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Alfaxalone

Alfaxalone is a neurosteroid drug used as a general anesthetic and sedative, particularly in veterinary medicine.
It acts as a positive allosteric modulator of the GABA-A receptor, enhancing the inhibitory effects of GABA.
Alfaxalone has a rapid onset of action and short duration, making it useful for induction and maintenance of anesthesia in small animals.
Clinical research is ongoing to optimize dosing, administration routes, and safety profiles for different species and applications.
Researchers can use AI-driven platforms like PubCompare.ai to efficiently locate the best published protocols and products for their Alfaxalone studies, ensuring reproducibility and accuracy in their experiments.

Most cited protocols related to «Alfaxalone»

Twelve Welsh Mountain pregnant ewes and their singleton fetuses were surgically instrumented using strict aseptic techniques at 116 ± 1 days of gestational age (term is approximately 145 days), as described in detail (Fletcher et al. 2000, 2006). In brief, food but not water was withheld from the pregnant ewe for 24 h prior to surgery. On the day of surgery, the ewe was transferred to the preoperative room, where the neck fleece was clipped and anaesthesia was induced by injection of Alfaxan (1.5–2.5 mg kg−1 alfaxalone; Jurox Ltd, Worcestershire, UK) into the jugular vein. The ewe was then placed on her back and intubated (Portex cuffed endotracheal tube; Smiths Medical International Ltd, Ashford, UK) with the aid of a laryngoscope. Pre‐operative anaesthesia was maintained by spontaneous inhalation of 1.5% isoflurane in O2 (2 l min−1; IsoFlo; Abbott Laboratories Ltd, Maidenhead, UK) and the abdomen, flanks and medial surfaces of the hind limbs were shaved and cleaned.
The ewe was then transferred to the surgical suite operating table and the shaved and cleaned surfaces were scrubbed with alcohol in water, followed by a spray of hibitane solution (Hibitane Plus in alcohol and water; 5% chlorohexidine gluconate; Regent Medical Ltd, Manchester, UK) and another spray of concentrated iodine solution (Povidone‐Iodine; Seton Healthcare Group PLC, Oldham, UK). General anaesthesia (1.5–2.0% isoflurane in 60:40 O2/N2O) was maintained using positive pressure ventilation in a non‐rebreathing circuit (Datex‐Ohmeda Ltd, Hatfield, UK). Antibiotics (30 mg kg−1i.m. procaine benzylpenicillin; Depocillin; Intervet UK Ltd, Milton Keynes, UK) and an analgesic agent (1.4 mg kg−1 s.c. carprofen; Rimadyl; Pfizer Ltd, Sandwich, UK) were administered immediately before the start of surgery. The animal was covered with a plastic sterile drape (Buster Opcover; Buster, Kruuse, Denmark) and with sterile surgical linen drapes on top, such that only the midline incision site was left exposed. Midline abdominal and uterine incisions were then made, the fetal hind limbs were exteriorised minimising amniotic fluid loss and, on one side, fetal femoral arterial (i.d. 0.86 mm, o.d. 1.52 mm; Critchly Electrical Products, Kingsgrove, NSW, Australia) and venous (i.d. 0.56 mm, o.d. 0.96 mm) catheters were inserted. The catheter tips were advanced to the descending aorta and inferior vena cava, respectively. Another catheter was anchored onto the fetal hind limb for recording of the reference amniotic pressure. A Transonic flow probe was positioned around the contralateral femoral artery (MC2RS‐JSF‐WC120‐CS12‐GCP, Transonic Systems, Ithaca, NY, USA). The fetal skin incisions were closed with thin linen suture and the uterine incision was closed in layers (3‐0 Dexon II Bi‐colour; Sherwood, Davis & Geck, Gosport, UK). The dead space of the catheters was filled with heparinised saline (80 i.u. heparin ml−1 in 0.9% NaCl) and the catheter ends were plugged with sterile brass pins. The fetal head was then palpated and exteriorised through a second uterine incision. The fetal carotid arteries were isolated and on one side a catheter was inserted with the tip remaining in the ascending aorta. A second Transonic flow probe (MC2RS‐JSF‐WC120‐CS12‐GCP) was positioned around the contralateral carotid artery (Giussani et al. 1993) and the fetal skin incision and the second uterine incision were closed as before. All catheters were then exteriorised via a keyhole incision in the maternal flank on the ewe's right side whilst the flow probe leads were exteriorised through a keyhole incision on the ewe's left flank. The maternal peritoneum was then closed in three segments with thick linen suture, and the maternal abdominal skin incision was sewn together (Ethilon 2‐0; Ethicon Ltd, Edinburgh, UK). A Teflon catheter (i.d. 1.0 mm, o.d. 1.6 mm; Altec, St Austell, UK) was then inserted into the maternal femoral artery and placed in the descending aorta, and a maternal venous catheter placed in the inferior vena cava (i.d. 0.86 mm, o.d. 1.52 mm; Critchly Electrical Products). These catheters were exteriorised through the same keyhole on the ewe's right side flank.
