Tuggle D W, Horton J W
Circ Shock. 1986;18(3):215-25.
Beta-endorphin has been implicated in the cardiovascular depression that occurs in shock. While pharmacologic doses of beta-endorphin cause hypotension, physiologic doses of beta-endorphin have not been studied. In this study, six dogs (group I) were given IV beta-endorphin (peak concentrations previously determined in canine shock, 3,200 pg/ml); 5 minutes prior to beta-endorphin infusion, four dogs (group II) were given naloxone, 2 mg/kg bolus, and continuous infusion, 2 mg/kg/hr. In group I, beta-endorphin decreased stroke volume (from 0.99 +/- .12 to 0.57 +/- .08 ml/kg), dP/dt (from 3,167 +/- 140 to 2,875 +/- 412 mmHg X sec), and coronary blood flow (from 2.5 +/- .47 to .68 +/- .11 ml/min/gm), while heart rate rose significantly. Naloxone pretreatment maintained dP/dt, stroke volume, and coronary blood flow with no change in heart rate or mean arterial pressure. This study confirms that beta-endorphin depresses contractility and coronary blood flow in normovolemic nonstressed dogs, suggesting that beta-endorphin is in part responsible for cardiovascular depression in shock.
β-内啡肽与休克时发生的心血管抑制有关。虽然药理剂量的β-内啡肽会导致低血压,但生理剂量的β-内啡肽尚未得到研究。在本研究中,六只狗(第一组)静脉注射β-内啡肽(先前在犬类休克中测定的峰值浓度为3200 pg/ml);在输注β-内啡肽前5分钟,四只狗(第二组)静脉注射纳洛酮,负荷剂量为2 mg/kg,持续输注剂量为2 mg/kg/小时。在第一组中,β-内啡肽使每搏量(从0.99±0.12降至0.57±0.08 ml/kg)、dp/dt(从3167±140降至2875±412 mmHg·秒)和冠状动脉血流量(从2.5±0.47降至0.68±0.11 ml/min/g)降低,而心率显著升高。纳洛酮预处理可维持dp/dt、每搏量和冠状动脉血流量,心率和平均动脉压无变化。本研究证实,β-内啡肽会降低血容量正常且未受应激的狗的心肌收缩力和冠状动脉血流量,提示β-内啡肽在一定程度上是休克时心血管抑制的原因。