Effects of serotonin on the cardio-circulatory system of the European eel (Anguilla anguilla) in vivo
Effects of serotonin on the cardio-circulatory system of the European eel (Anguilla anguilla) in vivo
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血清素对欧洲鳗（Anguilla anguilla）体内心脏循环系统的影响
DOI：
10.1007/bf00301176
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
P. Soulier
中科院分区：
文献类型：
--
作者：
J. Janvier;M. Peyraud;P. Soulier
研究了血清素对欧洲鳗体内连续记录的心脏参数（心率、心输出量、心搏量）、腹主动脉和背主动脉血压、鳃血管和全身血管阻力的影响。静脉注射血清素（30 μg·kg−1）引起明显的心动过缓（45%），同时心输出量（50%）、腹侧（35%）和背侧（50%）主动脉血压下降。支气管阻力明显增加（60%），全身阻力下降（30%）。心脏搏量保持不变。血清素对心脏的影响基本不变。羟色胺对心脏参数的影响被甲基塞吉特或双侧心脏迷走神经段抑制。心动过缓可以被认为是迷走神经机制的结果，由血清素作用于中枢甲基塞吉特敏感的血清素能受体。未观察到血清素的肌力作用。本文讨论了心肌收缩性改变的缺乏。迷走神经切断术可减轻5 -羟色胺介导的支气管血管收缩，而甲基塞吉特可抑制剩余的支气管阻力增加（40%）。5 -羟色胺介导的支气管血管收缩可能是由心输出量减少引起的被动机制（依从性）和涉及甲基塞吉特敏感的5 -羟色胺能受体的主动机制的结果。本文讨论了这种血管舒缩效应在鳃摄氧量中的可能参与。5-羟色胺诱导的全身性血管舒张对心脏迷走神经切开术或5-HT1/2、5-HT3和5-HT4受体拮抗剂不敏感，表明其参与的局部机制仍有待评估。
The effects of serotonin on continuously recorded cardiac parameters (heart rate, cardiac output, cardiac stroke volume), ventral and dorsal aortic blood pressures, branchial and systemic vascular resistances were investigated in the European eel in vivo. Intravenous administration of serotonin (30 μg · kg−1) caused a marked bradycardia (45%) and a simultaneous decrease in cardiac output (50%), ventral (35%) and dorsal (50%) aortic blood pressures. Branchial resistance was markedly increased (60%) and systemic resistance decreased (30%). Cardiac stroke volume remained unchanged. The effects of serotonin on cardiac mained unchanged. The effects of serotonin on cardiac parameters were suppressed either by methysergide or a bilateral section of the cardiac vagus. Bradycardia could then be regarded as the consequence of a vagal mechanism triggered by serotonin action on central methysergide-sensitive serotonergic receptors. No inotropic effect of serotonin was observed. This lack of myocardiac contractility modification is discussed. The serotonin-mediated branchial vasoconstriction was attenuated by vagotomy, whereas the residual increase in branchial resistance (40%) was suppressed by methysergide. The serotonin-mediated branchial vasoconstriction could be the consequence of both a passive mechanism (compliance) caused by the decrease in cardiac output and an active mechanism involving methysergide-sensitive serotonergic receptors of the branchial vasculature. A possible involvement of this vasomotor effect in gill oxygen uptake is discussed. The serotonin-induced systemic vasodilation was insensitive either to cardiac vagotomy or to 5-HT1/2, 5-HT3 and 5-HT4 receptor antagonists, suggesting the involvement of a local mechanism which remains to be assessed.