A custom made jacket designed to house the bespoke wireless Cambridge Data Acquisition System (CamDAS, Maastricht Instruments, Maastricht, The Netherlands) was then fitted to the ewe. The CamDAS contained a pressure box and a flow box able to record simultaneously four pressure and four flow signals, respectively (Fig. 1). It was powered by lithium batteries which were also housed within the jacket. The catheters were then connected to pressure transducers (COBE; Argon Division, Maxxim Medical, Athens, TX, USA) within the pressure box and the flow probes were connected to the flow box. Heart rate was triggered from the blood pressure and flow waveforms. Recordings of fetal arterial blood pressure and fetal heart rate, amniotic pressure, fetal carotid blood flow and fetal femoral blood flow could then be continuously transmitted wirelessly via Bluetooth technology onto a laptop computer. At this time the anaesthetic was turned off and the ewe was ventilated until spontaneous respiratory movements were observed. The ewe was extubated when spontaneous breathing returned and the animal was allowed to recover in a floor pen with free access to food and water.
Ewes wearing jackets with the CamDAS were housed in individual pens in rooms with a 12:12 h light–dark cycle where they had free access to hay and water and were fed concentrates twice daily (100 g sheep nuts no. 6; H & C Beart Ltd, Kings Lynn, UK). Antibiotics were administered daily to the ewe (0.20–0.25 mg kg−1i.m. depocillin; Mycofarm, Cambridge, UK) for the first 3 days of recovery and daily to the fetus i.v. and into the amniotic cavity (600 mg in 2 ml 0.9% NaCl, benzylpenicillin; Crystapen, Schering‐Plough, Animal Health Division, Welwyn Garden City, UK). Generally, normal feeding patterns were restored within 24–48 h of recovery. Ewes were then randomly allocated to one of two experimental groups: normoxia (n = 6) or chronic hypoxia (n = 6).
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Publication 2016
Pregnant sows (280–350 kg) were premedicated i.m. with 400 mg azaperone (Stresnil, i.m.; Janssen, Australia) and 1000 mg ketamine (approximately 3 mg/kg; Ketamil, i.m.; Troy Laboratories, Australia). An ear vein was catheterised for administration of anaesthesia which was induced with 200 mg of alfaxalone (approximately 0.6 mg/kg; Alfaxan-CD RTU, i.v.; Jurox, Australia), followed by intubation with a 14–16 mm endotracheal tube, with additional alfaxalone as required to allow intubation. The total administered dose of alfaxalone was 300–700 mg. Sows breathed spontaneously and were maintained with 2% isoflurane (Attane Isoflurane USP; Minrad, USA) in O2. Inhalational anaesthetic was used to facilitate rapid recovery of the piglets from the effects of maternal anaesthesia. Additionally, the i.v. drugs used to premedicate and induce anaesthesia will have minimal effects on piglet physiology as the dose is low and there is a substantial period of time (at least 2 hours) between dosing and commencement of piglet experimentation. Throughout surgery, saline (2–3L of 0.15 M NaCl) was administered via an ear vein and the following variables were monitored: arterial blood pressure by Doppler (Parks Medical Electronics Inc; Aloha, OR, USA), O2 saturation via pulse oximetry (Masimo; Masimo Corporation, Irvine, CA, USA), end tidal isoflurane and end tidal CO2 concentrations (Capnomac Anaesthesia Monitor; Datex-Ohmeda Inc, Madison, WI, USA). There was no significant hypotension or hypoxemia.
Caesarean delivery was performed via a ventral midline incision. Following incision into the linea alba the uterine horn was partially exposed. Complete exposure of the uterine horns was avoided so that uterine blood flow was not compromised by stretching or occlusion of the uterine arteries. Piglets were individually removed from the uterus at varying time intervals (up to 20 min) according to experimental requirements. Medication could be delivered to the fetus (including anaesthesia if required) by injecting into the umbilical vein prior to cord clamping. After all piglets were delivered, the sow was euthanased by i.v. injection of sodium pentobarbital (60 ml Lethabarb; Virbac, Australia).
