Cardiac hypertrophy alters myocardial response to ischaemia and reperfusion in vivo
1Department of Kinesiology, University of Illinois, Urbana 61801.
Insights
Cardiac hypertrophy, induced by aortic constriction or swimming, protected rat hearts against ischemia-reperfusion injury. Hypertrophied hearts showed better antioxidant status and energy metabolism, indicating enhanced resistance to I-R damage.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
- Oxidative Stress
Background:
- Cardiac hypertrophy can alter myocardial response to stress.
- Ischemia-reperfusion (I-R) injury is a critical concern in cardiovascular disease.
- Understanding protective mechanisms in hypertrophied hearts is vital.
Purpose of the Study:
- To investigate the impact of cardiac hypertrophy on myocardial biochemical and physiological responses to I-R.
- To compare the effects of different hypertrophy models (aortic constriction vs. swimming training) on I-R tolerance.
- To assess oxidative and antioxidant status, and energy metabolism during I-R in hypertrophied hearts.
Main Methods:
- Cardiac hypertrophy was induced in rats via aortic constriction (PH) or swimming training (TH).
- Open-chest rat hearts underwent 30 min ischemia followed by 15 min reperfusion (I-R) or sham operation.
- Myocardial biochemical markers (glutathione, ATP, adenine nucleotides) and physiological parameters (heart rate, pressure) were measured.
Main Results:
- I-R significantly depleted glutathione (GSH) and reduced the GSH/GSSG ratio in control hearts, alongside decreased ATP and energy charge.
- Hypertrophied hearts (PH and TH) showed no significant alterations in GSH status or adenine nucleotide metabolism post-I-R.
- TH rats exhibited preserved heart rate, peak systolic pressure, and energy charge during I-R compared to controls.
Conclusions:
- Well-functioning hypertrophied hearts demonstrate resistance to I-R-induced disturbances in oxidative and antioxidant functions.
- Hypertrophy may confer cardioprotection against I-R injury by maintaining cellular redox balance and energy homeostasis.
- These findings suggest potential therapeutic strategies targeting hypertrophy-related protective pathways.
Abstract:
The impact of cardiac hypertrophy on myocardial biochemical and physiological responses to ischaemia-reperfusion (I-R) was investigated in vivo. 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 oxidative and antioxidant status, or lipid peroxidation. However, I-R significantly decreased glutathione (GSH) content, increased glutathione disulfide (GSSG) content, and reduced GSH/GSSG ratio in the SC hearts. These alterations were associated with decreased activities of GSH peroxidase and GSSG reductase, and an increase in lipid peroxidation. Myocardial ATP, total adenine nucleotide content and energy charge in SC were significantly decreased after ischaemia, whereas levels of purine nucleotide derivatives, particularly adenosine, were elevated. No significant alteration of GSH status of adenine nucleotide metabolism occurred after ischaemia or I-R in hypertrophied hearts. In both PH and TH, glutathione content was significantly higher than in SC, whereas activities of GSH peroxidase and GSSG reductases were lower. TH rats maintained a higher heart rate (HR), peak systolic pressure, and energy charge during I-R. These data indicate that hypertrophied but well-functioned hearts may be more resistant to I-R induced disturbances of myocardial oxidative and antioxidant functions.
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