Khambatta H J, Stone J G, Khan E
Anesthesiology. 1979 Aug;51(2):127-30. doi: 10.1097/00000542-197908000-00007.
The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who recieved hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin-angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 +/- 2 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane-nitrous oxide anesthesia, mean arterial pressure decreased to 85 +/- 1 torr and plasma renin activity increased to 4.4 +/- 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 +/- 2 torr and plasma renin activity increased to 15.2 +/- 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 +/- 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 +/- 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.
作者们观察到，在术中停止输注用于诱导低血压的硝普钠后，平均动脉压升至低血压前水平之上。对12例接受低血压麻醉以进行脑动脉瘤手术矫正的患者进行了研究，以评估肾素-血管紧张素系统在这一现象中的作用。清醒状态下，平均动脉压为100±2托，血浆肾素活性为3.0±0.1纳克/毫升/小时。建立稳定的氟烷-氧化亚氮麻醉30分钟后，平均动脉压降至85±1托，血浆肾素活性升至4.4±0.1纳克/毫升/小时。在接下来的两小时手术过程中，两者均无明显变化。在硝普钠诱导的低血压期间，平均动脉压降至49±2托，血浆肾素活性升至15.2±0.2纳克/毫升/小时。停止输注硝普钠30分钟后，平均动脉压升至112±2托，不仅高于低血压前水平，而且显著高于清醒状态下记录的水平。此时的血浆肾素活性为10.9±0.1纳克/毫升/小时。由于血浆肾素的半衰期为15分钟，这些数据表明，血浆肾素活性持续升高可能是硝普钠诱导低血压后动脉压升高的原因。