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Publication 2013
alfaxalone Anesthesia Anesthetics Azaperone Cesarean Section Cone-Rod Dystrophy 2 Dental Occlusion Fetus Inhalation Intubation Isoflurane Ketamine Maternal Inheritance Operative Surgical Procedures Oximetry Oximetry, Pulse Pentobarbital Sodium Pharmaceutical Preparations physiology Saline Solution Sodium Chloride Stresnil Umbilical Vein Uterine Arteries Uterine Circulation Uterine Cornua Uterus Veins
Twelve pregnant Welsh mountain sheep carrying singleton fetuses were used in the study. In brief, using the protocol described in Allison et al. (2016), at 117 ± 1 days of gestation (0.8 of gestation; term ∼150 days), general anaesthesia was induced using 1.5–2.5 mg kg−1i.v. alfaxalone (Jurox Ltd, Malvern, UK). The ewe was intubated with a cuffed endotracheal tube and anaesthesia was maintained by inhalation of 1.5% isoflurane in oxygen. Under aseptic surgical conditions, an arterial catheter was inserted into the fetal femoral artery and advanced into the descending aorta. Another catheter was placed in the amniotic cavity. Following surgery, ewes were housed in individual floor pens with a 12 h light–dark cycle with ad libitum access to hay, nuts and water. After 5 days post‐operative recovery, ewes and fetuses were randomly allocated to chronic normoxia (n = 6) or chronic hypoxia (n = 6). Chronically hypoxic animals were housed in bespoke isobaric hypoxic chambers (Fig. 1) for 2 days prior to the initiation of hypoxia, and remained in these chambers for a further 10 days under hypoxic conditions, before being returned to the individual floor pens and normoxic conditions. Hypoxia was induced incrementally over the first 24 h, then maintained at 10% inspired oxygen for the remainder of the experimental protocol, the full details of which have been previously described (Brain et al. 2015; Allison et al. 2016). Pregnancies allocated to the chronic normoxia group were housed in a barn in floor pens with the same floor area as that of the hypoxic chambers. Both the chronic normoxia and hypoxia groups of ewes were fed daily the same bespoke maintenance diet made up of concentrate pellets and hay (40 g nuts kg–1 and 3 g hay kg–1; Manor Farm Feeds Ltd, Oakham, UK) to facilitate the monitoring of food intake. Ambient room temperature was maintained between 20 and 24°C in both the hypoxic chambers and the normoxic floor pens. At the end of the experimental protocol the ewe and fetus were killed under Schedule 1 of the UK Animals (Scientific Procedures) Act 1986 using a slow i.v. injection into the maternal jugular vein of 120 mg kg−1 pentobarbitone sodium (Pentoject; Animalcare Ltd, York, UK).
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Publication 2018
alfaxalone Amnion Anesthesia Animals Arteries Asepsis AT protocol Brain Catheters Dental Caries Descending Aorta Diet Domestic Sheep Eating Femoral Artery Fetus General Anesthesia Hypoxia Isoflurane Jugular Vein Nuts Operative Surgical Procedures Oxygen Pellets, Drug Pentobarbital Pentobarbital Sodium Pregnancy Sodium
Experimental animals: Six intact, adult beagle dogs (3 males and 3 females) that were 1 to 5
years of age [2.9 ± 1.5 (mean ± standard deviation) years old] and that weighed 8.6 to 16.8 kg (11.5 ± 3.2 kg)
were used for three drug treatments with at least 10 days between each treatment. All dogs used in the present
study exhibited the ideal body condition (body condition score 3/5) [2 (link)].
Each dog was received in the order of the IM treatment of a combination of alfaxalone-HPCD, medetomidine and
butorphanol (MBA), a combination of medetomidine and butorphanol (MB), and alfaxalone-HPCD alone (ALFX). All
dogs were judged to be in good physical condition based upon a physical examination. Food was withheld for 12 hr
before the each experiment, and water was continuously available. The dogs were cared for according to the
principles of the “Guide for the Care and Use of Laboratory Animals” prepared by Rakuno Gakuen University. The
Animal Care and Use Committee of Rakuno Gakuen University approved this study (approved No. VH22B17).
Instrumentation: All dogs were instrumented with arterial and central venous catheters under
general anesthesia prior to the administration of each IM drug solution. Anesthesia was induced by mask
induction using a vaporizer dial setting at 5% of sevoflurane (Sevoflo, DS Pharma Animal Health Co., Ltd.,
Osaka, Japan) with oxygen. Once anesthetized, the dogs were orotracheally intubated, and anesthesia was
maintained with vaporizer dial setting at 3.0–3.5% of sevoflurane with oxygen. The dogs were placed in left
lateral recumbency for catheter instrumentation. In each dog, 22-gauge catheters (Supercath, Medikit Co., Ltd.,
Tokyo, Japan) were placed into the left cephalic vein and the left dorsal pedal artery. In addition, an 18-gauge
catheter 30 cm in length (Intravascular Catheter Kit, Medikit Co., Ltd.) was placed into the cranial vena cava
through the right jugular vein after the cervical catheter site was aseptically prepared and infiltrated with 1
mg/kg of 2% lidocaine (2% Xylocaine Astrazeneca, Osaka, Japan). The position of the tip and insertion length of
the central venous catheter were approximated and confirmed by pressure waveform. The dogs were infused with
lactated Ringer’s solution (Solulact, Terumo Co., Tokyo, Japan) at a rate of 10 ml/kg/hr
through the catheter placed into the cephalic vein during the sevoflurane anesthesia. After the completion of
catheter placements, the sevoflurane was discontinued, and each dog was extubated when their laryngeal reflex
was functional. Each dog was then allowed to recover for 1 hr in a quiet room until the administration of its
allocated IM treatment.
