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ventricular arrhythmias were induced in dogs in which the capture energy used was 10 times as great as the pacing threshold. 8 Despite the fact that application of TCP for a period of 30 minutes appears not to induce serious myocardial injuries in dogs and

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in American Journal of Veterinary Research

a cardiac-specific marker for myocardial injury in many species, including rats, dogs, horses, and humans. 12–15 Assessment of circulating cTnI concentration has been used for diagnosis of ischemic heart disease (eg, myocardial infarction) in humans

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in American Journal of Veterinary Research

damage produced by free radicals. Results of a study 40 on cardiomyocyte viability after ischemia-reperfusion injury indicate that glutamine increases myocardial survival by protecting mitochondrial structure and function from oxidative damage. 40 The

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in American Journal of Veterinary Research

filament and consists of 3 subunits as follows: troponin C, troponin I, and troponin T. 12 Hematologic assays for cTnI and cardiac troponin T are used to specifically identify cardiac muscle injury in humans. 13,14 An increase in serum cardiac troponin

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in American Journal of Veterinary Research

regulatory protein complex in the contractile fibers of cardiomyocytes that controls the calcium-mediated interaction between actin and myosin. 14 It is a highly conserved biomarker of myocardial injury in mammals detectable by an immunoassay with high

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in American Journal of Veterinary Research

Cardiac troponin is a highly sensitive and specific biomarker of myocardial injury in humans. In patients with myocardial infarction, sepsis, or traumatic myocardial injury, assessment of circulating cTnI concentration is used to aid diagnosis and

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in American Journal of Veterinary Research

and oxidative damage. The process of mitochondrial injury is accelerated in humans with ischemic heart disease, 4 and many of the abnormally regulated genes on microarray data sets for heart failure are involved with mitochondrial dysfunction and

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in American Journal of Veterinary Research

-based substances that are associated with cardiac structure, function, and injury. Atrial natriuretic peptide and BNP are vasodilatory peptides that are released by myocardial tissue primarily in response to increased stress on the myocardial wall. Cardiac troponin

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in American Journal of Veterinary Research

further speculated that the localization of α-SMA–positive cells to the subendothelial layers may be in response to such signaling. 10,11 Indeed, it has long been recognized that in in vitro models of valve injury interstitial cells proliferate and

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in American Journal of Veterinary Research

external environment and respond to a host of mechanical and hormonal stimuli. The etiology of DMVD is unknown but may involve inherited connective tissue disorders, a proliferative response to repeated valve injury, or endothelial cell dysfunction. In

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in American Journal of Veterinary Research