Federici A, Rizzo A, Cevese A
J Auton Nerv Syst. 1985 Apr;12(4):333-45. doi: 10.1016/0165-1838(85)90048-7.
The present study was performed on conscious, chronically instrumented dogs, which underwent selective blockade of sympathetic adrenergic and vagal outflows. Excitements were performed on these animals in normal states (N), after chronic treatment with guanethidine, for sympathetic blockade (SB), after cold vagal blockade (VB), and after combined sympathetic and vagal blockade (SB + VB). Heart rate and arterial blood pressure were monitored in all the experiments, while a group of dogs was also tested with an electromagnetic flowmeter on the superior mesenteric artery. The role of the sympathetic and parasympathetic controls in the defence reaction was assumed from comparison of experiments performed in the presence or in the absence of each (or both) autonomic component(s). In the SB + VB condition, excitement was followed by sudden hypotension, without changes in heart rate. In VB experiments, a brief and transient hypotension appeared, followed by gradually developed hypertension, while heart rate progressively rose in about 5 s; there was no sudden increase in mesenteric vascular resistance, which contrasted with the very marked reaction in N experiments. Under vagal control alone (SB), the stimulus elicited prompt tachycardia and hypertension, followed by a period of moderately reduced blood pressure. We conclude that, while the defence reaction leads to a sudden fall of arterial blood pressure, in the absence of compensatory mechanisms, both branches of the autonomic nervous system play a protective role against hypotension. In addition, the modulation of the vagal outflow, leading to sudden changes in the heart performance, seems to be responsible for the initiation of the overall haemodynamic adjustments following excitements. The possibility that withdrawal of the parasympathetic outflow to the heart may raise arterial blood pressure was verified in a special experiment in which artificial vagal stimulation in a conscious (vagal blocked) dog, was turned off for brief periods, before and after guanethidine. This led to changes in blood pressure and heart rate very similar to those seen at the onset of the defence reaction, both in N and SB conditions.
本研究在清醒、长期植入仪器的犬只上进行,这些犬只接受了交感肾上腺素能和迷走神经传出纤维的选择性阻断。在正常状态(N)下、用胍乙啶进行慢性治疗以实现交感神经阻断(SB)后、冷刺激迷走神经阻断(VB)后以及交感和迷走神经联合阻断(SB + VB)后,对这些动物进行刺激。在所有实验中监测心率和动脉血压,同时一组犬还用电磁流量计对肠系膜上动脉进行检测。通过比较在存在或不存在每种(或两者)自主神经成分的情况下进行的实验,推测交感和副交感神经控制在防御反应中的作用。在SB + VB状态下,刺激后出现突然的低血压,心率无变化。在VB实验中,出现短暂的一过性低血压,随后逐渐发展为高血压,而心率在约5秒内逐渐升高;肠系膜血管阻力没有突然增加,这与N实验中的非常明显的反应形成对比。仅在迷走神经控制下(SB),刺激引发迅速的心动过速和高血压,随后血压有一段适度下降的时期。我们得出结论,虽然防御反应会导致动脉血压突然下降,但在没有代偿机制的情况下,自主神经系统的两个分支都对低血压起到保护作用。此外,迷走神经传出纤维的调节导致心脏功能突然变化,似乎是兴奋后整体血流动力学调整启动的原因。在一项特殊实验中验证了心脏副交感神经传出纤维撤离可能会升高动脉血压,该实验中,在胍乙啶给药前后,有意识(迷走神经阻断)的犬只短暂关闭人工迷走神经刺激。这导致血压和心率的变化与在N和SB状态下防御反应开始时观察到的变化非常相似。