Model 845

Manufactured by Harvard Apparatus

The Model 845 is a high-performance syringe pump designed for precise, repeatable fluid delivery in laboratory applications. It features a stepper motor-driven, lead screw-based mechanism that provides accurate control over flow rates, volumes, and infusion/withdrawal sequences. The pump is capable of accommodating a wide range of syringe sizes and can be programmed to deliver fluids at a constant rate or in complex multi-step protocols.

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Lab products found in correlation

Succinylcholine, by Henry Schein (4 mentions) Isoflurane, by Baxter (4 mentions) Buprenorphine, by Reckitt Benckiser (4 mentions) 29g 29g insulin syringe, by BD (2 mentions) Isoflurane, by Harvard Apparatus (2 mentions) 29g insulin syringe, by BD (2 mentions) 7 0 silk suture, by Johnson & Johnson (1 mentions) Low glucose dmem, by Thermo Fisher Scientific (1 mentions)

13 protocols using model 845

Pulmonary Ischemia-Reperfusion Injury Model

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Mice were anesthetized by intraperitoneal injection of ketamine (130mg/kg) and xylazine (7mg/kg). Buprenorphine (5mg/kg)
was given subcutaneously before skin incision. Mice were orotracheally intubated and connected to a rodent ventilator (Harvard
Apparatus, model 845) with tidal air volumes of 150 uL/g and respiratory rate set at 150 breaths per minute. A left dorsolateral
thoracotomy was performed in the fourth intercostal space and a microvascular clamp (Roboz Surgical Instrument, Gaithersburg, MD)
was applied across the pulmonary artery and vein to occlude the vasculature. The left lung was occluded for 30 minutes, and the
microvascular clamp was removed. The thoracotomy was closed and the mouse was removed from the ventilator and allowed to recover
for the 3-hour reperfusion period.

Hsu J., Krishnan A., Lee S.A., Dodd-o J.M., Kim B.S., Illei P., Yarnoff K., Hamad A.A., Rabb H, & Bush E.L. (2019). CD3+CD4−CD8− Double-Negative αβ T cells Attenuate Lung Ischemia-Reperfusion Injury. The Journal of thoracic and cardiovascular surgery, 161(1), e81-e90.

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Murine Myocardial Infarction Induction

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To induce MI, mice were anesthetized with isoflurane (1.0–1.5%) delivered via a nose cone, intubated and mechanically respirated (model 845, Harvard Apparatus) via an endotracheal tube with room air supplemented with 100% oxygen; to maintain anesthesia, isoflurane was delivered via the ventilator. The electrocardiogram (ECG; limb lead II configuration) was continuously recorded (Powerlab) using needle electrodes; rectal temperature was maintained at 37°C throughout the experiments using a servo-controlled heating pad. Before initiating surgery, mice were subcutaneously injected with sustained release meloxicam (4 mg/kg) to limit post-operative pain. Once anesthetized, thoracotomy was performed to the left of the sternum to expose the heart. This was followed by opening the pericardium, and, with assistance of a microscope, insertion of an 8.0 nylon suture beneath the left main coronary artery at a level below the tip of the left atrium; this placement was designed to target the lower half of the ventricle. Ischemia was then induced by ligating the suture with a double knot, after which coronary occlusion was verified by observation of myocardial blanching distal to the ligature, as well as by ST segment elevation per ECG. Following ligation, the chest wall was closed with polypropylene suture, and recovery was monitored until mice became fully ambulatory.

Wang X., Kulik K., Wan T.C., Lough J.W, & Auchampach J.A. (2024). Evidence of Histone H2A.Z Deacetylation and Cardiomyocyte Dedifferentiation in Infarcted/Tip60-depleted Hearts. bioRxiv.

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Murine Myocardial Infarction Model

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Mice with or without previous bone marrow transplantation were anesthetized with ketamine (55 mg/kg) and xylazine (15 mg/kg). Atropine (0.05 mg subcutaneously) was administered to reduce airway secretions. Animals were intubated and ventilated with room air (tidal volume, 250 μL; 120 breaths/min) with a mouse respirator (Model 845; Harvard Apparatus, Holliston, MA). A left intercostal thoracotomy was performed, and the left anterior descending coronary artery was ligated with a 7‐0 silk suture. For each experiment, a similar number of sham‐operated mice underwent the same surgery minus the coronary artery ligation. Rectal temperatures of the mice were maintained at 37°C by a Thermopad (Harvard Apparatus). Similar basal heart rates were observed in all animals, with values of 300 to 400 bpm, typical for anesthetized mice.

Moldovan N.I., Anghelina M., Varadharaj S., Butt O.I., Wang T., Yang F., Moldovan L, & Zweier J.L. (2014). Reoxygenation‐Derived Toxic Reactive Oxygen/Nitrogen Species Modulate the Contribution of Bone Marrow Progenitor Cells to Remodeling After Myocardial Infarction. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 3(1), e000471.