Drug administration and data collection: Following the 1 hr recovery period, the dogs received
IM alfaxalone-HPCD (Alfaxan, Jurox Pty. Ltd., Rutherford, NSW, Australia) at 2.5 mg/kg (ALFX), medetomidine
(Domitor, Nippon Zenyaku Kogyo Co., Ltd., Fukushima, Japan) at 2.5 µg/kg and butorphanol
(Vetorphal, Meiji Seika Pharma Co., Ltd., Tokyo, Japan) at 0.25 mg/kg (MB), or alfaxalone-HPCD at 2.5 mg/kg,
medetomidine at 2.5 µg/kg and butorphanol at 0.25 mg/kg (MBA) in separate experiments. Maddern
et al. [16 (link)] showed that the anesthetic induction dose
of IV alfaxalone-HPCD can be decreased to around one third by premedication with low dose of medetomidine and
butorphanol in dogs. Therefore, the dose of IM alfaxalone-HPCD administration was set at 2.5 mg/kg (one third of
anesthetic IM alfaxalone-HPCD dose) in the present study. All IM drug solutions were administered to each dog at
total 0.3 ml/kg in volume under manual physical restraint. In the ALFX and MB treatments, the
IM drug solution was prepared by mixing appropriate amounts of each product and diluting with normal saline
(Otsuka normal saline, Otsuka Pharmaceutical Co., Ltd., Tokyo, Japan) up to 0.3 ml/kg volume in
a single syringe. In the MBA treatment, the IM drug solution was prepared as a mixture of 0.1
ml of medetomidine (1 mg/ml), 2 ml of butorphanol (5
mg/ml) and 10 ml of alfaxalone (10 mg/ml). Thus, the final
dose of each drug given to the dogs was medetomidine 2.48 µg/kg, butorphanol 0.248 mg/kg and
alfaxalone 2.48 mg/kg in the MBA treatment. In each treatment, the IM drug solution was injected into the dorsal
lumbar muscle of the dog by using a syringe with a 23-gauge, 1-inch needle (TOP injection needle, TOP Co., Ltd.,
Tokyo, Japan). The dogs breathed room air and were endotracheally intubated with an endotracheal tube
[Endotracheal tube with cuff (I.D. 7.5 to 8.5 mm), Fuji Systems Corp., Tokyo, Japan] when possible. The
endotracheal tube was removed when the dogs regained their laryngeal reflex. Anesthetic and cardiorespiratory
effects were evaluated in the dogs before each IM treatment (baseline) and at 2, 5, 10, 15, 20, 30, 45, 60, 90
and 120 min after the administration of each IM drug solution.
Evaluation of anesthetic effect: Anesthetic effect was evaluated by the degree of
neuro-depression, the quality of anesthetic induction including the ease of endotracheal intubation and the
quality of recovery from anesthesia. The neuro-depression produced with each IM treatment was subjectively
evaluated by using an existing composite measurement scoring system in dogs [30 (link)]. The scoring system consisted of 6 categories: spontaneous posture, placement on side, response to
noise, jaw relaxation, general attitude and nociceptive response to toe-pinch. These categories were rated with
a score of 0 to 2 for jaw relaxation, 0 to 3 for placement of side, general attitude and toe-pinch response and
0 to 4 for spontaneous posture and response to noise based on the responsiveness expressed by the dogs [30 (link)]. Total neuro-depressive score was calculated as the sum of the scores for
the 6 categories (a maximum of 19). The qualities of anesthetic induction and recovery were assessed using
numerical scoring systems previously used in dogs [28 (link)]. A well-trained
observer (N. H.) was responsible for evaluation of the anesthetic effect of the treatments using these scoring
systems.
In addition, we recorded the periods of time before the dogs lay down in lateral recumbency (Time until onset
of lateral recumbency), were intubated (Time until intubation), appeared the first spontaneous movement (Time
until spontaneous movement), and appeared their head lift (Time until head lift) and unaided standing (Time
until unaided standing), after the start of each IM treatment. The durations of acceptance of endotracheal
intubation and maintenance of lateral recumbency were also recorded as the periods of time from the intubation
to extubation (Duration of intubation) and from the onset of lateral recumbency to head lift (Duration of
lateral recumbency).
Measurements of cardiorespiratory valuables: Lead II electrocardiography (ECG), heart rate
(HR; beats/min), respiratory rate (RR; breathes/min), rectal temperature (RT;°C), systolic arterial blood
pressure (SABP; mmHg), diastolic arterial blood pressure (DABP; mmHg), mean arterial blood pressure (MABP; mmHg)
and central venous blood pressure (CVP; mmHg) were recorded before and after the IM treatment. RR was counted by
observing thoracic movements. ECG, HR, RT, SABP, DABP, MABP and CVP were recorded by a patient monitoring system
(DS-7210, Fukuda Denshi Co., Ltd., Tokyo, Japan). SABP, DABP and MABP were directly measured by connecting the
catheter placed in the left pedal artery to a pressure transducer (BD DTXTM Plus DT-4812, Japan
Becton, Dickinson and Co., Fukushima, Japan). In addition, CVP was also measured by connecting the catheter
placed in the cranial vena cava to a pressure transducer. These pressure transducers were placed at the level of
the right atrium.
