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Biomedical subjects

W Bernauer

Publications and source records attributed to W Bernauer.

113 records · Page 7Linked to original sources
PubMedDate not supplied

Differential effects of superoxide dismutase on high energy phosphates, creatine kinase release, and arrhythmias during post-ischaemic reperfusion in isolated rat hearts.

In isolated rat hearts, 25 min of global ischaemia led to significant decreases in the ATP, creatine phosphate (CP), and glycogen contents and increased glucose-6-phosphate (G-6-P) and lactate in the myocardium. During a subsequent reperfusion for 15 min only the CP level, but not ATP and glycogen were restored. G-6-P and lactate were reduced, but remained still elevated in comparison with non-ischaemic hearts. The post-ischaemic coronary flow volume and creatine kinase (CK) release increased significantly compared with preischaemic values. Arrhythmias such as extrasystoles, ventricular tachycardia, flutter and fibrillation, occurred, especially during the first few minutes of reperfusion. Application of the oxygen radical scavenger, superoxide dismutase (SOD), enhanced the myocardial creatine phosphate content during reperfusion. In fibrillating hearts, SOD also increased the ATP content in comparison with non-treated hearts. Superoxide dismutase was effective only during reperfusion and not during the preceding ischaemia. Neither the CK release nor reperfusion arrhythmias were decreased by the radical scavenger. The results suggest that the superoxide radical is involved in the reduction of high energy phosphates during post-ischaemic reperfusion and that this effect can be antagonised by the superoxide anion scavenger superoxide dismutase.

Animals↗
PubMedDate not supplied

Myocardial damage by ventricular fibrillation in isolated perfused rat hearts, and its underlying mechanisms.

In isolated perfused rat hearts ventricular fibrillation (VF), elicited electrically and persisting further spontaneously, led to an extensive release of creatine kinase (CK). Coronary flow volume and oxygen consumption were increased. In contrast, the CK release was only very small in hearts which were stimulated permanently with rhythmic impulses of 10 Hz, whereas the increase in coronary flow and oxygen consumption was significantly greater. When a relative ischemia was induced by perfusion at a low pressure, the CK release from fibrillating hearts was not greater, but less than at a higher perfusion pressure. It appeared unlikely, therefore, that the CK release from fibrillating hearts was simply due to an oxygen deficiency, although a decrease of ATP and glycogen, and an increase of glucose-6-phosphate and lactate in the myocardium were found. When VF was interrupted by lidocaine, the enzyme leakage was reduced only in the experiments with the higher perfusion pressure. A partial restoration of the myocardial metabolites after 1 h was observed. Findings in maximally ischemic hearts further supported the idea that the enzyme release in fibrillating hearts was not merely due to a lack of oxygen. Complete interruption of the coronary perfusion led to the release of only small CK activities during subsequent coronary reperfusion, whereas the metabolic alterations were more distinct than in fibrillating hearts. Mechanisms responsible for the enzyme release during fibrillation, besides a moderate oxygen deficiency, are discussed.

Adenosine Triphosphate↗
PubMedDate not supplied

Post-ischemic release of nucleosides and oxypurines in isolated rat hearts. Possible involvement of ventricular fibrillation.

In isolated perfused rat hearts global ischemia for 2, 5, and 15 min was produced. Depending on the duration of the ischemia, postischemic reperfusion led to the release of adenosine and its catabolites, and to more or less severe ventricular tachyarrhythmias. When ventricular fibrillation occurred, a highly significant increase in the purine release was observed compared with non-fibrillating hearts. Prevention of fibrillation by antiarrhythmic drugs decreased the purine release in a highly significant way. After only 2 min of ischemia, reperfusion did not lead to ventricular fibrillation. Electrical induction of fibrillation during the reperfusion in these hearts provoked the release of very high amounts of the purine compounds. A similar effect of electrically-induced fibrillation was also obtained in hearts without a previous ischemic period. The findings suggest that ventricular fibrillation is able to induce the release of purine derivatives from the heart.

Adenosine↗
PubMedDate not supplied

Effect of antiarrhythmic drugs on the postischaemic metabolic recovery of isolated rat hearts.

In isolated perfused rat hearts, global ischaemia for 20 or 40 min led to a substantial decrease of myocardial ATP, creatine phosphate and glycogen, and to an increase in lactate and glucose-6-phosphate. Subsequent coronary reperfusion was associated with severe tachyarrhythmias (ventricular fibrillation occurring in 40% of the hearts after 20 min of ischaemia, and in 100% after 40 min of ischaemia) and the release of great activities of creatine kinase. Metabolic recovery was obtained only in hearts in which reperfusion-induced fibrillation was lacking. Significant improvement of the metabolic recovery during reperfusion was obtained with corynanthine, a stereoisomer of yohimbine, given in concentrations which prevented reperfusion-induced fibrillation. Moreover, a highly significant decrease of the enzyme release was observed. Similar results were obtained with quinidine. Lidocaine (30 mumol/l) failed to prevent ventricular fibrillation and had no beneficial effect on myocardial metabolism. The effects of these antiarrhythmic drugs are discussed in view of the importance of ventricular fibrillation on postischaemic metabolic recovery.

Adenosine Triphosphate↗