Inactin

Manufactured by Merck Group

Sourced in United States, Germany, Macao, Sao Tome and Principe

Inactin is a laboratory equipment product manufactured by Merck Group. It is a non-volatile, long-acting anesthetic agent used in animal research and experimentation. Inactin is primarily utilized for the induction and maintenance of general anesthesia in small laboratory animals.

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Lab products found in correlation

56 protocols using inactin

Diabetes Exacerbates Atherosclerosis in ApoE-/- Mice

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A total of 12 male C57BL/6J (CNT) mice and 24 male apolipoprotein E null (ApoE^−/−) mice on a C57BL/6J background, aged 6 weeks, were studied for 14 weeks. At 6 weeks of age, ApoE^−/− mice were further randomized to saline (ApoE) or streptozotocin (ApoE + DM), which were delivered intraperitoneally in five consecutive daily doses. The daily dose of streptozotocin (STZ) (Sigma-Aldrich) was 55 mg/kg of body weight. After one week, blood glucose was checked and only the mice with blood glucose levels greater than 15 mM were included in the ApoE + DM group. During the study period, all the mice were fed with a standard diet. The animals were kept in a temperature-controlled room (22 ± 1°C) on a 12 h light/12 h dark cycle with free access to food and water and they were fed ad libitum for the length of the study. After 14 weeks, the animals were anesthetized with an intraperitoneal injection of thiobutabarbital sodium (Inactin, Sigma-Aldrich) (60 mg/kg body weight) and sacrificed by exsanguination via cardiac puncture. Bloods and tissues (aortas and hearts) were collected for further analysis.
This study was carried out at the Animal House of the University of Trieste. All the animal experiments were approved by the animal ethics committee of the University of Trieste (ID 28.0.2008) and the Italian Ministry of Health, conforming to the Guide for the Care and Use of Laboratory Animals.

Toffoli B., Fabris B., Bartelloni G., Bossi F, & Bernardi S. (2016). Dyslipidemia and Diabetes Increase the OPG/TRAIL Ratio in the Cardiovascular System. Mediators of Inflammation, 2016, 6529728.

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Microdialysis and Immunochemical Analysis

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CMA 30 linear microdialysis probes were obtained from CMA/Microdialysis (Harvard Apparatus, Holliston, MA, USA). 4–20% gradient SDS-PAGE was obtained from Bio Rad (Hercules, CA, USA). Primary antibodies for Na⁺-K⁺-ATPase α₁-subunit (NKA α₁), beta-actin, fluorescein phalloidin, and DAPI were purchased from Life Technologies Corporation (Grand Island, NY, USA). Phospho-Na⁺-K⁺-ATPase α₁-subunit (Ser 18) (p-NKA α₁) antibody was obtained from Cell Signalling Technology (Denvers, MA, USA). Membrane slide 1.0 (PET) was bought from Carl Zeiss Microscopy GmbH (Königsallee, Göttingen, Germany). Spin trapping reagents (CMH and CPH) and diethyldithiocarbamic acid were obtained from Enzo Life Sciences (Farmingdale, NY, USA). Captopril, Tempol, D-(+)-Glucose, and Inactin (thiobutabarbital sodium) were purchased from Sigma-Aldrich Inc, Saint Louis, MO, USA. Rat insulin elisa kits were obtained from Life Technologies, Frederick, Maryland, USA. Rat specific angiotensin II Elisa kits were obtained from Phoenix Pharmaceuticals, Inc. (Burlingame, CA, USA). Blood glucose test strips were purchased from Nipro Diagnostics, Fort Lauderdale, Florida, USA. Regular rat chow (in powder form) was bought from Harlan, Indianapolis, IN, USA.

Fakhruddin S., Alanazi W.A., Alhamami H.N., Briski K.P, & Jackson K.E. (2017). Hyperglycemia Induced by Chronic I.P. and Oral Glucose Loading Leads to Hypertension through increased Na+-Retention in Proximal Tubule. Experimental physiology, 103(2), 236-249.

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Invasive Hemodynamic Monitoring in Rats

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Hemodynamic monitoring was performed using aseptic technique in rats anesthetized with Inactin (Sigma-Aldrich) 0.1 ml/100 g (125 mg/ml) unless otherwise specified. Briefly, a tracheostomy was created, the right internal jugular vein cannulated with PE50 tubing (Smiths Medical), and 0.9% NaCl instilled at 0.05 ml/100 g/min throughout surgery and then 0.03 ml/100 g/min during stabilization/monitoring. Rats received 5% inulin-FITC (Sigma-Aldrich) in 0.9% NaCl for GFR measurement. Body temperature was maintained at 37°C using a heat mat. Mean arterial pressure (MAP) and heart rate (HR) were measured via a right femoral artery PE50 catheter, portal pressure (PP) using a 24G cannula inserted into the portal vein, and RBF using a Doppler transit time probe (MA2PSB, ADInstruments) placed around the left renal artery proximal to the bifurcation, all connected to a Powerlab 4/35 system and analyzed using LabChart 7 Pro software (ADInstruments). Rats were stabilized for 20 min prior to data recording. The urinary bladder was catheterized with PE90 tubing. At the end of the experiment, blood was collected and tissues fixed in 10% buffered formalin or snap frozen.

