CARDIAC-HYPERTROPHY ALTERS MYOCARDIAL RESPONSE TO ISCHEMIA AND REPERFUSION IN-VIVO

Citation
Ll. Ji et al., CARDIAC-HYPERTROPHY ALTERS MYOCARDIAL RESPONSE TO ISCHEMIA AND REPERFUSION IN-VIVO, Acta Physiologica Scandinavica, 151(3), 1994, pp. 279-290
Citations number
39
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
151
Issue
3
Year of publication
1994
Pages
279 - 290
Database
ISI
SICI code
0001-6772(1994)151:3<279:CAMRTI>2.0.ZU;2-#
Abstract
The impact of cardiac hypertrophy on myocardial biochemical and physio logical responses to ischaemia-reperfusion (I-R) was investigated in v ivo. Hypertrophy was produced by aortic constriction (PH) or swimming training (TH). Open-chest rat hearts in PH, TH and a sedentary control group (SC) were subjected: (1) to ischaemia, by surgical occlusion of the main descending branch of the left coronary artery for 30 min; (2 ) to I-R, by releasing the occluded blood vessel for 15 min; or (3) to a sham operation. Ischaemia per se had little effect on heart oxidati ve and antioxidant status, or lipid peroxidation. However, I-R signifi cantly decreased glutathione (GSH) content, increased glutathione disu lfide (GSSG) content, and reduced GSH/GSSG ratio in the SC hearts. The se alterations were associated with decreased activities of GSH peroxi dase and GSSG reductase, and an increase in lipid peroxidation. Myocar dial ATP, total adenine nucleotide content and energy charge in SC wer e significantly decreased after ischaemia, whereas levels of purine nu cleotide derivatives, particularly adenosine, were elevated. No signif icant alteration of GSH status or adenine nucleotide metabolism occurr ed after ischaemia or I-R in hypertrophied hearts. In both PH and TH, glutathione content was significantly higher than in SC, whereas activ ities of GSH peroxidase and GSSG reductase were lower. TH rats maintai ned a higher heart rate (HR), peak systolic pressure, and energy charg e during I-R. These data indicate that hypertrophied but well-function ed hearts may be more resistant to I-R induced disturbances of myocard ial oxidative and antioxidant functions.