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Biomedical subjects

U C Czubek

Publications and source records attributed to U C Czubek.

2 recordsLinked to original sources

[Functioning of the transplanted heart].

There are significant differences between functioning of transplanted and healthy hearts. Assessment of such a heart and therapeutic possibilities in heart recipients require understanding of these differences. Vegetative denervation of heart increases its sensitivity to the circulation humoral substances, especially catecholamines. In the early postoperative period, filling pressures of the right and left ventricle are elevated. An increase in pulmonary resistance accompany noted pulmonary hypertension, leading subsequently to the right ventricular failure and mitral valve insufficiency. Normalization of these disorders begins in the majority of cases about 4 months following heart transplantation. A type of immunosuppression has an important effect on circulatory hemodynamics. A systemic blood hypertension is a frequent complication of immunosuppression with cyclosporine A in heart recipients. Heart contraction frequency is usually higher in heart recipients than that in control group, and its resting mean value is 90 beats per minute. Moreover, a mild circadian changes in this frequency by about 20% is noted in heart recipients. Cardiac arrhythmias following heart transplantation are associated with the degree of denervated heart transplant to arrhythmia is rather improbable. Cardiac drugs acting with mediation of vegetation system have no effect on the transplanted heart. Heart transplant is fully capable to maintain proper body functioning.

Arrhythmias, Cardiac↗

[Reperfusion injury to the myocardium].

Reperfusion injury is of increasing importance due to new techniques of restoring blood flow to acutely ischaemic areas by means of thrombolysis, angioplasty, or acute coronary artery bypass surgery. Reperfusion of ischaemic myocardium can results in the acceleration of surrounding reversibly injured myocytes and endothelial cells to irreversibly injured cells. The complex group of phenomena associated with reperfusion include: no-reflow, arrhythmias, "stunned" myocardium-impaired contractile power and abnormalities of relaxation. Experimental studies have demonstrated that microvascular damage may play an important role in the pathogenesis of this phenomenon. The causal factors of reperfusion injury are not clarified, but include free radicals, calcium and various inflammatory mediators. The deleterious effects of reperfusion are related importantly to the action of oxygen-derived free radicals. These effects can be reduced or even prevented with scavengers of free radicals. However, the value of these agents in patients remains to be tested. Prophylactic chronic treatment of patients at high risk of coronary occlusion with a beta-adrenergic blocking agent or a calcium antagonist slow cell death causing limitation of infarct size.

Animals↗