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Induction of Myocardial Infarction in Mice

Cited 1 time

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Myocardial infarctions were produced as described previously Xiao et al. (2011 (link)). In brief, mice were anesthetized by intramuscular injection with a mixture of ketamine (9 mg/100 g), Acepromazine (4 mg/100 g), atropine (0.06 mg/100 g), and prepared for sterile surgery. Animals were intubated with a 20G catheter and ventilated with a mixture of O₂ and room air, using a model 845 ventilator (Harvard Apparatus, Holliston, MA). The stroke volume was set at 0.3 mL and the respiratory rate was 125 breaths/min. After a left anterior thoracotomy, the heart was exposed and the location of the left coronary artery (LCA) on the surface of LV anterior wall was identified. A 7–0 silk suture (Ethicon) was placed around the LCA and was tightened. Occlusion of the LCA was confirmed by change in the color at the involved LV wall. Lungs were expanded to displace air before the chest was closed; the mouse was then extubated. Mice were allowed to recover from the surgery in an oxygen‐filled chamber over a heating pad. Sham‐operated mice underwent similar surgery without occlusion of the LCA.

Mousa T.M., Schiller A.M, & Zucker I.H. (2014). Disruption of cardiovascular circadian rhythms in mice post myocardial infarction: relationship with central angiotensin II receptor expression. Physiological Reports, 2(11), e12210.

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Murine Myocardial Infarction Model

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MI was induced, or sham surgery performed, in 10- to 12-week-old male mice under general anesthesia with isoflurane (1.5-2.0%) and mechanical respiration (model 845, Harvard Apparatus) via an endotracheal tube with room air supplemented with 100% O₂. Electrocardiograms (ECGs; limb lead II configuration) were continuously recorded (Powerlab) via needle electrodes. Rectal temperature was maintained at 37°C using a servo-controlled heating pad. Following anesthesia onset, mice were subcutaneously injected with sustained release meloxicam (4 mg/kg) to manage postoperative pain. A left-sternal thoracotomy was performed to expose the heart, and the pericardium was opened. To target the MI to the lower half of the ventricle, an 8-0 nylon suture was threaded beneath the left main coronary artery at a level below the tip of the left atrium, with the aid of a microscope. Ischemia was induced by tying a permanent suture with a double knot. Coronary occlusion was verified by visually observing blanching of the myocardium distal to the ligature, and by elevation of the ST segment on the ECG. For sham experiments, the sutures were placed as described above but they were not tightened to occlude the artery. The chest wall was closed using polypropylene suture. Recovery was monitored until mice became fully ambulatory.

Wang X., Wan T.C., Kulik K.R., Lauth A., Smith B.C., Lough J.W, & Auchampach J.A. (2022). Pharmacological inhibition of the acetyltransferase Tip60 mitigates myocardial infarction injury. Disease Models & Mechanisms, 16(5), dmm049786.

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Murine Myocardial Infarction Model

Cited 1 time

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To induce MI, we performed permanent ligation of the left anterior descending coronary artery or to a sham operation without ligation. Briefly, mice were anesthetized with 3.5% isoflurane, endotracheal intubation performed and then mechanical ventilation started and kept throughout the operation via small animal ventilator (Harvard Apparatus, model 845). Pre-operational analgesics (0.05 mg/kg Buprenorphine) and paralytics (1 mg/kg Succinylcholine) were administrated prior to operation. A thoracotomy was performed on the 3rd or 4th intercostal space. A 8-0-polyethylene suture was advanced sub-epicardially and perpendicular to the left anterior descending coronary artery. For permanent occlusion, a ligation was done around the artery. The immediate impact was verified by myocardial bleaching and decreased contractility below the occlusion. The chest and skin were closed with a 6-0 nylon suture. Those procedures were performed by the same surgeon, who was also blinded to the experimental design (GC). Mice that died during recovery from anesthesia were excluded from the analysis. Sham-operated animals underwent a similar procedure but without coronary artery ligation (55 (link)).

Bracamonte-Baran W., Chen G., Hou X., Talor M.V., Choi H.S., Davogustto G., Taegtmeyer H., Sung J., Hackam D.J., Nauen D, & Čiháková D. (2019). Non-cytotoxic Cardiac Innate Lymphoid Cells Are a Resident and Quiescent Type 2-Commited Population. Frontiers in Immunology, 10, 634.

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Transmural MI Model in Mice

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A transmural regional MI model was generated by left anterior descending coronary artery ligation in C57BL/6 female mice (8–10 weeks) under general anesthesia (0.01 mL/g of a solution containing ketamine 10 mg/mL, xylazine 2 mg/mL by intraperitoneal injection), as described previously [15] (link). Animals were mechanically ventilated using a rodent ventilator (Model 845, Harvard Apparatus, South Natick, MA) connected to an endotracheal tube. The heart was exposed by a left side limited thoracotomy and the left anterior descending artery (LAD) was ligated with a 6-0 polyester suture 1 mm from tip of the normally positioned left auricle. Immediately after MI induction, an iPSC-derived monolayer CM sheet was apposed to the surface of LAD distribution overarching the MI area. The mice were randomly divided into four groups, as follows: 1) Sham operated mice had a loose suture placed around LAD (Sham group); 2) MI operated mice (MI group); 3) MI plus cell sheet without receiving NCX1 promoter (MI + iPSC^Null group), and 4) MI plus cell sheet with receiving NCX1 (MI + iPSC^NCX1).

