Delle M, Thorén P, Ricksten S E
Department of Physiology, University of Göteborg, Sweden.
Acta Physiol Scand. 1988 Dec;134(4):493-501. doi: 10.1111/j.1748-1716.1998.tb08523.x.
Central haemodynamics were studied in one group of morphine-dependent rats, and in a non-dependent control group, before and after administration of repeated bolus doses of naloxone. Dependence was induced by s.c. morphine pellet implantations. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO) and mean transit time (MTT) were measured in the conscious state, after induction of chloralose anaesthesia and after the administration of naloxone (0.005, 0.05, 0.5 and 5 mg kg-1 i.v.). Total peripheral resistance (TPR), stroke volume (SV) and central blood volume (CBV) were subsequently calculated. The haemodynamic variables did not differ significantly in the conscious state, except for a lower SV, when compared with the non-dependent control group. However, in response to anaesthesia the dependent rats exhibited a greater fall in MAP, mainly due to a TPR decrease. Naloxone elicited a marked increase in MAP in the morphine-dependent group, which was mainly caused by an increase in TPR. Naloxone induced no significant change compared with the control group in CO and CBV, while SV increased concomitantly with a lowered HR after naloxone in the morphine-dependent group. These results suggest that the withdrawal hypertension during morphine abstinence was mainly explained by an increase in TPR, reflecting an augmented tone of the resistance vessels. The minor changes in CBV indicate that the tone of the venous capacitance vessels was largely unaffected by naloxone-induced morphine abstinence.
在一组吗啡依赖大鼠和一个非依赖对照组中,研究了反复静脉推注纳洛酮前后的中心血流动力学。通过皮下植入吗啡丸诱导产生依赖性。在清醒状态、氯醛糖麻醉诱导后以及静脉注射纳洛酮(0.005、0.05、0.5和5 mg·kg⁻¹)后,测量平均动脉压(MAP)、心率(HR)、心输出量(CO)和平均通过时间(MTT)。随后计算总外周阻力(TPR)、每搏输出量(SV)和中心血容量(CBV)。与非依赖对照组相比,清醒状态下血流动力学变量无显著差异,只是SV较低。然而,在麻醉状态下,依赖大鼠的MAP下降幅度更大,主要是由于TPR降低。纳洛酮使吗啡依赖组的MAP显著升高,这主要是由TPR增加引起的。与对照组相比,纳洛酮对CO和CBV无显著影响,而在吗啡依赖组中,纳洛酮注射后SV增加,同时HR降低。这些结果表明,吗啡戒断期间的戒断性高血压主要是由TPR增加所致,反映了阻力血管张力增强。CBV的微小变化表明,静脉容量血管的张力在很大程度上不受纳洛酮诱导的吗啡戒断的影响。