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Biomedical subjects

V Kékesi

Publications and source records attributed to V Kékesi.

At least 37 records · Page 2Linked to original sources
PubMed1995

Ventricular tachycardias induced by intracoronary administration of endothelin-1 in dogs.

In 12 anesthetized, open-chest mongrel dogs, endothelin-1 (ET-1) was infused into the left anterior descending coronary artery through an indwelling catheter at a dose of 30 pmol.min-1 for 30 min (n = 8). In four dogs the ET-1 dose was increased to 60 pmol/min for 10 min. Programmed electrical stimulation was used for electrophysiologic studies. Coronary blood flow was reduced by 32% on average without any ischemic ECG signs. QT time (186 +/- 3 ms vs. 218 +/- 6, p < 0.05, and 225 +/- 9, p < 0.05, p < 0.05). Ventricular irritability increased in all cases; ventricular extrasystoles, and nonsustained and sustained tachycardias occurred and, in 11 cases, ventricular fibrillation terminated the experiments. In two dogs, early afterdepolarization was recorded. Therefore, ET-1 is capable of inducing fatal ventricular arrythmias at least partly independent of its vasoconstrictor effect. QT prolongation appears to have a pathophysiologic role in this arrythmogenic effect.

Action Potentials↗
PubMed1994

Coronary arteriopathy after lymphatic blockade: an experimental study in dogs.

The effects of lymph stasis on the histological and biochemical properties of the coronary arterial wall and on the coronary circulation were studied in 72 dogs. Cardiac lymph stasis was produced in 52 dogs by cardiac lymphatic blockade whereas in 20 dogs only a sham operation was performed. Blockade of cardiac lymph drainage promoted characteristic injury to the coronary arteries including subendothelial edema with plasma inbibition, interstitial and intracellular edema in the tunica media with degeneration in the smooth muscle layer, swelling of the adventitial space with dilated lymph vessels and, later, fibrosis. The biochemical properties of the coronary arterial wall also were adversely affected by cardiac lymph stasis. Thus, the collagen and hexosamine content of the coronary arteries increased and the metabolism of the coronary wall shifted in an anaerobic direction. Whereas coronary blood flow was slightly decreased with lymph blockade, the coronary circulatory reserve capacity and the adaptability of the coronary vascular system was markedly reduced. The histological changes were most apparent in the smaller coronary arteries. The coronary microvasculature was also pathologically altered with the development of numerous coronary arteriovenous microshunts. These findings in conjunction with other experimental and clinical information suggest that impaired cardiac lymph drainage contributes to the pathogenesis and progression of coronary artery disease.

Animals↗
PubMed1993

Effect of antioxidant treatment on the myocardium during reperfusion in dogs.

Open chest dogs undergoing 30-min occlusion of the left anterior descending coronary artery (LAD), followed by 20-min reperfusion, received silibinin (2 mg/kg body weight), allopurinol (100 mg for two days as pretreatment, 20 mg/kg body weight during ischemia and reperfusion), superoxide dismutase (SOD, 5 and 0.5 mg/kg body weight, starting from the last minute of ischemia over 6 min). Control and treated dogs were comparable with respect to myocardial regional contractile force (strain gauge), malondialdehyde (MDA) and creatinine kinase (CK) levels of sinus coronarius blood samples, heart rate, and blood pressure. Allopurinol and large doses of SOD produced significant improvement in contractility and decreased MDA levels, which might suggest free radical mediated reactions during reperfusion.

Allopurinol↗
PubMed1992

The effect of superoxide dismutase in the myocardium during reperfusion in the dog.