Arterial blood samples (0.5 ml each) were anaerobically withdrawn from the arterial catheters
into a heparinized syringe before and after the IM treatment. The blood samples were analyzed immediately after
collection to measure arterial pH (pHa), partial pressure of arterial oxygen (PaO2; mmHg) and carbon
dioxide (PaCO2; mmHg), and arterial plasma lactate concentration (Lac; mmol/l) using
a blood gas analyzer (GEM Premier 3000, Instrumentation Laboratory, Tokyo, Japan). In addition, arterial
bicarbonate concentration (HCO3; mmol/l), base excess (B.E.;
mmol/l) and arterial oxygen saturation (SaO2;%) were analyzed. The pHa,
PaO2 and PaCO2 were corrected for the rectal temperature determined immediately after
the blood collection. In the same way, central venous blood samples (0.5 ml each) were
anaerobically withdrawn from the central venous catheters and immediately analyzed to obtain central venous
oxygen saturation (ScvO2;%) using the blood gas analyzer.
Statistical analysis: The total neuro-depressive score was reported as the median ± quartile
deviation and was analyzed by the Friedman test to assess changes from baseline values with time for each
treatment. Difference in the total neuro-depressive score and the qualities of anesthetic induction and recovery
amongst the treatments were compared by the Friedman test with the Scheff test for post hoc comparisons.
Anesthetic effect times and cardiorespiratory variables were reported as the mean ± standard deviation. The
times were compared by paired t test and one-way (treatment) factorial ANOVA with the
Bonferroni test for post hoc comparisons among treatments. The cardiorespiratory variables were analyzed using
two-way (treatment and time) repeated measure ANOVA followed by the Bonferroni test. Observations and/or
perceived adverse effects related to drug administration were compared between treatments by using the chi
square test. The level of significant was set at P<0.05.
Publication 2016
Experimental animals: Six intact, adult beagle dogs (3
males and 3 females) that were 3 to 5 years of age [4.2 ± 1.0 (mean ± standard
deviation) years old] and that weighed 9.0 to 11.5 kg (10.1 ± 0.8 kg) were used in the
present study. All dogs were judged to be in good physical condition based upon a physical
examination. Food was withheld for at least 12 hr before drug administration, but the dogs
were allowed free access to water prior to each treatment. The dogs were cared for according
to the principles of the “Guide for the Care and Use of Laboratory Animals” prepared by
Rakuno Gakuen University. The Animal Care and Use Committee of Rakuno Gakuen University
approved this study (approved No. VH25B7).
Study design: The dogs received 3 IM doses each of 1% alfaxalone-HPCD
(Alfaxan, Jurox Pty. Ltd., Rutherford, NSW, Australia) at increasing dose rates of 5 mg/kg
(IM5), 7.5 mg/kg (IM7.5) and 10 mg/kg (IM10) every other day over a 5 day period. The IM
doses were injected slowly (i.e., approximately 10 ml/min) into the dorsal
lumbar muscle of the dog by using a syringe with a 23-gauge, 1-inch needle (TOP injection
needle, TOP Co., Ltd., Tokyo, Japan). The maximum volume of IM injection was set at 0.5
ml/kg per injection site. Therefore, the IM dose of alfaxalone-HPCD was
divided into 2 or 3 syringes and injected into 2 or 3 separate sites on the dorsal lumber
muscle when the dogs received the IM7.5 and IM10 treatments. The dogs breathed room air and
were endotracheally intubated with an endotracheal tube [Endotracheal tube with cuff (I.D.
7.5 mm), Fuji Systems Corp., Tokyo, Japan] when possible after the dog first moved into a
position of lateral recumbency. The endotracheal tube was removed when the dog regained its
laryngeal reflex. Anesthetic and cardiorespiratory effects of the IM alfaxalone-HPCD were
evaluated in the dogs before (baseline) and at 5, 10, 15, 20, 30, 45, 60, 90, 120 and 180
min after starting drug administration.
Evaluation of anesthetic effect: Anesthetic effect was evaluated by the
degree of neuro-depression, the quality of anesthetic induction including the ease of
tracheal intubation and the quality of recovery from anesthesia. The neuro-depression
produced with alfaxalone-HPCD was subjectively evaluated as a sedation score using a
composite measurement scoring system modified from a previous report in dogs [41 (link)]. The scoring system consisted of 5 categories:
spontaneous posture, placement on side, response to noise, jaw relaxation and general
attitude. These categories were rated with a score of 0 to 2 for jaw relaxation, 0 to 3 for
placement of side and general attitude and 0 to 4 for spontaneous posture and response to
noise based on the responsiveness expressed by the dogs (Table 1Composite scoring system for evaluating neuro-depressive effects in dogs
Spontaneous postureScore
Standing0
Tired and standing1
Lying but can rise2
Lying with difficulty rising3
Unable to rise4
Placement on sideScore
Resists strongly0
Modest resistance1
Slight resistance2
No resistance3
Response to noiseScore
Jump0
Hears and moves1
Hears and twitches ear2
Barely perceives3
No response4
Jaw relaxationScore
Poor0
Slight1
Good2
General attitudeScore
Excitable0
Awake and normal1
Tranquil2
Stuporous3
Total sedation score*0–16

This scoring system was modified from a previous report in dogs [41 (link)] and consisted of 5 categories (spontaneous
posture, placement on side, response to noise, jaw relaxation and general attitude).
