Tani M, Asakura Y, Hasegawa H, Shinmura K, Ebihara Y, Nakamura Y
Department of Geriatric Medicine, Keio University School of Medicine, Tokyo, Japan.
Cardiovasc Res. 1996 Feb;31(2):263-9.
We previously reported that a brief period of hypoxic perfusion (BHP) prior to ischemia in rat hearts improved functional recovery upon reperfusion with reduced Ca2+ overload. The present study was designed to determine whether the effect of BHP would be associated with a reduction in reperfusion arrhythmias and a preservation of function of the sarcoplasmic reticulum (SR).
Hearts were subjected to 40 min of global ischemia and 30 min of reperfusion after a 20 min period of oxygenated perfusion (oxygenated group: OG), or a 10 min period of oxygenation and 10 min of hypoxic perfusion (hypoxic group: HG). We evaluated the release of Ca2+ by SR blocked by ryanodine, the recovery of left ventricular function, and the reperfusion induced ventricular tachycardia/fibrillation (VT/VF).
Functional recovery improved and the incidence and duration of reperfusion VT/VF were reduced in HG. In HG the uptake of Ca2+ in SR decreased during ischemia, but this decrease was less than that in OG. However, recovery of Ca2+ uptake after reperfusion did not differ between groups. The release of Ca2+ by SR blocked by ryanodine was inhibited in HG throughout the ischemia-reperfusion sequence.
Observations suggest that the benefits of BHP on recovery of function and reperfusion arrhythmias were associated with a decrease in release of Ca2+ by SR blocked by ryanodine.
我们之前报道过，大鼠心脏在缺血前进行短时间的缺氧灌注（BHP）可改善再灌注时的功能恢复，并减少钙超载。本研究旨在确定BHP的作用是否与再灌注心律失常的减少以及肌浆网（SR）功能的保留有关。
心脏在经过20分钟的氧合灌注后（氧合组：OG），或10分钟的氧合和10分钟的缺氧灌注后（缺氧组：HG），进行40分钟的全心缺血和30分钟的再灌注。我们评估了由ryanodine阻断的SR释放Ca2+的情况、左心室功能的恢复以及再灌注诱导的室性心动过速/心室颤动（VT/VF）。
HG组的功能恢复得到改善，再灌注VT/VF的发生率和持续时间降低。在HG组中，缺血期间SR对Ca2+的摄取减少，但这种减少小于OG组。然而，再灌注后Ca2+摄取的恢复在两组之间没有差异。在整个缺血-再灌注过程中，HG组中由ryanodine阻断的SR释放Ca2+受到抑制。
观察结果表明，BHP对功能恢复和再灌注心律失常的益处与由ryanodine阻断的SR释放Ca2+的减少有关。