The aim of the study was to investigate the pathological role of free radicals during myocardial reperfusion. Low (0.5 mg/kg body weight) and high doses (5 mg/kg) of superoxide dismutase (SOD) were infused into the left atrium of mongrel dogs for 4 min starting 29 min after ligation and 1 min before reperfusion of the left anterior descending coronary artery (LAD). Arterial blood pressure, heart rate, electrocardiogram, and the regional contractile force of the left ventricle were monitored throughout the ligation (30 min) and reperfusion periods (20 min). Concentrations of creatine kinase (CK) and malondialdehyde (MDA) in the coronary sinus blood were determined before (0 min) and during ligation (15 and 25 min) and during reperfusion of the LAD (2, 7, and 20 min). In other groups of dogs, the effect of the two doses of SOD on epicardial blood flow was investigated during ligation and reperfusion by the measurement of epicardial temperature using a thermocardiograph. Experimental subjects were mongrel dogs of either sex (n = 25), weight 10-35 kg. Compared to controls (mean +/- SEM, 43.1 +/- 1.2; n = 7), the number of ventricular extrasystoles during the first 5 min of reperfusion was significantly (p < .001) decreased in dogs treated with the high dose (15.01 +/- 2.14; n = 5), but not in those receiving the low dose of the drug (34.6 +/- 5.66; n = 5). The concentrations of CK increased gradually until the end of reperfusion without differences among the different groups. Plasma MDA was the highest in control dogs 7 min after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Endothelin-induced long-lasting mesenteric vasoconstriction: a hypothetical mechanism of non-occlusive intestinal infarction.

The in vivo mesenteric vascular effect of the novel, endothelium-derived endogenous polypeptide, endothelin-1 (ET-1) was examined in experiments performed on pentobarbital-anesthetized dogs. Blood supply to a segment of the small bowel was measured simultaneously with an electromagnetic flow probe and computer-assisted thermography which senses flow-dependent infrared irradiation. It was found that close mesenteric arterial injections of ET-1 produced long-lasting flow decreases of considerable magnitude: the single dose of 1 nmol reduced blood flow by nearly 90 percent, and even the minimal single amount of 1 pmol produced statistically significant vasoconstriction. The thermographic analysis proved the homogenous character of these reactions. Unlike vascular responses elicited by most of the known vasoconstrictive agents, the ET-1-induced spastic effects were maintained without a continuous exposure (drug infusion). All features that characterize the spastic ET-1 action qualify the peptide for a hypothetical candidate of mediating the nonocclusive mesenteric ischemic syndrome.

Animals↗
PubMed1991

Dopamine-induced aggravation of myocardial ischaemia in the paced heart: cardiosurgical perspectives.

The action of dopamine on the blood supply to acutely ischemic cardiac areas was investigated at arbitrarily selected, fixed heart rates. The A-V node of open chest dogs was crushed and the ventricles were paced between 30 and 220 beats per minute (bpm). Ischemic blood supply was assessed by computer-aided infrared thermography. It was found that the ischemic (collateral-dependent) blood flow paralleled overall myocardial blood supply (coronary sinus outflow) and was directly related to heart rate between 30 and 100-140 bpm; above this frequency it decreased moderately. Dopamine (10 micrograms/kg i.v.) elicited a marked increase of ischemic flow in the heart paced at 60 bpm, whereas the drug action was characterized by a long-lasting flow decrease (preceded by a slight dilation) at 200 bpm. It was concluded that the treatment of the tachycardic heart with dopamine, as it frequently occurs in postbypass cardiac and coronary surgery, may place the non-completely revascularized myocardium at risk.

Animals↗
PubMed1991

Lymphatic arteriopathy: damage to the wall of the canine femoral artery after lymphatic blockade.

The effect of lymph stasis on the histological, biochemical, and elastic properties of the femoral artery were studied after regional lymphatic blockade in 36 dogs. Dogs were sacrificed 4-21 days after operation. Histologic changes of the femoral arterial wall (interstitial edema, degeneration in the muscle layer or media, thickened adventitia with dilated lymph vessels, and fibrosis) developed after regional lymphatic blockade. Characteristic metabolic alterations of the arterial wall (anaerobic catabolism of carbohydrate, increased lactate and glycosamine content) accompanied the morphological changes. Distensibility of the femoral artery decreased and greater elastic stiffness developed after regional lymphatic blockade. These results in conjunction with other experimental and clinical data support the concept that insufficient lymphatic transport within the blood vessel wall may contribute to the genesis and progression of arteriopathies.