Chang D., Wen Z., Wang Y., Cai W., Wani M., Paul C., Okano T., Millard R.W, & Wang Y. (2014). Ultrastructural Features of Ischemic Tissue following Application of a Bio-Membrane Based Progenitor Cardiomyocyte Patch for Myocardial Infarction Repair. PLoS ONE, 9(10), e107296.

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Murine Myocardial Infarction Model

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To induce MI, mice were respirated (model 845, Harvard Apparatus) via an endotracheal tube with room air supplemented with 100% oxygen to maintain blood gases within normal physiological limits. The electrocardiogram (ECG; limb lead II configuration) was continuously recorded (Powerlab) using needle electrodes, and rectal temperature was maintained at 37°C throughout the experiments using a servo-controlled heating pad. When anesthetized, thoracotomy was performed to the left of the sternum to expose the heart, followed by opening of the pericardium and placement of an 8.0 nylon suture beneath the left main coronary artery at a level below the tip of the left atrium to target the lower half of the ventricle, with the aid of a microscope. Ischemia was induced by carefully tying the suture with a double knot, after which coronary occlusion was verified by visual observation of blanching of the myocardium distal to the ligature and by ST segment elevation on the ECG. After ligation, the chest wall was closed with polypropylene suture and recovery was monitored until mice became fully ambulatory. Immediately prior to initiating the surgical procedure to produce MI, mice were injected subcutaneously with sustained release meloxicam (4 mg/kg) to limit post-operative pain.

Wang X., Lauth A., Wan T.C., Lough J.W, & Auchampach J.A. (2020). Myh6-driven Cre recombinase activates the DNA damage response and the cell cycle in the myocardium in the absence of loxP sites. Disease Models & Mechanisms, 13(12), dmm046375.

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Mouse Model of Heart Failure

Cited 2 times

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To create a mouse heart failure model, permanent left anterior descending coronary artery occlusion was used to induce myocardial infarction [30 (link)]. Mice were anesthetized by intraperitoneal injection of 2,2,2-tribromoethanol (0.5 mg/g) and then intubated with an 18-gauge intra-arterial catheter. A rodent ventilator (Model 845, Harvard Apparatus) with 60% oxygen was used during the surgical procedure. Following anesthesia, the chest was opened by a horizontal incision via the space between the fourth and fifth ribs, and the LAD coronary artery was ligated with a 6-0 silk suture. Successful ischemia was verified by the presence of a pale myocardium and dyskinesis of the ischemic region. The sham operation group performed the same operation, but the LAD coronary artery was not ligated. For cell culture studies, the OGD model was established by placing H9C2 cells in low-glucose DMEM (Gibco, Inc., Chengdu, Sichuan, China) and hypoxic environment (1% O₂, 5% CO₂, and 94% N₂) for 6 hours. [31 (link)].

Li Q., Liu Y., Huang Q., Yi X., Qin F., Zhong Z., Lin L., Yang H., Gong G, & Wu W. (2022). Hypoxia Acclimation Protects against Heart Failure Postacute Myocardial Infarction via Fundc1-Mediated Mitophagy. Oxidative Medicine and Cellular Longevity, 2022, 8192552.

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Transfer of Cardiac Cell Therapy

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WT or IL-17Ra^–/– BALB/c mice on day 21 of EAM were depilated and anesthetized with 3.5% isoflurane (Baxter). The mice were subsequently endotracheally intubated, 100% oxygen and 2% isoflurane were provided to the animals throughout the operation by mechanical ventilation (Model 845, Harvard Apparatus). Pre-operational analgesics (0.05 mg/kg Buprenorphine, Reckitt Benckiser) and paralytics (1 mg/kg Succinylcholine, Henry Schein) were administered prior to operation. Mice were subjected to a thoracotomy, typically around the 4th or 5th intercostal space to expose the heart ventricles. Roughly 1.5 – 2 × 10⁵ cells were injected with a 29G 29G ½ insulin syringe (BD) into 2 – 3 ventricular locations. Mice were placed under the heat lamp to recover post-surgery, post-operational analgesics (0.05 mg/kg Buprenorphine, Reckitt Benckiser) were administered. Mice were sacrifice at 40 hours or at 160 hours post-surgery to assess cell transfer outcomes.

Hou X., Chen G., Bracamonte-Baran W., Choi H.S., Diny N.L., Sung J., Hughes D., Won T., Wood M.K., Talor M.V., Hackam D.J., Klingel K., Davogustto G., Taegtmeyer H., Coppens I., Barin J.G, & Čiháková D. (2019). The Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in Myocarditis. Cell reports, 28(1), 172-189.e7.

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