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monocrotaline/инфаркт
Веза се чува у привремену меморију
7 резултати
YM598, an orally active ET(A) receptor antagonist, ameliorates the progression of cardiopulmonary changes and both-side heart failure in rats with cor pulmonale and myocardial infarction.
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The effects of the novel, selective endothelin-A (ETA) receptor antagonist YM598 on both-side heart failure were investigated. Right-side heart failure secondary to pulmonary hypertension was produced by a single subcutaneous injection of 60 mg/kg monocrotaline, and post-ischemic congestive
Enhanced expression and activity of xanthine oxidoreductase in the failing heart.
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The molecular basis for heart failure is unknown, but oxidative stress is associated with the pathogenesis of the disease. We tested the hypothesis that the activity of xanthine oxidoreductase (XOR), a free-radical generating enzyme, increases in hypertrophied and failing heart. We studied XOR in
[New animal models for drug discovery research: focus on cardiovascular diseases].
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Development of novel drugs relies on research to discover new drugs. Testing and evaluating new drugs on human subjects are usually impossible because of ethical concerns. Therefore, for drug discovery research, it is essential to establish animal models of human diseases. Numerous animal models
Right Atrial Mechanisms of Atrial Fibrillation in a Rat Model of Right Heart Disease.
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Ghrelin and the heart.
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Ghrelin, a growth hormone-releasing peptide that was first discovered in the stomach of rats in 1999, is an endogenous ligand of growth hormone secretagogue receptor. Ghrelin exerts its potent growth hormone-releasing and orexigenic activities by binding to specific receptors in the brain.
Right ventricular oxygen supply parameters are decreased in human and experimental pulmonary hypertension.
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BACKGROUND
In pulmonary arterial hypertension (PAH), high right ventricular (RV) power output requires increased myocardial oxygen consumption. Oxygen supply, however, does not increase in proportion. It is unknown what cellular mechanisms underlie this lack of adaptation. We therefore determined
Current animal models for the study of congestion in heart failure: an overview.
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Congestion (i.e., backward failure) is an important culprit mechanism driving disease progression in heart failure. Nevertheless, congestion remains often underappreciated and clinicians underestimate the importance of congestion on the pathophysiology of decompensation in heart failure. In
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