Larsen R, Drobnik L, Teichmann J, Radke J, Kettler D
Anaesthesist. 1979 Oct;28(10):494-6.
Arterial hypotension to about 50 mm Hg mean pressure was induced in anaesthetized and artificially ventilated dogs by halothane, nitroprusside, and trimethaphan to study their effects on cerebral blood flow and intracranial pressure during hypotension. During nitroprusside induced hypotension there was a 32% increase in cerebral blood flow above control and a marked decrease in cerebral arteriovenous oxygen content difference indicating luxury perfusion of the brain. Cerebral blood flow remained high even 30 min after termination of hypotension. During halothane and trimethaphan hypotension cerebral blood flow remained unchanged. In all groups epidural pressure did not change substantially during hypotension but increased during recovery from nitroprusside hypotension by a maximum of 72% above control. It is concluded that during and after nitroprusside hypotension loss of cerebral autoregulation occurs which may result in a marked rise in intracranial pressure. Special vulnerability seems to exist shortly after termination of induced hypotension when arterial pressure begins to rise and brain perfusion follows a pressure-flow relationship.
通过氟烷、硝普钠和阿方那特使麻醉并人工通气的犬的动脉血压降至平均约50 mmHg，以研究低血压期间它们对脑血流量和颅内压的影响。在硝普钠诱发的低血压期间，脑血流量比对照增加32%，脑动静脉氧含量差显著降低，表明脑的过度灌注。即使在低血压终止后30分钟，脑血流量仍保持较高水平。在氟烷和阿方那特诱发的低血压期间，脑血流量保持不变。在所有组中，硬膜外压力在低血压期间没有显著变化，但在从硝普钠低血压恢复过程中增加，最高比对照高出72%。得出的结论是，在硝普钠低血压期间及之后会发生脑自动调节功能丧失，这可能导致颅内压显著升高。当动脉压开始上升且脑灌注遵循压力-流量关系时，在诱发低血压终止后不久似乎存在特殊的易损性。
