Gelman S, Reves J G, Harris D
Anesth Analg. 1983 Feb;62(2):135-9.
Experiments were performed on nine dogs instrumented with pulmonary artery Swan-Ganz catheters and catheters placed into the distal aorta and posterior caval vein. Electromagnetic flowmeter probes were placed around the portal vein and hepatic artery, and the portal vein was cannulated. A week later, systemic and splanchnic circulatory variables were studied before and after 10 mg/kg of midazolam given intravenously. Three minutes after injection, heart rate increased 26% (P less than 0.006), cardiac index decreased 15% (P less than 0.001), portal flow increased 19% (P greater than 0.05), and hepatic arterial flow decreased slightly (P less than 0.002). Later, portal blood flow decreased 17% below baseline values (P less than 0.006). The biphasic response of portal blood flow to midazolam is probably related to redistribution of blood within the splanchnic system (blood mobilization from spleen and intestine). It is suggested that because maintenance of cardiac output during midazolam anesthesia depends on compensatory mechanisms, failure to increase cardiac output with compensatory increases in heart rate, contractility, and blood volume mobilization from the splanchnic circulation could result in decreased cardiac output.
对九条狗进行了实验,这些狗均植入了肺动脉 Swan-Ganz 导管以及置于主动脉远端和后腔静脉的导管。电磁流量计探头置于门静脉和肝动脉周围,并对门静脉进行插管。一周后,在静脉注射 10mg/kg 咪达唑仑前后研究全身和内脏循环变量。注射后三分钟,心率增加 26%(P<0.006),心脏指数降低 15%(P<0.001),门静脉血流量增加 19%(P>0.05),肝动脉血流量略有下降(P<0.002)。随后,门静脉血流量比基线值降低 17%(P<0.006)。门静脉血流量对咪达唑仑的双相反应可能与内脏系统内的血液重新分布(脾脏和肠道的血液动员)有关。有人认为,由于咪达唑仑麻醉期间心输出量的维持依赖于代偿机制,若不能通过心率、收缩力的代偿性增加以及内脏循环中血容量的动员来增加心输出量,可能会导致心输出量下降。