摘要
The effects of hypoxic preconditioning (HP) on the functions of myocardial mitochondria and ATP content were studiedin the rat. Rats were exposed to a simulated altitude of 4000m (with a barometric pressure of 43 kPa) for 1d. The myocardialmitochondrial respiratory function was determined with the Clark type O2 electrode, mitochondrial membrane fluidity (MMF) wasassayed with fluorescence polarizative method, and the myocardial content of ATP, ADP and AMP were measured with high performance liquid chromatography. It was found that after the administration of HP, the ATP content was increased from 31.89±2.42/mg·g-1 to 60. 55±3.52/mg·g-1 (P<0.01 ), mitochondrial respiratory control rate (RGR) was increased from 1.84 ±0.58 to4. 55 ± 0. 32 (P<0.01), MMF was significantly increased (P< 0.05) and the activities of FO F1 -ATPase and Na+ -K+ -ATPasewere increased by 66% and 25%, respectively. It is concluded that HP is efficacious to improve myocardial energy metabolismthrough the mechanism of the increase of mitochondrial membrane fluidity and the improvement of mitochondrial respiratory function.
The effects of hypoxic preconditioning (HP) on the functions of myocardial mitochondria and ATP content were studiedin the rat. Rats were exposed to a simulated altitude of 4000m (with a barometric pressure of 43 kPa) for 1d. The myocardialmitochondrial respiratory function was determined with the Clark type O2 electrode, mitochondrial membrane fluidity (MMF) wasassayed with fluorescence polarizative method, and the myocardial content of ATP, ADP and AMP were measured with high performance liquid chromatography. It was found that after the administration of HP, the ATP content was increased from 31.89±2.42/mg·g-1 to 60. 55±3.52/mg·g-1 (P<0.01 ), mitochondrial respiratory control rate (RGR) was increased from 1.84 ±0.58 to4. 55 ± 0. 32 (P<0.01), MMF was significantly increased (P< 0.05) and the activities of FO F1 -ATPase and Na+ -K+ -ATPasewere increased by 66% and 25%, respectively. It is concluded that HP is efficacious to improve myocardial energy metabolismthrough the mechanism of the increase of mitochondrial membrane fluidity and the improvement of mitochondrial respiratory function.
