Toth P D, Hamburger S A, Judy W V
Circ Shock. 1986;20(1):35-42.
Naloxone reverses the hypotension in various types of hemorrhagic shock models. What has yet to be firmly established is the mechanism by which naloxone reverses the hypotension. In a canine hemorrhagic shock model, impedance cardiography and invasive methods were used to measure various cardiovascular parameters. All dogs (beagles, 10-15 kg) were bled to and maintained at a mean arterial blood pressure (MAP) of 60 mmHg for 90 min and were then given either naloxone (2 mg/kg; n = 6) or an equivalent volume of saline (n = 6) intravenously (IV). After another 90 min observation period, the shed blood was reinfused. No significant differences in the preshock and shock cardiodynamics were noted between the naloxone and the control animals. During the treatment period, MAP was significantly increased in the naloxone group. There was no increase in cardiac output (CO), stroke volume (SV), end diastolic volume (EDV), dP/dt max, dP/dt/P, or HI (the impedance contractility index) over control animals. The most significant parameter improvement was total peripheral resistance (TPR). The data suggest that naloxone in this hemorrhagic shock model improves hemodynamics primarily by increasing vascular resistance.
纳洛酮可逆转各种类型失血性休克模型中的低血压状态。然而，纳洛酮逆转低血压的机制尚未完全明确。在犬失血性休克模型中，采用阻抗心动图和侵入性方法测量各种心血管参数。所有犬（比格犬，体重10 - 15千克）放血至平均动脉血压（MAP）为60 mmHg并维持90分钟，然后静脉注射（IV）纳洛酮（2毫克/千克；n = 6）或等量生理盐水（n = 6）。在另外90分钟的观察期后，回输放出的血液。纳洛酮组和对照组动物在休克前和休克时的心脏动力学无显著差异。在治疗期间，纳洛酮组的MAP显著升高。与对照组动物相比，心输出量（CO）、每搏输出量（SV）、舒张末期容积（EDV）、dP/dt max、dP/dt/P或HI（阻抗收缩性指数）均无增加。最显著改善的参数是总外周阻力（TPR）。数据表明，在此失血性休克模型中，纳洛酮主要通过增加血管阻力来改善血流动力学。