Animals↗
PubMed1989

The effect of atrial dilatation on the genesis of atrial arrhythmias.

The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.

Animals↗
PubMed1989

The dopamine-induced coronary vasoconstrictor response is potentiated by adenosine administration in the dog heart.

The ineffectiveness of beta-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 micrograms.kg-1.min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg.kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary beta-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heart emission. However, both types of effects were moderate, and only the hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 micrograms.kg-1.min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventional beta-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.

Adenosine↗
PubMed1989

The role of coronary alpha 1-adrenoceptors of the dog heart in dopamine-induced cardiostimulation evidenced by treatment with prazosin.

To assess the participation of postjunctional coronary alpha 1-adrenoceptors in the dopamine-induced general circulatory stimulation, pentobarbital-anesthetized open chest dogs were infused with the agent (1-16 micrograms.kg-1.min-1 i.v.) before and after the administration of the alpha 1-selective adrenergic antagonist prazosin (0.15 mg.kg-1). Coronary responses were characterized by the changes of blood flow (electromagnetic flowmeter) and those of calculated vascular conductance. Left ventricular contractile force was measured with a strain gauge arch. In the control state, whereas coronary blood flow increased simultaneously with the dose-dependent hypertensive effect of dopamine, the calculated augmentation of coronary vascular conductance was relatively slight (maximum: greater than or equal to 50%) compared to the very great increase of cardiac inotropism (up to greater than or equal to 250%) and myocardial O2 consumption (up to greater than or equal to 250%). After blocking the alpha 1-adrenoceptors, in spite of the elimination of the hypertensive effect, the inotropic and blood flow actions of dopamine remained unaltered and the calculated value of vascular conductance indicated an enhanced vasodilation (up to 200%). The alpha 2-blocker yohimbine (0.5 mg.kg-1) failed to elicit actions of similar magnitude. It was concluded that postjunctional alpha-adrenoceptor-dependent coronary vasoconstrictor influences compete with metabolically coupled vasodilation during the cardiostimulatory action of dopamine.

Animals↗
PubMed1989

Factors influencing the vascular action of dopamine in the canine mesenteric bed.

The effect of dopamine on the mesenteric arterial bed was investigated in dogs anaesthetized with pentobarbital sodium. The vascular responses to dopamine in a branch of the superior mesenteric artery supplying a segment of the small intestine were measured with a flowmeter probe and visualized by infrared telethermography or, in a separate series of dogs, were obtained by the direct determination of arterial resistance--changes during perfusion with constant flow. It was found that the mesenteric action of dopamine (given i.v. in the submaximal dose of 16 micrograms.kg-1.min-1 or intraarterially up to a dose of 40 micrograms.min-1) is primarily mediated via dopaminergic vasodilator and a alpha-adrenergic vasoconstrictor receptors, the net result of this competition usually being moderate vasodilation under natural conditions. The contribution of beta-adrenergic vasodilation to the mesenteric dopamine action is minimal as evidenced by beta-blockade with oxprenolol. By blocking the alpha-component with phentolamine (1.0 mg.kg-1) an almost threefold increase of the vasodilation was obtained in resistance. Because of the concomitant reversal of the systemic hypertensive dopamine action to hypotension, the net flow increase remained essentially unchanged. It was concluded that unless the degree of alpha-stimulation is restrained and proper control of blood pressure is ensured, it is not possible to recommend that dopamine be used in the therapy of mesenteric vascular disorders.

Animals↗
PubMed1989

Effect of atrial dilatation on the tendency of atrial arrhythmias.

