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Amelioration of Chronic Intermittent Hypobaric Hypoxia on DecreasedL-type Ca^(2+) Currents by Ischemia/Reperfusion in Cardiomyocytes ofDeveloping Rat
摘要
The aim of the present study was to observe the effect of chronic intermittent hypobaric hypoxia (CIHH) on L-type calcium channel current (I_(CaL)) in developing rat in order to investigate the ionic mechanism of the car-dioprotective effect of CIHH. Age- and body weight-matched postnatal male Sprague-Dawleyrats were divided into four groups: 28-day CIHH group (CIHH28), 42-day CIHH group (CIHH42), 28-day control group (CON28) and 42-day control group (CON42). CIHH neonatal rats were experienced a CIHH treatment simulating 3000-m altitude (P_B = 525 mmHg, P_(O2) = 108.8 mmHg, 5 h/day) in a hypobaric chamber for 28 and 42 days, respectively. Whole-cell patch clamp technique was used to record I_(CaL) in ventricular myocytes of neonatal rats. The results showed: There were no differences of peak current, current-voltage (I-V) relationship curve, and dynamics of I_(CaL) between CON and CIHH cardiomyocytes under normal external solution (P ＞ 0.05). The peak I_(CaL) was decreased and I-V relationship curve was shifted upward during simulated ischemia/reperfusion (I/R) (P ＜ 0.05), but the change of I_(CaL) was much smaller in CIHH cardiomyocytes than in CON cardiomyocytes (P ＜ 0.05). The steady-state inactivation curve of I_(CaL) was shifted to the left during I/R in CON28 and CON42 cardiomyocytes (P ＜ 0.05), but not in CIHH28 and CIHH42 cardiomyocytes (P ＞ 0.05). In conclusion, CIHH has no effect on I_(CaL) in ventricular myocytes of developing rat under basic condition, but effectively antagonizes the inhibition of simulated I/R on I_(CaL), which might be one of the ionic mechanisms for CIHH cardiac protection against I/R injury in developing rats.
延伸閱讀
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