Induction of remifentanil by bradycardia and hypotension through distinct biochemical mechanisms

Induction of remifentanil by bradycardia and hypotension through distinct biochemical mechanisms
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通过不同的生化机制诱导瑞芬太尼出现心动过缓和低血压

DOI:
10.5897/ajpp12.498
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发表时间:
2012-10
影响因子:
--
通讯作者:
Ru-Ping Dai
Ru-Ping Dai
中科院分区:
--
文献类型:
--
作者:
Yong Yang;Di Fu;Qu-Lian Guo;Wu Hui;Ru-Ping Dai

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众所周知,与其他阿片类药物相比,瑞芬太尼可引起更显著的心动过缓和低血压。然而,其基本机制仍然知之甚少。本研究假设瑞芬太尼导致心动过缓和低血压具有不同的机制,并旨在验证这一假设。验证这一假设将拓宽我们对瑞芬太尼潜在作用机制的理解,并可能为瑞芬太尼的临床应用提供一些指导。在麻醉家兔给药前和给药后的指定时间测量平均动脉压和心率。迷走神经切断组,暴露双侧颈部迷走神经,分别切断一侧迷走神经。瑞芬太尼立即引起轻微但显著的心动过缓,并在1分钟内完全恢复。另一方面,推注瑞芬太尼导致严重的低血压,持续超过5分钟。双侧迷走神经切断可延迟瑞芬太尼介导的心动过缓的恢复,但对瑞芬太尼诱发的低血压无明显影响。非特异性阿片受体拮抗剂纳洛酮预处理可完全预防瑞芬太尼介导的低血压,但仅部分逆转瑞芬太尼介导的心动过缓。瑞芬太尼引起的心动过缓和低血压具有不同的生理生化机制。瑞芬太尼诱导的心动过缓是通过阿片受体依赖性和非依赖性途径介导的,而瑞芬太尼诱导的低血压仅通过阿片受体依赖性途径介导。
Remifentanil has been well known to cause much more significant bradycardia and hypotension as compared with other opioids. However, the underlying mechanism is still poorly understood. The present study hypothesized that remifentanil led to bradycardia and hypotension with distinct mechanisms and aimed to test this hypothesis. Testing the hypothesis would broaden our understanding the underlying mechanism of remifentanil and may provide some guidance in the use of remifentanil clinically. Mean arterial pressure and heart rate were measured before and at the indicated time after drug treatment in the anesthetized rabbits. In the vagotomy group, bilateral vagus in the neck was exposed and one section of the vagus severed respectively. Remifentanil caused slight but significant bradycardia immediately which recovered entirely within one minute. On the other hand, bolus injection of remifentanil led to severe hypotension which sustained for more than five minutes. Bilateral vagotomy could delay the recovery of remifentanil-mediated bradycardia but did not affect remifentanil-evoked hypotension significantly. Pretreatment with naloxone, a non-specific opioid receptor antagonist could entirely prevent the remifentanil-mediated hypotension but only partially reversed remifentanil-mediated bradycardia. Remifentanil induces bradycardia and hypotension with distinct physiological and biochemical mechanisms. Remifentanil-induced bradycardia is mediated by opioid receptor-dependent and -independent pathways; however, remifentanil-induced hypotension is only through opioid receptor-dependent pathway.
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