Maron M B, Hakim T S, Dawson C A
J Appl Physiol Respir Environ Exerc Physiol. 1979 Jan;46(1):84-8. doi: 10.1152/jappl.1979.46.1.84.
To investigate the possibility that a pulmonary vasomotor reflex contributes to the pulmonary hemodynamic response to elevated cerebral spinal fluid pressure (PCSF), we studied 10 chloralose-anesthetized dogs in which the left lower lobe (LLL) perfusion was isolated to eliminate the influence of passive factors and of circulating vasoactive agents. Left lower lobe neural integrity was tested by electrically stimulating the stellate ganglion. This resulted in a 35.5% increase in lobar vascular resistance and a 29.1% increase in systemic vascular resistance. Elevating the PCSF to 137 Torr caused the systemic vascular resistance to increase 33.0%, but resulted in no change in LLL vascular resistance. In the intact right lung, this PCSF elevation resulted in increases in pulmonary artery and left atrial pressures, but no change in right lung vascular resistance. Because the neurally intact LLL did not respond to PCSF elevation and the responses of the right lung could be accounted for by passive mechanisms, we conclude that no pulmonary vascular reflex was elicited by PCSF elevation in this preparation.
为了研究肺血管运动反射是否有助于肺血流动力学对脑脊液压升高(PCSF)的反应,我们对10只水合氯醛麻醉的犬进行了研究,在这些犬中,左下叶(LLL)灌注被分离以消除被动因素和循环血管活性物质的影响。通过电刺激星状神经节来测试左下叶神经的完整性。这导致叶血管阻力增加35.5%,全身血管阻力增加29.1%。将脑脊液压升高到137 Torr会使全身血管阻力增加33.0%,但左下叶血管阻力没有变化。在完整的右肺中,这种脑脊液压升高导致肺动脉和左心房压力升高,但右肺血管阻力没有变化。由于神经完整的左下叶对脑脊液压升高没有反应,并且右肺的反应可以用被动机制来解释,我们得出结论,在该制备中,脑脊液压升高未引发肺血管反射。