The arrhythmogenic effect of atrial dilatation was studied by electrophysiological investigations carried out on 24 dogs. Atrial distension was evoked by increasing the pressure in the right atrium (12 to 14 mm Hg) or by the balloon dilatation of the left atrium. Programmed electrical stimulation of the heart was used for the electrophysiological investigations. In addition to the superficial ECG leads also atrial and ventricular epicardial electrograms were obtained for the ECG recording. Acute atrial dilatation led to shortening of the atrial refractory period, whereas neither impulse conduction of the heart, nor pacemaker activity of the sinus node exhibited any alteration. Atrial dilatation resulted in pathological atrial irritability, and early or frequent atrial stimulation caused atrial tachycardia of shorter (non sustained) or longer (sustained) duration. Repetitive atrial extrasystoles in response to early stimuli could also frequently be observed during atrial dilatation. The obtained results indicate that atrial dilatation is arrhythmogenic and may lead to the development of atrial tachycardia.

Animals↗
PubMed1989

Motility, haemodynamics and responsibility to vasoactive agents after revascularization of autotransplanted small intestine segments in the dog.

Functional and haemodynamic changes occurring after revascularization of an autotransplanted small intestine segment were studied in acute experiments performed in 10 dogs under pentobarbital anaesthesia. Intestinal motility and mesenteric blood flow of the segment were measured with intraluminal pressurized balloon and electromagnetic flowmeter, respectively. The time-course of observations was divided, according to the findings, into three main periods (phases 1 to 3). In the initial phase (1) the bowel exhibited very slight spontaneous motility which was found to increase moderately but significantly after denervation and isolation of the graft still left in situ before transplantation (phase 2). After declamping of anastomoses of the retransplanted graft (which was protected by cooling to 4 degrees C after being removed from the body) a short period (approximately 2 min) of reactive hyperaemic flow increase was observed in association of vigorous bowel movements lasting for a more prolonged (approximately 15 min) period of time (phase 3a and 3b). Reactivity of the retransplanted vasculature as compared to the denervated control revealed a marked relative shift in adrenergic balance, tested by dopamine, to the vasoconstrictor range, but it showed no change in responses to general haemodynamic or haemorheologic interventions, tested by veratrine and pentoxifylline, respectively. However, the basic levels of blood supply (controlled also by thermography) and systemic blood pressure remained unaltered after transplantation. Regarding the critical role of functional changes immediately after transplantation in determining the survival of bowel grafts, these observations may contribute to a more effective monitoring of surgical interventions.

Animals↗
PubMed1988

Reversal of isoproterenol-induced calorigenic action in the heart during myocardial ischemia.

With the aid of infrared thermography, a powerful new tool for studying the biological state of cardiac regulatory mechanisms, the reversal of the isoproterenol-induced calorigenic action in the in situ dog heart was demonstrated after establishing acute myocardial ischemia. The thermographic manifestations indicated a modified activity pattern of the cardiac (coronary) beta-mechanism with a preserved sensitivity to its specific pharmacologic blockade. Results provide new evidence of the transformation (plasticity) of adrenoceptor qualities under pathologic circumstances.

Animals↗
PubMed1988

Prevention by a stable prostacyclin analogue, 7-oxoprostaglandin I2 of the platelet loss during experimental cardiopulmonary bypass.

A great percentage of circulating platelets is lost through activation and aggregation during total body perfusion used in cardiac surgery. The effect on platelet count of a chemically stable prostacyclin analogue, 7-oxoprostaglandin I2 was investigated in anaesthetized dogs subjected to cardiopulmonary bypass of 120 min duration. In control (untreated) dogs the perfusion decreased the amount of circulating platelets by more than 60% of their initial value. This loss was completely prevented by i.v. infusion of the analogue (50 micrograms.kg-1.min-1) without affecting the haemodynamic state of the preparation. With the infusion of native prostacyclin at the same rate, a similar protective action was found to be associated with significant arterial hypotension. It was concluded that 7-oxoprostaglandin I2 is an useful pharmacological tool for maintaining physiological platelet counts and thus preserving haemostatic stability in open heart surgery.

Animals↗