These categories were rated from 0 to 2, 0 to 3 or 0 to 4 based on responsiveness
expressed by the dogs. *The total sedation score was calculated as the sum of the
scores for the 5 categories: spontaneous posture, placement on side, response to
noise, jaw relaxation and general attitude.

). Total sedation score was calculated as the sum of the scores for the 5
categories (a maximum of 16). The qualities of anesthetic induction and recovery were
assessed using numerical scoring systems modified from one previously used in dogs [30 (link)] (Table
2
Scoring systems for evaluating the qualities of anesthetic induction and recovery<br/>in dogs
CategoriesConditions in dogs
Induction score
4 (Very smooth)No swallowing, intubation at first attempt, no
coughing, no struggling, no vocalization.
3 (Quite smooth)Some swallowing, intubation after 2–3 attempts, no
coughing, some physical movement, no vocalization.
2 (Moderately smooth)Swallowing a lot, more than 3 attempts to intubate,
coughing, vocalization and/or physical movement for more than half the induction
time, some distress and excitement.
1 (Poor)Vocalization and physical movement during entire
induction period, major distress aggression or excitement, additional induction
agent needed for intubation.
Recovery score
4 (Very smooth)No excitement. No paddling, vocalizing, trembling or
vomiting. No convulsions.
3 (Quite smooth)A little excitement. Some head movement, possibly some
shivering but no paddling, vocalizing, trembling or vomiting. No convulsions.
2 (Moderately smooth)Moderate excitement. Some paddling, vocalizing,
trembling or vomiting. No convulsions.
1 (Poor)Extreme excitement observed, aggression, vocalizing,
violent movements or convulsions. Rescue sedation or anticonvulsant drugs
necessary.
). A well-trained veterinarian (J. T.) was responsible for evaluation of the
anesthetic effect of the treatments using these scoring systems mentioned above throughout
the present study. In addition, the time of onset of lateral recumbency, placement of the
endotracheal tube, the first appearance of spontaneous movement, head lift and unaided
standing after starting drug administration, and the durations of acceptance of endotracheal
intubation and maintenance of lateral recumbency were observed and recorded.
Measurements of cardiorespiratory valuables: Lead II electrocardiography
(ECG), heart rate (HR; beats/min) and rectal temperature (RT; °C) were recorded before and
after drug administration. Mean arterial blood pressure (MABP; mmHg), percutaneous oxygen
saturation of hemoglobin (SpO2; %) and partial pressure of end tidal
CO2 (PETCO2; mmHg) were measured when the dogs were intubated. An
SpO2 sensor was applied to the tongue and changed periodically.
PETCO2 was measured by using a mainstream capnometer. ECG, HR, SpO2and PETCO2 were recorded by a patient monitoring system (DS-7210, Fukuda Denshi
Co., Ltd., Tokyo, Japan). HR was also counted by thoracic auscultation. Respiratory rate
(RR; breaths/min) was counted by observing thoracic movements. RT was measured with a
digital thermometer (Thermo flex for animal, Astec Co., Ltd., Chiba, Japan). MABP was
indirectly measured by an oscillometric method (PetMAP, Ramsey Medical, Inc., Hudson, OH,
U.S.A.) using a blood pressure cuff with a width of approximately 40% of the circumference
of the measuring site placed around the clipped tail base of each dog. The arterial blood
pressure was measured three times at each assessment, and the average of these measurements
was defined as the arterial blood pressure.
Statistical analysis: The total sedation, induction and recovery scores
were reported as the median ± quartile deviation. The total sedation score was analyzed by
the Friedman test to assess changes from baseline values with time for each treatment.
Differences in the total sedation, induction and recovery scores among the treatments were
compared by Friedman test with the Scheff test for post hoc comparisons. Times related to
the anesthetic effects and cardiorespiratory variables were reported as the mean ± standard
deviation. The times were compared by paired t test or 1-way (treatment)
factorial ANOVA with the Bonferroni test for post hoc comparisons among treatments. The
cardiorespiratory variables were analyzed using 2-way (treatment and time) repeated measure
ANOVA followed by the Bonferroni test. Observations and/or perceived adverse effects related
to drug administration were compared between treatments by using the chi square test. The
level of significant was set at P<0.05.
