Intracisternal naloxone and cardiac nerve blockade prevent vasodilatation during simulated haemorrhage in awake rabbits.
Intracisternal naloxone and cardiac nerve blockade prevent vasodilatation during simulated haemorrhage in awake rabbits.
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脑池内纳洛酮和心脏神经阻滞可防止清醒兔子模拟出血期间的血管舒张。
DOI：
10.1113/jphysiol.1989.sp017481
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
S. Potocnik
中科院分区：
文献类型：
--
作者：
R. Evans;J. Ludbrook;S. Potocnik
1.在5只未麻醉的家兔中模拟急性出血，通过对下腔静脉上的袖带充气，使心输出量每分钟下降其静息水平的8.3%。模拟出血后进行假治疗，分级剂量的静脉内和脑池内纳洛酮，并与心包内普鲁卡因心脏神经阻滞后。2.假处理后，对模拟出血的血流动力学反应是双相的。在第一阶段，全身血管传导性稳步下降，心率稳步上升，动脉压仅略有下降。当心输出量下降到其静息水平的约55%时，第二失代偿期突然开始。血管传导性急剧上升，心率缓慢下降，动脉压急剧下降。3.纳洛酮给药（静脉注射，0.04 - 0.4 mg kg-1;脑池内注射，0.2 - 2 μ g kg-1）对模拟出血的血流动力学反应的任一阶段均无影响。4.接受较大剂量纳洛酮（静脉注射，4 - 8 mg kg-1;脑池内注射，4 - 69 mg kg-1）治疗后，第一阶段未受影响，但第二阶段不再发生。在整个模拟出血过程中，全身血管传导性稳步下降，心率上升，动脉压保持良好。防止第二阶段的脑池内纳洛酮剂量比相应的静脉注射剂量低90 - 900倍。第二阶段也被心脏神经阻滞所阻止。5.我们的结论是，内源性阿片机制是负责的血流动力学失代偿时发生的心输出量福尔斯下降到一个临界水平。该机制位于中枢神经系统内。它由心脏发出的信号触发。
1. Acute haemorrhage was simulated in five unanaesthetized rabbits, by inflating a cuff on the inferior vena cava so that cardiac output fell by 8.3% of its resting level per minute. Simulated haemorrhage was performed after sham treatment, after graded doses of intravenous and intracisternal naloxone, and after cardiac nerve blockade with intrapericardial procaine. 2. After sham treatment, the haemodynamic response to simulated haemorrhage was biphasic. During the first phase, systemic vascular conductance fell steadily, heart rate rose steadily, and arterial pressure fell only slightly. A second decompensatory phase began abruptly when cardiac output had fallen to approximately 55% of its resting level. Vascular conductance rose steeply, heart rate fell slowly, and arterial pressure fell precipitately. 3. Treatment with naloxone (intravenous, 0.04‐0.4 mg kg‐1; intracisternal, 0.2‐2 micrograms kg‐1) did not affect either phase of the haemodynamic response to simulated haemorrhage. 4. After treatment with larger doses of naloxone (intravenous, 4‐8 mg kg‐1; intracisternal, 4‐69 micrograms kg‐1), the first phase was unaffected, but the second phase no longer occurred. Throughout simulated haemorrhage, systemic vascular conductance fell steadily, heart rate rose, and arterial pressure was well maintained. The dose of intracisternal naloxone which prevented the second phase was 90‐900 times less than the corresponding intravenous dose. The second phase was also prevented by cardiac nerve blockade. 5. We conclude that an endogenous opiate mechanism is responsible for the haemodynamic decompensation that occurs when cardiac output falls to a critical level. The mechanism is located within the central nervous system. It is triggered by a signal from the heart.
清醒兔低血压出血期间阿片受体介导的肾神经活动减少。
影响因子：
20.1
作者：
Morita,H;Nishida,Y;Motochigawa,H;Uemura,N;Hosomi,H;Vatner,SF
通讯作者：
Vatner,SF