Schadt J C, McKown M D, McKown D P, Franklin D
Am J Physiol. 1984 Sep;247(3 Pt 2):R497-505. doi: 10.1152/ajpregu.1984.247.3.R497.
The central and peripheral hemodynamic effects of rapid hemorrhage and subsequent opiate receptor blockade were studied in conscious rabbits. With hemorrhage of less than 12 ml/kg, mean arterial blood pressure (BP) was maintained by an increase in total peripheral resistance (TPR). Cardiac output (CO) declined in spite of an increase in heart rate (HR). Blood loss greater than 13 ml/kg resulted in an abrupt decrease in BP that was largely due to a decline in TPR. CO continued to decline gradually as it did early in hemorrhage. HR also decreased at the transition to hypotension. Subsequent opiate receptor blockade with naloxone (3 mg/kg) produced a prompt increase in BP and a decrease in HR. An increase in TPR accounted for the rise in BP. CO did not change significantly after naloxone. Therefore the hypotension associated with hemorrhage results from a decline in peripheral vascular resistance that is reversible by opiate receptor blockade with naloxone. These results are consistent with the involvement of opiate receptors and endogenous opiate peptides centrally and/or peripherally in control of vascular resistance during acute hemorrhagic hypotension.
在清醒兔中研究了快速失血及随后阿片受体阻断的中枢和外周血流动力学效应。失血少于12 ml/kg时,平均动脉血压(BP)通过总外周阻力(TPR)增加得以维持。尽管心率(HR)增加,但心输出量(CO)仍下降。失血超过13 ml/kg导致BP突然下降,这主要是由于TPR下降所致。CO如在失血早期一样继续逐渐下降。在转变为低血压时HR也下降。随后用纳洛酮(3 mg/kg)阻断阿片受体使BP迅速升高,HR下降。TPR增加导致BP升高。纳洛酮后CO无明显变化。因此,与失血相关的低血压是由于外周血管阻力下降所致,而这种下降可通过用纳洛酮阻断阿片受体来逆转。这些结果与阿片受体和内源性阿片肽在急性失血性低血压期间对血管阻力控制的中枢和/或外周参与是一致的。