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Biomedical subjects

T Fazekas

Publications and source records attributed to T Fazekas.

At least 73 records · Page 4Linked to original sources
PubMed1991

Study on dysphagia after proximal selective vagotomy.

The authors examined one of the characteristic complications--dysphagia--of proximal selective vagotomy widely applied in the surgical treatment of duodenal ulcerations. To gain a better knowledge of the causes of this type of complications measuring the pH value for 24 hours and manometric examinations of the lower esophageal sphincter were performed in 12 patients without complaints following operation and in 22 with the complaint of dysphagia. No significant changes were observed between the two groups either in basal sphincter pressure or in the two parameters characteristic for reflux activity, e.g. the number of reflux episodes and reflux index. Operation resulted in a slight increase of the basal pressure and the decrease of reflux activity in both groups. It is likely that postvagotomical dysphagia has a multifactorial background: denervation or mechanical trauma of the lower oesophagus and the uncoordinated and insufficient relaxation of the lower oesophageal sphincter following swallowing.

Adult↗
PubMed1990

Analysis of the proarrhythmic action of lidoflazine (Clinium).

The mechanism of the proarrhythmic action of the Na+ and Ca++ channel blocking agent lidoflazine (Clinium) in animal experiments was analysed. Lidoflazine pretreatment was found to increase the electrically induced atrial fibrillatory threshold in the intact cat, but to decrease this parameter in the ventricular heart muscle. The changes induced by lidoflazine in the ventricular repolarization of the normoxic dog heart (T wave flattening, appearance of prominent U waves, T-U fusion, QT/QTU prolongation) are considered to be proarrhythmic ECG signs.

Animals↗
PubMed1989

[Anti-arrhythmia therapy with Ca++-antagonists].

A minireview is given of the theoretical and clinical knowledge relating to antiarrhythmic therapy with Ca++-antagonists. Following a brief recall of the basic cardiac electrophysiological elements, some primarily Ca++- and 'slow response'-dependent electropathological phenomena (ischaemia-induced local conduction delay, ST-T-alternans, early and delayed after depolarizations) are presented, to which roles are attributed in the development of re-entry, triggered automaticity and human cardiac arrhythmias. Next, those types of heart rhythm disturbances are discussed which can be treated in the hope of success with Ca++ entry blocking (class IV) antiarrhythmic agents.

Arrhythmias, Cardiac↗
PubMed1989

Effects of the lipolysis inhibiting agent beta-pyridylcarbinol (Ronicol) in acute myocardial ischaemia.

The antilipolytic, nicotinic acid analogue beta-pyridylcarbinol (Ronicol) has previously been reported to decrease the free fatty acid (FFA) concentration of the arteria-blood, and to moderate the FFA-uptake and O2-consumption of the myocardium; on this basis, the drug may be expected to exert a cardioprotective action. The cardiac effects of Ronicol were therefore studied on a self-control, 'single-vessel' coronary artery ligature dog model. The left anterior descending coronary artery (LAD) was prepared in the in situ heart of anaesthetized, thoracotomized animals. Following the control ligation, a stabilization period and Ronicol infusion (1 mg/kg iv. during 10 minutes), the LAD was repeatedly ligated. The duration of the individual occlusions was 10 minutes. Ronicol significantly decreased the arterial FFA concentration and the epicardial ST segment elevation; its antilipolytic and anti-ischaemic effects were protracted and were still observed 120 minutes after pretreatment. The drug did not decrease the inhomogeneity of ventricular depolarization in the ischaemic myocardium and in the dose applied it had no influence on the heart rate, arterial blood pressure, left ventricular end-diastolic pressure and left ventricular contractility (LV dP/dtmax). In the canine myocardial infarction model employed it was observed that the duration of the anti-ischaemic effect of Ronicol (1 mg/kg iv.) is about 120 minutes. It has the advantage that it does not possess the unwanted cardiovascular side-effects displayed by nicotinic acid observed by us too in this model earlier (Cardiol. Hung. 13, 33-41, 1984).

Animals↗
PubMed1988

Effect of chloroquine in experimental myocardial ischaemia.

The cardiac effects of the phospholipase A2 inhibiting agent chloroquine were studied in dogs, rats and cats. During left anterior descending coronary artery occlusion produced in anaesthetized mongrel dog, chloroquine pretreatment considerably reduced the epicardial ST-segment elevation in the ischaemic area, as well as the number of premature ventricular contractions. In conscious male Sprague-Dawley CFY rats it diminished the duration and prolonged the latency of appearance of the early post-infarction arrhythmias and increased the survival rate following coronary artery ligation. Chloroquine failed to affect the ventricular fibrillation threshold in the normoxic cat heart. The cardioprotective action of chloroquine could be explained at least partly by its antiphospholipase activity.

Animals↗
PubMed1986

Effects of L-carnitine in acute myocardial ischaemia.

Data in the literature suggest that exogenous L-carnitine improves the metabolic function of ischaemic heart cells: it enhances the transport of long-chain fatty acids into the mitochondria, stimulates the slowed beta-oxidation, and moderates the accumulation of amphiphilic acyl esters. A study has therefore been made of the cardiac effects of L-carnitine in dog experiments (n = 8). The left anterior descending coronary artery (LAD) was isolated in anaesthetized, thoracotomized animals in situ. After a control occlusion and equilibration period, the LAD was again ligated at the time of L-carnitine infusion (100 mg/kg iv. during 10 min). The agent diminished the maximal conduction delay and the degree of epicardial ST-segment elevation in the ischaemic myocardial region, and the free fatty acid concentration of the arterial blood, but it did not influence the frequency of ventricular extrasystoles. The anti-ischaemic effect of L-carnitine was manifest only during the infusion, and its discontinuation was immediately followed by an enhanced ST-segment elevation. In the dose applied, the substance did not affect the heart rate, systemic mean arterial pressure, left ventricular end-diastolic pressure (LVEDP), or left ventricular contractility (LV dP/dtmax). In the canine myocardial infarction model employed it was observed that the duration of the anti-ischaemic effect of L-carnitine (100 mg/kg iv.) is very short, and it has no significant antiarrhythmic action.

Acute Disease↗