Haouzi P, Huszczuk A, Gille J P, Chalon B, Marchal F, Crance J P, Whipp B J
Laboratoire de Physiologie, Faculté de Médecine, Unité INSERM 14, Vandoeuvre-lès-Nancy, France.
Respir Physiol. 1995 Jan;99(1):41-50. doi: 10.1016/0034-5687(94)00083-c.
It has recently been proposed that afferent fibers from skeletal muscle could sense the state of the microvascular circulation, linking ventilation to the degree of peripheral perfusion or vascular distension (Huszczuk et al., Respir. Physiol., 91:207-226, 1993). Ventilatory and circulatory responses to manipulation of peripheral vascular pressures in the hind limbs of anaesthetized (sodium thiopental) sheep were examined. Inflatable balloons were placed at the caudal ends of the abdominal aorta and the vena cava (Vc). Aortic (Ao) occlusion induced a consistent normocapnic decrease in minute ventilation (VE). In contrast, VE increased significantly during vena cava obstruction, leading to hypocapnia. Small changes in systemic blood pressure were observed (+7 mmHg for Ao occlusion and -12 mmHg during Vc obstruction). Moreover, inflation of the caval balloon superimposed on a previously established Ao occlusion, preventing venous drainage of anastomotic inflow, resulted in a significant rise in distal vascular pressures with trivial changes in systolic blood pressure. This led to a gradual rise of VE, despite further reduction of the CO2 flux to the lungs. The subsequent deflation of the aortic balloon, exposing the hindlimb vasculature to aortic pressure, resulted in an even more profound hypocapnic hyperpnea. The concurrent arterial blood pressure changes were too small to possibly involve the ventilatory component of the arterial baroreflex. We therefore hypothesize, that perfusion-related afferent signals within the muscles could contribute to respiratory homeostasis by maintaining ventilation of the lungs commensurate with the circulatory state of the muscular apparatus.
最近有人提出,来自骨骼肌的传入纤维能够感知微血管循环状态,将通气与外周灌注程度或血管扩张联系起来(胡斯楚克等人,《呼吸生理学》,91:207 - 226,1993)。对麻醉(硫喷妥钠)绵羊后肢外周血管压力进行操纵时的通气和循环反应进行了研究。在腹主动脉和腔静脉(Vc)的尾端放置了可充气气球。主动脉(Ao)阻断导致分钟通气量(VE)出现一致的正常碳酸血症性下降。相反,腔静脉阻塞期间VE显著增加,导致低碳酸血症。观察到全身血压有微小变化(Ao阻断时升高7 mmHg,Vc阻塞时降低12 mmHg)。此外,在先前建立的Ao阻断基础上对腔静脉气球进行充气,阻止吻合口流入的静脉回流,导致远端血管压力显著升高,而收缩压仅有微小变化。这导致VE逐渐升高,尽管进入肺部的二氧化碳通量进一步减少。随后对主动脉气球进行放气,使后肢血管系统暴露于主动脉压力下,导致更严重的低碳酸血症性呼吸增强。同时发生的动脉血压变化太小,不可能涉及动脉压力感受器反射的通气成分。因此,我们假设,肌肉内与灌注相关的传入信号可能通过维持与肌肉器官循环状态相称的肺通气来促进呼吸稳态。