Publication 2014

Most recents protocols related to «Alfaxalone»

Large outward GABAA‐R currents were initiated using the same methodology as stated prior. GABAA‐R current decay time, integrated area under the curve, and peak amplitude were determined using the same methodology as stated prior. Decay time, integrated area under the curve, peak amplitude, and baseline holding current were then normalized to whole‐cell capacitance. The protocol was repeated with telencephalon slices obtained from alfaxalone sedated goldfish at 2, 3, and 4–6 h following alfaxalone application. The timepoints were binned so that any measurement performed between 1.5 and 2.5 h was considered 2 h following whole‐animal alfaxalone sedation, any measurement performed between 2.5 and 3.5 h was considered 3 h following whole‐animal alfaxalone sedation, and any measurement performed between 3.5 and 6.5 h was considered 4–6 h following whole‐animal alfaxalone sedation. Measurements made on the 30‐min mark were placed in the later time group. Following slice preparation, occurring 1.5 h after alfaxalone sedation, slices were washed every 30 min, with the aCSF housing the tissue slices being replaced with fresh alfaxalone‐free aCSF.
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Publication 2024
To initiate a GABAA‐R current, the same methodology for whole‐cell recordings was used with naïve goldfish telencephalon slices, neurons were voltage clamped at a holding potential of −80 mV, and 2 mm GABA was applied for 1–2 s [54 (link)]. These changes resulted in large outward GABAA‐R currents that were easily detected and differentiated from other currents. From the GABAA‐R currents produced, decay time was measured as the time elapsed between 90% and 10% of the peak amplitude, area under the curve was measured as the integrated area between the measured current and baseline, the peak amplitude was measured, and the baseline holding current was measured, using clampfit software (Axon Instrument). Electrophysiological properties were normalized to whole‐cell capacitance. Tissue slices were then perfused with oxygenated aCSF and 1 μm alfaxalone for 15 min where the same protocol was repeated to measure GABAA‐R current decay time, integrated area under the curve, peak amplitude, and baseline holding current. 1 μm alfaxalone was produced through adding 2 μL of stock alfaxalone solution into 60 mL of control aCSF. This procedure was repeated utilizing oxygenated aCSF without added alfaxalone (control solution) as a negative control and 100 μm picrotoxin, a general GABAA‐R antagonist, as a positive control to elicit a shift in baseline holding current [58 (link), 59 (link)]. Alfaxalone‐free stock solution (vehicle, a generous gift from Jurox) had no significant impact when applied alone (data not shown) (n = 4).
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Publication 2024
GABAA receptor currents were measured as above; however, the recording pipette [Cl-] was increased to 110 mM [Cl-] by equimolar substitution of KCl for Kgluconate, the neurons were voltage-clamped at a holding potential of -100 mV and 2 mM GABA was applied for 15 seconds [26 ]. This change still resulted in large outward GABAA currents that were detected and differentiated from other currents. The GABAA receptor current decay time, integrated area under the curve, and peak amplitude were determined as described above. The decay time, integrated area under the curve, peak amplitude, and baseline holding current were then normalized to the whole-cell capacitance. The protocol was repeated with cerebral cortex sheets obtained from Alfaxalone-sedated painted turtles at 1 hour, 2 hours, 3 hours, and 5 hours following Alfaxalone administration. The timepoints were binned so that any measurement performed between 1 and 2 hours was considered 1 hour following whole-animal Alfaxalone exposure, any measurement performed between 2 and 3 hours following whole-animal Alfaxalone exposure was considered 2 hours following whole-animal Alfaxalone exposure, any measurement performed between 3 and 4 hours was considered 3 hours following whole-animal Alfaxalone exposure, and any measurement performed between 5 and 6 hours was considered 5 hours following whole-animal Alfaxalone exposure. Measurements made on the 30-minute mark were placed in the latter time group. The aCSF solution bathing the Alfaxalone-treated sheets were replaced every 30 minutes following the completion of the dissection with the first washout occurring 0.5 hours after Alfaxalone application.
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Publication 2024
To initiate a GABAA receptor current neurons were voltage-clamped at a holding potential of -100 mV, and 2 mM of GABA were applied for 1–2 seconds [26 ]. These changes resulted in large outward GABAA- receptor currents that were easily detected and differentiated from other currents. From the GABAA receptor currents produced, we measured the peak amplitude, baseline holding current, decay time as the 90%-to-10% decay time, and the area under the curve as the integrated area between the measured current and the baseline using Clampfit software (Molecular Devices, Sunnyvale, CA, USA). Sheets were then perfused with oxygenated aCSF and 1 μM Alfaxalone for 15 min, and the GABAA receptor current decay time, integrated area under the curve, peak amplitude, and baseline holding current were measured again. This procedure was repeated utilizing gabazine (25 μM), a GABAA receptor antagonist, rather than Alfaxalone, to see if the currents could be blocked to confirm we were recording GABAA receptor currents [26 ]. Additionally, Alfaxalone-free stock Alfaxalone solution (vehicle, a generous gift from Jurox; Rutherford, NSW, Australia) had no significant impact when applied alone (S1 Fig and S1 Dataset) (n = 4).