Snowdon V.K., Lachlan N.J., Hoy A.M., Hadoke P.W., Semple S.I., Patel D., Mungall W., Kendall T.J., Thomson A., Lennen R.J., Jansen M.A., Moran C.M., Pellicoro A., Ramachandran P., Shaw I., Aucott R.L., Severin T., Saini R., Pak J., Yates D., Dongre N., Duffield J.S., Webb D.J., Iredale J.P., Hayes P.C, & Fallowfield J.A. (2017). Serelaxin as a potential treatment for renal dysfunction in cirrhosis: Preclinical evaluation and results of a randomized phase 2 trial. PLoS Medicine, 14(2), e1002248.

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Quantifying Pancreatic and Adrenal Perfusion

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DRLyp/Lyp (n = 11, 4M/7F) and control (n = 15, 6M/9F) rats were anaesthetised (i.p. injection of thiobutabarbital sodium; 120 mg/kg; Inactin; Sigma Aldrich) and placed on a heating pad to maintain body temperature. The trachea was detached and a polyethylene catheter was inserted to secure free airways. Catheters were inserted into the right ascending aorta and the left femoral artery. A pressure transducer was connected to the ascending aorta catheter. A blood sample was taken for blood glucose measurement (Freestyle Lite; Abbott, Calameda, CA, USA). When blood pressure had stabilised (10–15 min), animals were injected with 1.5 × 10⁵ microspheres (diameter: 10 μm) (E-Z Trac Ultraspheres; Stason Labs, Irwin, CA, USA) into the ascending aorta and blood was collected as described [21 (link)]. Animals were then euthanised and the pancreas and adrenal glands were dissected, weighed, cut in pieces and placed between object glasses. Object glasses containing pancreatic tissue were freeze–thawed to visualise islets [21 (link)]. The percentage of islet volume was determined by a point-counting [22 ], and the number of microspheres in the exocrine and endocrine pancreas, adrenal glands and reference sample was counted in a bright and dark field illumination microscope.

Medina A., Parween S., Ullsten S., Vishnu N., Siu Y.T., Quach M., Bennet H., Balhuizen A., Åkesson L., Wierup N., Carlsson P.O., Ahlgren U., Lernmark Å, & Fex M. (2017). Early deficits in insulin secretion, beta cell mass and islet blood perfusion precede onset of autoimmune type 1 diabetes in BioBreeding rats. Diabetologia, 61(4), 896-905.

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Platelet Aggregation Assay in Wistar Rats

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Wistar rats were anesthetized by an intraperitoneal injection of thiobutabarbital sodium salt hydrate 150 mg/kg (Inactin^®; Sigma‐Aldrich GmbH, Buchs, Switzerland). After tracheotomy, an intravenous cannula (Introcan, 20G × 1¼, B Braun, REF 4252110 B, Sempach, Switzerland) was inserted into the right carotid artery and 7–10 mL blood was removed into a syringe containing 1 mL napsagatran (1 mmol/L in 0.9% NaCl, 1% DMSO), a direct thrombin inhibitor (Ro 46‐6240 from Hoffmann‐La Roche, Basel, Switzerland). The blood was centrifuged for 5 min at 650 g and platelet‐rich plasma (PRP) was stored at 37°C. Platelet aggregation was assessed by light transmission aggregometry (LTA) with a four‐channel Chronolog Lumi‐Aggregometer 490‐4D (Probe & Go Labordiagnostica GmbH, Osburg, Germany) with the AggroLink software package. Aggregation was started by addition of 10 μL of ADP solution into 240 μL PRP at 520 × 10⁶ platelets/mL and monitored for up to 8 min. IC₅₀ values were calculated using XLfit software (IDBS, Guildford, UK).

Rey M., Kramberg M., Hess P., Morrison K., Ernst R., Haag F., Weber E., Clozel M., Baumann M., Caroff E., Hubler F., Riederer M.A, & Steiner B. (2017). The reversible P2Y12 antagonist ACT‐246475 causes significantly less blood loss than ticagrelor at equivalent antithrombotic efficacy in rat. Pharmacology Research & Perspectives, 5(5), e00338.

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Anesthetic and Neurotransmitter Compounds

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Isoflurane was obtained from Henry Schein (Melville, NY). Inactin, L-glutamate, bicuculline methiodide, sodium nitroprusside, hexamethonium, and atropine were obtained from Sigma Chemical (St. Louis, MO). L-glutamate, bicuculline, and gabazine were dissolved in artificial cerebrospinal fluid at a pH of 7.3–7.5.

