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V Kékesi

Publications and source records attributed to V Kékesi.

45 records · Page 3Linked to original sources

Experimental investigation of the effect of cardiac glycosides on the ischemic coronary circulation.

The paper presents new evidence of the vasoactivity of cardiac glycosides in the myocardium. Experiments were performed on the in situ dog heart. The present study primarily focuses on the analysis of K-strophantoside induced topo-optical and thermographic alterations in acute myocardial ischemia. The strong binding of K-strophantoside to the coronary vessel wall and the endothelial cells was found to be accompanied by vasoconstriction in the regionally ischemic heart muscle. The potential clinical impact of these findings on therapy is briefly evaluated.

Animals↗

Haemodynamic and thermographic signs of intramyocardial venous outflow redistribution induced by coronary sinus occlusion in the canine heart.

Short occlusions of the coronary sinus (CS) were performed in open chest dogs in order to study the clinico-physiologic aspects of changes induced by this manoeuvre both in intracoronary pressure distribution and myocardial blood supply. It was found that when mean CS blood flow (EM flowmeter) was plotted against mean CS pressure during the gradual blockade of the CS outflow, a perfectly linear relation could be established between these variables beyond the physiologic CS pressure range (greater than 10 mmHg). Inotropic stimulation (adrenaline administration), without affecting its basic characteristics, shifted this line to higher pressure-flow ranges. On occluding the sinus, intracoronary arterial pressure distal to the ligated LAD branch also increases, but to a lesser degree than CS outflow pressure; within the ischaemic zone this results in a complete reversal of the arteriovenous pressure gradient during a considerable part of the cardiac cycle. Blood supply to the non-ischaemic heart was estimated with the aid of the computerized thermographic method developed by the authors. It was demonstrated that cardiac heat emission reflecting changes in subepicardial blood flow is singularly little affected by CS occlusion. From all these findings it is evident that occlusion of the CS involves a drastic coronary outflow redistribution but not a drastic inflow reduction in the heart. The results were interpreted in terms of newly developed cardiosurgical procedures aimed at to preserve myocardial viability, and it was concluded that the occurrence of adverse coronary actions offsetting the potential benefits of these procedures is of very low probability.

Animals↗

Thermographic study of haemodynamic changes due to arteriovenous shunt.

The authors made thermographic studies on the haemodynamic changes due to arteriovenous shunt in animal experiments under different conditions. The effects due to acute and chronic fistulas in reaction-free and inflammatory environments were registered. Observations of diagnostic value were made on the haemodynamic changes due to arteriovenous shunt. These are of differential diagnostic importance also in human medical practice, therefore thermography is recommended to be used as new noninvasive diagnostic tools.

Animals↗

Computer-aided thermographic evaluation of disturbances of the coronary adaptive reserve: an experimental study.

Brief episodes of severe ischaemic loads have been reported to attenuate or abolish the vascular autoregulatory capacity, including reactive hyperaemic vasodilation, in the coronary bed. It is suggested that the developed loss of the coronary adaptive reserve and the consecutive ultrastructural alterations can be considered an experimental model for the human effort anginal attacks occurring without significant mechanical constriction of the vessels. The functional morphologic patterns in this state were analysed by the new quantitative technique which is based on the computerized evaluation of cardiac thermograms taken with a thermovision (AGA 750) equipment. In the isolated perfused heart of rabbits, the total adaptive loss developed in the overall flow (cessation of reactive hyperaemia) was found to be associated with slow reacting coronary vessels in the cardiac surface, a delayed shift of the computerized thermographic profiles to warmer ranges during reactive hyperaemia. The pattern strongly suggested a redistribution of flow from the subendocardium. In further observations, simulated emergency coronary bypass operations on dog hearts revealed another distinct thermographic pattern: a reduced vascular adaptive range without considerable delay in reactivity. The studies demonstrated the usefulness of quantitative thermography in visualising and differentiating the various types of coronary dysfunction.

Adaptation, Physiological↗

Effect of the Ca2+ chelators EDTA and EGTA on sinoatrial-node activity and heart irritability.

The effect of the Ca-chelators EDTA and EGTA on sinoatrial activity and heart irritability was studied in dog experiments by perfusing the artery supplying the sinoatrial node. Beside the usual ECG recordings left and right atrial and left and right ventricular epicardial electrograms, His-bundle electrogram and the early activity of the sinoatrial node were recorded. In addition action potentials were recorded from the left auricle and right ventricle of the dog hearts. Local application around the sinoatrial and atrio-ventricular nodes of EDTA and EGTA caused sinus bradycardia and later sinus arrest within 1 min after introduction of the drugs. For substitution of the sinus rhythm junctional (seldom lower atrial) escape rhythm developed. One to two minutes later it was followed by atrial premature beats and even later atrial flutter and fibrillation could be recorded. In one third of the cases atrial fibrillation was followed by secondary ventricular fibrillation. Atrio-ventricular impulse conduction was prolonged in the av node by EDTA and EGTA. Atrial action potentials and the slow (Ca dependent) ventricular action potentials were depressed by EDTA and EGTA.

Animals↗

Pharmacologic assessment of the functional state in stenosed coronary circulation of the dog.