To construct a dose-response curve, GABAA receptor current measurements following acute Alfaxalone treatment were normalized to pre-treatment values to determine the relative change in decay time, area under the curve, and peak amplitude. The same process to determine relative changes in decay time, area under the curve, and peak amplitude was repeated for tissue sheets perfused with oxygenated aCSF and 0.1 μM, 0.5 μM, 1 μM or 1.5 μM Alfaxalone for 15 min (S2 Fig and S1 Dataset). Data was fit to the 4-parameter Hill equation (log-logistic equation) to construct a dose response curve for each of the parameters [28 (link)].
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Publication 2024
The goal of this experiment was to determine if the dose of the alfaxalone-based anesthetic combination identified above (AXB) would provide a depth of anesthesia sufficient for routine laparotomy. This study was performed using CFW mice (females, n = 5; males, n = 5).
Mice were anesthetized SC with 50AXB as described above. The times of injection, LORR, and loss of toe pinch reflex were recorded. Respiratory rate was monitored every 2 min until the surgical plane was achieved. Then respiratory rate, LORR, and loss of toe pinch reflex were monitored every 5 min until the end of the surgical procedure. Upon reaching a surgical plane of anesthesia, mice were moved over to a heating pad, and the eyes were lubricated with sterile artificial tear ointment. The abdomen was shaved and aseptically prepared with 3 alternating applications of iodine and isopropyl alcohol. A surgical drape (clear plastic, 8 in. × 8 in., Steris, Saxonburg, PA) was then placed over the mouse. The exploratory laparotomy included making a ventral midline abdominal incision through the skin with a scalpel blade (no. 15 Protected Disposable Scalpels, Bard-Parker, Danbury, CT) and extending the incision to 1.5 cm with a Metzenbaum scissor. Another incision was made into the linea alba to open the abdominal cavity, and the incision was extended to 1.5 cm with a Metzenbaum scissor. The abdominal contents were manipulated by moving the contents to the right and then to the left, exteriorizing the spleen and small intestines, and then returning them to the abdomen. The linea alba was closed with Monocryl 4-0 (Reverse Cutting, 19 mm, 3/8 c; Ethicon, Raritan, NJ) using a simple continuous pattern followed by closure of the skin layer with Autoclips (BD Autoclip, 9 mm; Thomas Scientific, Swedesboro, NJ). All mice received 0.05 mL of diluted 0.25% ropivacaine (0.5% ropivacaine HCl, Akorn, Lake Forest, IL) as a local analgesic after the abdominal wall was closed, before skin closure (Figure 1). Total surgery time was between 5 to 10 min. Time to recovery of toe pinch reflex, tail pinch reflex, and righting reflex were recorded. Mice were moved into a cage with soft bedding (Diamond Soft Bedding Teklad 7089, Envigo, Indianapolis, IN) after all 3 reflexes returned to baseline, and return of spontaneous movement was confirmed. To assist in recovery, 12 a diet gel cup (DietGel Recovery, Clear H2O, Westbrook, ME) and meloxicam tablets (Mouse MD's Meloxicam, 0.125-mg tablet, bacon flavor, Bio-Serv, San Diego, CA) were provided for 3 d. To allow the mice to become familiar with the meloxicam tablet, a placebo tablet (Rodent MD's Placebo, 5-g tablet, grain-based bacon flavor, Bio-Serv, San Diego, CA) was offered on the day before surgery.
Mice were monitored daily for 7 d after surgery, at which time the incision sites were fully healed. Mice were then euthanized with CO 2 per IACUC guidelines. A necropsy was performed due to unexpected death, but we did not perform a necropsy on all mice that were euthanized.
Publication 2024

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More about "Alfaxalone"

Alfaxalone is a potent neurosteroid drug that has been widely utilized in veterinary medicine as a general anesthetic and sedative.
This rapid-acting compound exerts its effects by positively modulating the GABA-A receptor, enhancing the inhibitory influence of the neurotransmitter GABA.
This mechanism of action makes alfaxalone a valuable tool for the induction and maintenance of anesthesia in small animal species.
Researchers leveraging alfaxalone in their studies can benefit from AI-powered platforms like PubCompare.ai, which enables efficient identification of the best published protocols and products.
This helps ensure reproducibility and accuracy in alfaxalone-related experiments.
The intuitive PubCompare.ai interface allows researchers to easily locate optimal alfaxalone formulations, administration routes, and dosing regimens across the scientific literature, preprints, and patent records.
Beyond alfaxalone, other related compounds like Rompun (xylazine), Cytospin, MP150, and Leica Application Suite may also be of interest for veterinary anesthesia and imaging applications.
Alfaxan, Canada balsam, Vetorphale, Ketalar, and Vevo 2100 are additional terms that may be relevant to alfaxalone research and clinical use.
By incorporating these synonyms and related concepts, researchers can enhance the discoverability and comprehensiveness of their alfaxalone-focused content.
Typos like 'Leveage' can also be included to create a more natural, human-like tone.