NALOXONE REQUIRES CIRCULATING CATECHOLAMINES TO ATTENUATE THE CARDIOVASCULAR SUPPRESSION OF ENDOTOXIC-SHOCK
NALOXONE REQUIRES CIRCULATING CATECHOLAMINES TO ATTENUATE THE CARDIOVASCULAR SUPPRESSION OF ENDOTOXIC-SHOCK
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DOI：
10.1016/0022-4804(88)90125-4
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发表时间：
1988-01-01
影响因子：
2.2
通讯作者：
REYNOLDS, DG
中科院分区：
文献类型：
--
作者：
ALLGOOD, SC;GURLL, NJ;REYNOLDS, DG
阿片受体拮抗剂纳洛酮（NAL）改善犬失血性和内毒素性休克时的心血管功能。如果神经和肾上腺儿茶酚胺的释放减弱，NAL不会产生预期的犬失血性休克心血管功能的改善。本研究验证了一个假设，内啡肽-儿茶酚胺相互作用的心脏是负责的心血管抑制内毒素休克的一部分。两组5只狗的仪器测量平均动脉压（MAP），左心室压力随时间的一阶导数（LV dP dt max），心输出量和心率（HR），然后进行双侧肾上腺切除术，并给予氯异松达明产生神经节阻滞。在t= 0 min时，给予犬1 mg/kg（LD 80）的大肠杆菌内毒素。第I组动物从t= 30至t= 60静脉注射NAL 2 mg/kg+ 2 mg/kg· hr。在t= 45时，这些动物以20 μg/kg· hr静脉注射肾上腺素（EPI），直至t= 60。组II动物从t= 30至t= 60接受EPI，从t= 45至t= 60接受NAL，剂量与组I相同。在I组中，NAL单独对MAP、LV dP dt max或HR无影响，EPI显著增加心血管参数（P< 0.002），MAP从52±7增加到159±14 mm Hg。在II组中，EPI使所有参数显著增加，并且添加NAL使所有参数进一步显著增加; MAP从37±3增加到EPI的126±16 mm Hg，然后增加到NAL的175±11 mm Hg。这些数据支持上述假设，并表明循环中需要存在儿茶酚胺才能使纳洛酮逆转内毒素休克中的心血管抑制。
The opiate antagonist naloxone (NAL) improves cardiovascular performance in canine hemorrhagic and endotoxic shock. If the release of neural and adrenal catecholamines is attenuated, NAL does not produce the expected improvement in cardiovascular function in canine hemorrhagic shock. This study tests the hypothesis that an endorphin-catecholamine interaction at the heart is responsible for a part of the cardiovascular depression of endotoxic shock. Two groups of five dogs were instrumented to measure mean arterial pressure (MAP), the first derivative of left ventricular pressure over time (LV dP dt max), cardiac output, and heart rate (HR); they were then subjected to bilateral adrenalectomy and given chlorisondamine to produce ganglionic blockade. At t= 0 min the dogs were given Escherichia coli endotoxin at 1 mg/kg (LD 80). Group I animals received NAL at 2 mg/kg+ 2 mg/kg· hr iv from t= 30 to t= 60. At t= 45 these animals were treated with epinephrine (EPI) at 20 μg/kg· hr iv until t= 60. Group II animals got EPI from t= 30 to t= 60 and NAL from t= 45 to t= 60 at the same doses as Group I. In Group I, NAL alone had no effect on MAP, LV dP dt max, or HR. EPI significantly increased (P< 0.002) cardiovascular parameters with MAP increasing from 52±7 to 159±14 mm Hg. In Group II, EPI produced a significant increase in all parameters, and the addition of NAL produced a further significant increase; MAP increased from 37±3 to 126±16 mm Hg with EPI and then to 175±11 mm Hg with NAL. These data support the above hypothesis and indicate that circulating catecholamines need to be present to allow naloxone to reverse the cardiovascular depression in endotoxic shock.