Postischemic reperfusion may profoundly alter cardiac function. Principal mediators of this phenomenon are oxygen radicals and neutrophils, Upon reflow, oxygen radicals are generated in large amounts, overwhelming cel...
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Postischemic reperfusion may profoundly alter cardiac function. Principal mediators of this phenomenon are oxygen radicals and neutrophils, Upon reflow, oxygen radicals are generated in large amounts, overwhelming cellular defenses and inducing oxidative tissue damage;biochemical markers of oxygen radical formation and attack can be found in postischemic myocardium, Reintroduction of neutrophils in postischemic tissues is accompanied by their activation, with release of lytic enzymes that directly induce tissue damage and proinflammatory mediators that amplify the local inflammatory reaction. Neutrophils may also plug capillaries, mechanically blocking flow. Oxidants can also modulate various events, ultimately leading to tissue injury, such as nitric oxide formation, platelet-activating Factor metabolism, tissue factor synthesis, and exposure of adhesion molecules. In the clinical setting, important consequences of postischemic reperfusion are reversible contractile dysfunction ("stunning"), which is mostly caused by oxygen radical attack, and impairment to flow at the microvascular level ("no-reflow") secondary to neutrophil plugging and vasoconstriction.
An experimental model of right heart failure was developed to determine the effects of fluid loading and aminophylline on right heart function. We hypothesised that aminophylline would specifically improve right heart...
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An experimental model of right heart failure was developed to determine the effects of fluid loading and aminophylline on right heart function. We hypothesised that aminophylline would specifically improve right heart function through a decrease in pulmonary vascular resistance and, possibly, an increase in cardiac contractility. Right heart infarct was induced in ten experimental pigs and seven control pigs by ligating branches of the right coronary artery. The effect of fluid loading with a colloid solution and subsequent bolus doses of aminophylline on haemodynamics was observed. Fluid loading improved haemodynamics as expected. Aminophylline transiently improved cardiac index and pulmonary vascular resistance, but simultaneously caused an increase in heart rate and a decrease in stroke volume. Although aminophylline may reduce right heart afterload, it did not improve overall cardiac function in this experimental model of right heart infarction.
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