1,721,022 research outputs found
Myocardial damage during ischaemia and reperfusion
No full textReperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may, however, cause further damage. We attempted to identify the nature and time-course of metabolic changes occurring during ischaemia followed by reperfusion either in isolated and perfused rabbit hearts or in coronary artery disease (CAD) patients undergoing intracoronary thrombolysis or aortocoronary bypass grafting. In isolated hearts, reperfusion after prolonged ischaemia causes exacerbation of cell damage, leading to a breakdown of the permeability barrier of ions as well as of larger molecules, such as creatine phosphokinase. As consequence, reperfusion results in a large increase in intracellular calcium, leading to mitochondrial calcium overload with subsequent damage to the mitochondrial structure and loss of the ability to produce adenosine triphosphate (ATP). The ultimate mediator of the membrane damage is not known. It has been suggested that myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and the intracellular pool of reduced glutathione. Consequently, reperfusion results in severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of the human heart. During surgical reperfusion of CAD patients, we observed a prolonged and sustained release of oxidized glutathione; the degree of oxidative stress can inversely correlated with recovery of mechanical and haemodynamic function.(ABSTRACT TRUNCATED AT 250 WORDS
The neuroendocrine and sympathetic nervous system in congestive heart failure
No full textA review of recent randomized clinical trials has shown that neurohormonal activation starts early in the natural history of left ventricular dysfunction and levels of the circulating hormones increase in proportion to the severity of heart failure. Most studies suggest that high levels of neurohormones predict a poor prognosis. Among the several neurohormones, the sympathetic system is the one which is activated earlier, it increases in proportion to the severity of the disease and has a negative prognostic implication. These concepts have been also proven in untreated patients. Augmented sympathetic activity in the syndrome of heart failure is initially beneficial, appears to be adaptive and helps support blood pressure and cardiac output. Prolonged and excessive sympathetic activation has deleterious effects with adverse consequences at both cardiac and vascular levels which aggravates the clinical status of the syndrome and negatively affects its prognosis. Evidence is accumulating that, contrary to popular belief, beta-blockers may be beneficial in heart failure by inhibiting sympathetic activation. In addition to neuroendocrine activation, another class of biologically active molecules, termed cytokines, are excessively secreted by cells in heart failure. Important among these cytokines are tumour necrosis factor-alpha and interleukin-6. They appear to exert deleterious effects on the heart and circulation which may be also involved in the progression of heart failure
Il ruolo del defibrillatore impiantabile nella prevenzione della mortalità cardiaca in pazienti con pregresso infarto miocardio
No full text[The double face of oxygen. An introduction to cardiac pathology caused by oxidation injury]
No full textThe double face of oxygen. An introduction to cardiac pathology caused by oxidation injury
[Comparative protective effect of gallopamil in myocardial ischemia and reperfusion]
No full text[Comparative protective effect of gallopamil in myocardial ischemia and reperfusion
Hormonal response in untreated myocardial infarction
No full textPlasma levels of a variety of hormones have been measured in patients within two hours of the onset of symptoms of myocardial infarction and before commencement of any treatment. Increased plasma concentrations were found for norepinephrine, epinephrine, glucagon, aldosterone, vasopressin, atrial natriuretic peptide, corticotrophin, prolactin, cortisol and substance P while plasma renin activity was raised. The plasma concentrations of insulin, growth hormone, neurotensin, bombesin and vasointestinal peptide were normal
New findings on calcium antagonism
No full textThe family of calcium antagonist substances is continuously increasing. Often it is difficult, if not impossible, to have clear, objective criteria to differentiate between the available molecules. We have considered some molecular aspects of calcium channels and of the effects of calcium antagonists which may be relevant for the clinical utilization of these drugs. In particular, differences between L and T type of calcium channels in the myocytes and between VOC and ROC calcium channels in the smooth muscle are described. Then we have considered the main differences in the mechanism of action and clinical use of the three prototypes of calcium antagonists: phenilalkilamines, dihydropyridines and benzothiazepines. Finally, we have synthetically depicted the characteristic of the second generation agents such as nisoldipine, amlodipine, felodipine, isradipine, lacidipine and gallopamil
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