Ll. Ji et al., CARDIAC-HYPERTROPHY ALTERS MYOCARDIAL RESPONSE TO ISCHEMIA AND REPERFUSION IN-VIVO, Acta Physiologica Scandinavica, 151(3), 1994, pp. 279-290
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.