Kulkarni S.S., Mischel N.A, & Mueller P.J. (2023). Revisiting differential control of sympathetic outflow by the rostral ventrolateral medulla. Frontiers in Physiology, 13, 1099513.

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Renal Clearance Experiments in Mice

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Renal clearance experiments were performed as previously described (3 (link)). Mice were anesthetized with Inactin (thiobutabarbital sodium salt hydrate, Sigma), and catheters were inserted into the trachea, jugular vein, carotid artery, and bladder. A bolus dose (0.1 ml/10 g body wt) of physiological saline solution was given via the jugular catheter as soon as intravenous access was established followed by a continuous infusion of 0.2 ml·10 g⁻¹·h⁻¹. This infusate contained 146 mM Na⁺, 5 mM K⁺, 113 mM Cl⁻, 15 mM HCO₃⁻, 0.25% (wt/vol) FITC-inulin, and 0.5% (wt/vol) p-aminohippuric acid sodium salt (PAH; Sigma) at pH 7.4. Mean arterial blood pressure was recorded from the carotid catheter in real time.

Hunter R.W., Craigie E., Homer N.Z., Mullins J.J, & Bailey M.A. (2014). Acute inhibition of NCC does not activate distal electrogenic Na+ reabsorption or kaliuresis. American Journal of Physiology - Renal Physiology, 306(4), F457-F467.

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Tissue Plasminogen Activator Inhibition Protocol

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The recombinant tissue-type plasminogen activator (rtPA, Actilyse^®) was purchased from Boehringer Ingelheim (Mannheim, Germany). Inactin^® (thiobutabarbital sodium), heparin, penicillin G, and stannous chloride dehydrate were purchased from Sigma (St. Louis, MO, USA). Fe (II) chloride tetrahydrate (≥99%), Fe (III) chloride hexahydrate (≥97%), and α-Naphthylisothiocyanate were purchased from Acros Organics (Morris Plains, NJ, USA). Isoflurane (FORAND^®) was purchased from Aesica Queenborough Limited (Queenborough, UK). The recombinant human plasminogen activator inhibitor-1 was purchased from Calbiochem (La Jolla, CA, USA). The chitosan polymer (150 kDa) with a degree of deacetylation of 95% was obtained from Fluka (Buchs, Switzerland). The chromogenic substrate, S-2288^TM, was obtained from Chromogenix (Milano, Italy).

Lin M.L., Wu S.Y., Chen J.P., Lu Y.C., Jung S.M., Wey S.P., Wu T, & Ma Y.H. (2024). Targeted Thrombolysis with Magnetic Nanotherapeutics: A Translational Assessment. Pharmaceutics, 16(5), 596.

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Inactin® Dissolved in Buffered Saline

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Inactin® and all other salts were purchased from Sigma (St. Louis, MO). All drugs were dissolved in sterile isotonic phosphate buffered saline (PBS; in mM: 147.6 NaCl, 83.3 NaH₂PO₄, 12.9 KH₂PO₄).

Swartz E.M, & Holmes G.M. (2014). Gastric vagal motoneuron function is maintained following experimental spinal cord injury. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 26(12), 1717-1729.

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Measurement of Endocochlear Potential in Mice

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These were performed as previously described by Teubner et al40 (link). Briefly, mice were intraperitonealy anaesthetised with sodium thiobutabarbital (0.1 mg g⁻¹ bodyweight) (Inactin, Sigma, Deisenhofen, Germany). The cochleae were exposed by a ventral approach and access to the basal scala media gained by thinning the bone over the SL. Borosilicate capillaries filled with 0.5 M NaCl were used as glass electrodes connected to a FD223 (World Precision Instruments) differential electrometer, which was used to measure the endocochlear potential.

Potter P.K., Bowl M.R., Jeyarajan P., Wisby L., Blease A., Goldsworthy M.E., Simon M.M., Greenaway S., Michel V., Barnard A., Aguilar C., Agnew T., Banks G., Blake A., Chessum L., Dorning J., Falcone S., Goosey L., Harris S., Haynes A., Heise I., Hillier R., Hough T., Hoslin A., Hutchison M., King R., Kumar S., Lad H.V., Law G., MacLaren R.E., Morse S., Nicol T., Parker A., Pickford K., Sethi S., Starbuck B., Stelma F., Cheeseman M., Cross S.H., Foster R.G., Jackson I.J., Peirson S.N., Thakker R.V., Vincent T., Scudamore C., Wells S., El-Amraoui A., Petit C., Acevedo-Arozena A., Nolan P.M., Cox R., Mallon A.M, & Brown S.D. (2016). Novel gene function revealed by mouse mutagenesis screens for models of age-related disease. Nature Communications, 7, 12444.

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