Use of the Ferret in Cardiovascular Research

Morgan, James P.

doi:10.1002/9781118782699.ch27

Cited by 5 publications

(5 citation statements)

References 83 publications

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“…F1A–D in “Ferret Study”). We chose Ferrets because their cardiac function is more closely associated with that of humans than are mouse cardiac properties [39]. GsMTx4-D showed no significant changes in any hemodynamic parameters at any concentration compared to vehicle injected animals.…”

Section: Resultsmentioning

confidence: 99%

“…We observed a transient (first 15 min after reperfusion) concentration-dependent increase in HR in the ischemia challenged mice anesthetized with pentobarbital, but the HR was the same as controls after 24 and 48 h of reperfusion. No effect on HR was observed in isoflurane anesthetized mice, nor in normal free roaming ferrets which have cardiac properties more closely associated with humans [39]. …”

Section: Discussionmentioning

confidence: 99%

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GsMTx4-D is a cardioprotectant against myocardial infarction during ischemia and reperfusion

Wang

Sachs

et al. 2016

Journal of Molecular and Cellular Cardiology

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GsMTx4 is a selective inhibitor of cationic mechanosensitive ion channels (MSCs) and has helped establish the role of MSCs in cardiac physiology. Inhomogeneous local mechanical stresses due to hypercontracture and swelling during ischemic reperfusion injury (IRI) likely induce elevated MSC activity that can contribute to cation imbalance. The aim of this study was to determine if the D enantiomer of GsMTx4 can act as a cardioprotectant in a mouse IRI model. Ischemia and reperfusion involved ligating a coronary artery followed by release of the ligature. GsMTx4-D was tested by either acute intravenous injection during the ischemic event or by two day pretreatment by intraperitoneal injection, both methods achieving similar results. Based on pharmacokinetic studies, GsMTx4-D dosage was set to achieve expected plasma concentrations between 50 and 5000 nM and heart tissue concentrations between 1 and 200 nM by intravenous injection. Relative to vehicle injected animals, GsMTx4-D reduced infarct area by ~40% for acute and pretreated animals for both 20 and 45 min ischemic challenges. Many indicators of cardiac output were indistinguishable from sham-treated control hearts after GsMTx4-D treatment showing improvement at both 4 and 48 h post ischemia, and premature ventricular beats immediately following reperfusion were also significantly reduced. To determine if GsMTx4-D cardioprotection could act directly at the level of cardiomyocytes, we tested its effects in vitro on indicators of IRI damage like cation influx and activation of inflammatory kinases in isolated myocytes cultured under hypoxic conditions. Hypoxia challenged cardiomyocytes treated with 10 μM GsMTx4-D showed improved contractility and near normal contraction-related Ca2+ influx. GsMTx4-D inhibited indicators of ischemic damage such as the apoptotic signaling system JNK/c-Jun, but also inhibited the energy response signaling system Akt kinase. We conclude that GsMTx4-D is a potent cardioprotectant in vivo that may act directly on cardiomyocytes and potentially be useful in multidrug strategies to treat IRI.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

GsMTx4-D is a cardioprotectant against myocardial infarction during ischemia and reperfusion

Wang

Sachs

et al. 2016

Journal of Molecular and Cellular Cardiology

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“…Apart, a demand for more complex physiological environment could be fulfilled using suitable animal models, including mice, humanized mice, hamsters, ferrets, non-human primates [ 259 ]. Since ferrets commonly develop cardiac diseases such as dilated cardiomyopathy, arrhythmias and ferret myocardium has positive force–frequency relationship (FFR) that is quite analogous to human [ 263 ], it represents a suitable model to investigate myocardial injury, induced during SARS-CoV-2 infection. Certain strains of Syrian hamster (Bio TO-2) exhibit progressive development of cardiac dysfunctions, including musculocutaneous blood flow associated with the cardiac remodeling that includes atrial hypertrophy and left ventricular dilation, wall thinning, increased collagen density, and decreased mean arterial pressure [ 264 ].…”

Section: Different Models To Study the Sars-cov-2 Virus Interaction With The Cardiovascular Systemmentioning

confidence: 99%

The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications

Veluswamy

Wacker

Stavridis

et al. 2021

Viruses

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The SARS-CoV-2 virus causing COVID-19 disease has emerged expeditiously in the world and has been declared pandemic since March 2020, by World Health Organization (WHO). The destructive effects of SARS-CoV-2 infection are increased among the patients with pre-existing chronic conditions and, in particular, this review focuses on patients with underlying cardiovascular complications. The expression pattern and potential functions of SARS-CoV-2 binding receptors and the attributes of SARS-CoV-2 virus tropism in a physio-pathological state of heart and blood vessel are precisely described. Of note, the atheroprotective role of ACE2 receptors is reviewed. A detailed description of the possible detrimental role of SARS-CoV-2 infection in terms of vascular leakage, including endothelial glycocalyx dysfunction and bradykinin 1 receptor stimulation is concisely stated. Furthermore, the potential molecular mechanisms underlying SARS-CoV-2 induced clot formation in association with host defense components, including activation of FXIIa, complements and platelets, endothelial dysfunction, immune cell responses with cytokine-mediated action are well elaborated. Moreover, a brief clinical update on patient with COVID-19 disease with underlying cardiovascular complications and those who had new onset of cardiovascular complications post-COVID-19 disease was also discussed. Taken together, this review provides an overview of the mechanistic aspects of SARS-CoV-2 induced devastating effects, in vital organs such as the heart and vessels.

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“…Literature reviews undertaken in 1967Literature reviews undertaken in , 1969Literature reviews undertaken in , 1973Literature reviews undertaken in , and 1985, however, revealed an increasing appreciation for the ferret's usefulness and versatility in the study of human physiologic, anatomic, and disease mechanisms (Hahn and Wester, 1969;Marshall and Marshall, 1973;Shump et al, 1974;Frederick and Babish, 1985). The domesticated ferret has been and continues to be used extensively in studies involving virology, neuroscience, carcinogenesis, cardiovascular physiology, and emesis (Morgan and Travers, 1998). The document was designed to serve as a reference tool for individuals involved in the care or use of ferrets in the laboratory setting.…”

Section: B Use In Researchmentioning

confidence: 99%