Dogs were subjected to exercise on a treadmill, using a protocol in which the speed and slope were increased every 3min, and which elevated both heart rate (to a mean of 198±14beatsċmin-1) and mean arterial blood pressure (to 150±4mmHg). Then, 24 or 48h later, the dogs were anaesthetized with a mixture of α-chloralose and urethane and subjected to a 25min occlusion of the left anterior descending coronary artery. The control dogs (instrumented but not exercised) were subjected to the same procedure. In some dogs the nitric oxide synthase inhibitor aminoguanidine (50mgċkg-1; intravenous) was administered 30min before occlusion. Baroreflex sensitivity (BRS) was determined by the rapid bolus injection of phenylephrine 60min before, and again 3min after, the onset of occlusion. Exercise markedly reduced the consequences of coronary artery occlusion 24h (but not 48h) later, without modifying myocardial tissue blood flow. In the exercised dogs there were reductions in arrhythmia severity [ventricular fibrillation (VF) during occlusion, 0%; survival from the combined ischaemia/reperfusion insult, 70%] compared with controls (VF during occlusion, 36%; survival, 9%). BRS was preserved during occlusion in the exercised dogs (before occlusion, 1.60±0.54msċmmHg-1; 3min after occlusion, 1.37±0.4msċmmHg-1), but not in controls (before occlusion, 1.28±0.29msċmmHg-1; 3min after occlusion, 0.45±0.12msċmmHg-1; P < 0.05), and other ischaemic changes (inhomogeneity of electrical activation and changes in the ST-segment, recorded over the ischaemic region) were also less marked in the exercised dogs. Exercise-induced cardioprotection was abolished by aminoguanidine (VF during occlusion, 25%; survival, 0%). The results show that even a single period of exercise affords delayed protection against ischaemia/reperfusion-induced VF and other ischaemic changes. Since this protection is abolished by aminoguanidine, and since (inducible) NO synthase activity was elevated 3-fold in left ventricular samples 24h after exercise, we suggest that this protection is mediated by nitric oxide.
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March 08 2002
Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide
László BABAI;
László BABAI
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert Szent-Györgyi Faculty of Medicine, Dóm tér 12, P.O. Box 427, H-6701 Szeged, Hungary
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Zsolt SZIGETI;
Zsolt SZIGETI
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert Szent-Györgyi Faculty of Medicine, Dóm tér 12, P.O. Box 427, H-6701 Szeged, Hungary
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James R. PARRATT;
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert Szent-Györgyi Faculty of Medicine, Dóm tér 12, P.O. Box 427, H-6701 Szeged, Hungary
†Department of Physiology and Pharmacology, Strathclyde Institute for Biomedical Sciences, 27 Taylor Street, Glasgow G4 ONR, U.K.
Correspondence: Professor Emeritus J. R. Parratt, at Strathclyde Institute for Biomedical Sciences (e-mail [email protected]).
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Ágnes VÉGH
Ágnes VÉGH
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert Szent-Györgyi Faculty of Medicine, Dóm tér 12, P.O. Box 427, H-6701 Szeged, Hungary
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Publisher: Portland Press Ltd
Received:
October 11 2001
Accepted:
November 28 2001
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2002
2002
Clin Sci (Lond) (2002) 102 (4): 435–445.
Article history
Received:
October 11 2001
Accepted:
November 28 2001
Citation
László BABAI, Zsolt SZIGETI, James R. PARRATT, Ágnes VÉGH; Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide. Clin Sci (Lond) 1 April 2002; 102 (4): 435–445. doi: https://doi.org/10.1042/cs1020435
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