In open chest dogs under sodium pentobarbital anaesthesia the interaction of mechanical constriction on a large coronary branch and autoregulatory capacity of the relevant small resistance vessels was analyzed. Coronary blood flow (CBF) was measured with an electromagnetic flowmeter. Step-by-step mechanical constriction gradually abolished adenosine-induced coronary vasodilation, whereas the resting level of mean CBF remained unaltered. At this point verapamil (0.2 mg/kg i.v.), a vasodilator with a strong potency of blocking adenosine action, eventually decreased CBF and increased coronary resistance. Similar results were obtained with these drugs injected directly into a bypass established between the carotid and left common coronary arteries. The results suggest that (i) adenosine affects the same coronary segments which accomplish compensatory autoregulation (ii); with critical stenosis verapamil augments indirectly coronary resistance by inhibiting an "intrinsic" adenosine effect (iii); the functional state of stenosed coronaries can be assessed with the aid of these pharmacologic tests.

Animals↗

Increased susceptibility of the heart to arrhythmia in response to QT-prolongation associated with unhomogeneous repolarization: further data concerning the pathomechanism of arrhythmias associated with long QT-syndrome.

The pathomechanism of arrhythmias consecutive to a prolonged electrical systole --the long QT syndrome--was studied by local hypothermia in the heart. Local increase in the QT-interval (long QT with unhomogeneous repolarisation) was induced at a circumscribed area of the right ventricle by perfusion of the mid- and end-sections of the right coronary with cooled blood. The effect of local prolongation of QT on the arrhythmic susceptibility of the heart was studied by means of programmed electrical stimulation. Induced local hypothermia of the heart was found to increase the QT-interval of the ECG-tracings, also if QT had been corrected for heart rate. The local ECG tracings showed a considerable increase of the QT-interval at the selected right ventricular area under the effect of induced hypothermia but in relation to QT (ERP/QT) it diminished. The long QT in association with an unhomogeneous repolarization went hand in hand with an increased irritability of the heart. Early ventricular impulses were found to elicit extrasystolic runs, ventricular tachycardia or ventricular fibrillation. The results indicate that the cause of tachyarrhythmias consecutive to the long QT-syndrome may be ascribed to the inhomogeneity of repolarization on the one hand, and to the shortness of ERP in relation to the QT-duration on the other.

Animals↗

The effect of atrial dilatation on reperfusion arrhythmias: development of supraventricular tachycardias on reperfusion with atrial stretching.

UNLABELLED: The study was aimed at investigating the effect of atrial dilatation on the genesis of supraventricular tachyarrhythmias following myocardial reperfusion. Experiments were carried out in 26 mongrel dogs under pentobarbital narcosis with artificial ventilation. Electrophysiological study was performed for studying the arrhythmic condition of the heart. Investigations were carried out: (i) in normal condition, (ii) during atrial stretching (balloon dilatation of the left atrium), (iii) in reperfusion following myocardial ischemia, (iv) in reperfusion combined with atrial stretching. On reperfusion the irritability of the atrium increased moderately (on atrial extrastimuli in 3 dogs non-sustained atrial tachycardia, in 7 dogs repeated atrial responses could be induced). Reperfusion with atrial stretching, however, very markedly enhanced the atrial vulnerability, and in 19 dogs atrial tachycardia appeared spontaneously. Comparison of the effect of atrial stretching to that of atrial stretching + reperfusion showed that the reperfusion significantly augmented the arrhythmia-inducing effect of atrial stretching. CLINICAL INVESTIGATIONS: Aortocoronary bypass operations were followed by development of supraventricular tachycardia in 41 out of 428 operated cases. Atrial dilatation was detected in 37 cases, mostly before the appearance of atrial tachycardia. The data seem to prove that atrial dilatation has an important part in the pathogenesis of supraventricular tachyarrhythmias following reperfusion of myocardial ischemia.

Animals↗

Dopamine-induced coronary effects in the dog heart attributed to beta- and alpha-adrenergic mechanisms.

Open chest anesthetized dogs were given dopamine (DA) in intravenous (i.v., 2-16 micrograms.kg-1.min-1) and intracoronary (i.c., 10-40 micrograms.min-1) infusions. The drug effect was analyzed using the nonselective beta-adrenoceptor antagonist oxprenolol (0.5 mg.kg, i.v.) and the nonselective alpha-adrenoceptor antagonist phentolamine (1.0 mg.kg-1, i.v.). Coronary blood flow (CBF, electromagnetic flowmeter), arterial pressure and left ventricular contractile force (strain gauge) were measured. Coronary vascular responses were characterized by changes of CBF and calculated coronary vascular resistance (CVR). In the control state, DA-induced arterial hypertension (i.v. administration) and augmented inotropism (i.v. and i.c. administration) were accompanied by a dose-dependent coronary vasodilatation (increase of CBF and decrease of CVR). Oxprenolol converted coronary vasodilatation to vasoconstriction during DA infusions and blocked the inotropic action; the hypertensive DA effect remained unaffected. Similar alterations were observed after a transitory (45 min) regional myocardial ischemia, elicited by coronary occlusion. On the other hand, phentolamine-pretreatment potentiated the DA-induced coronary vasodilatation and converted hypertension to hypotension; the inotropic component of the DA action was not affected. After combined beta- and alpha-blockade, DA failed to increase CBF and decrease CVR during the infusion periods. Instead, the drug elicited a very slight coronary vasoconstriction. I.c. (but not i.v.) infusions of DA were regularly followed by a rebound-like, transient CBF increase, even after combined beta- and alpha-blockade. These results show that all of the multifactorial determinants of the direct, steady state coronary effects of DA can be ascribed to alpha- and beta-adrenoceptor stimulation, whereas the hypothetical dopaminergic coronary vascular receptors do not seem to play a decisive role in these responses. However, undefined after-effects provoked by i.c. DA, may be connected with specific dopaminergic effects.

Animals↗