Maron M B, Dawson C A
J Appl Physiol Respir Environ Exerc Physiol. 1980 Jul;49(1):73-8. doi: 10.1152/jappl.1980.49.1.73.
Previously we found that raising cerebrospinal fluid pressure (PCSF) caused pulmonary vasoconstriction mediated by adrenal catecholamines. To localize the site of this vasoconstriction we used the outflow occlusion technique to divide changes in the pulmonary arteriovenous pressure gradient (Pa-v) into upstream and downstream pressure drops. Experiments were conducted in 10 dogs in which the animal's left lower lung lobe was denervated and perfused at constant flow and outflow pressure with blood pumped from the dog's pulmonary artery. Raising PCSF to 218 Torr caused Pa-v to rise from 9.0 to 12.5 Torr. Most (83%) of this increase resulted from an increase in the downstream pressure drop. Previous studies have indicated that changes in the upstream and downstream pressure drops, as measured by this technique, are highly correlated with changes in the resistance of the arterial and venous sides of the vascular bed. Thus, it appears that elevated PCSF caused primarily pulmonary venoconstriction. Similar results were obtained with norepinephrine and epinephrine infusion. This is consistent with previous studies, indicating that adrenal catecholamines are responsible for the increase in Pa-v in response to PCSF in this preparation.
此前我们发现,升高脑脊液压力(PCSF)会导致由肾上腺儿茶酚胺介导的肺血管收缩。为了确定这种血管收缩的部位,我们采用流出道阻塞技术,将肺动静脉压力梯度(Pa-v)的变化分为上游和下游压力降。在10只犬身上进行了实验,这些犬的左下肺叶去神经支配,并以恒定流量和流出压力,用从犬肺动脉泵出的血液进行灌注。将PCSF升高到218托会导致Pa-v从9.0托升至12.5托。这种升高的大部分(83%)是由下游压力降增加所致。先前的研究表明,用该技术测量的上游和下游压力降的变化与血管床动脉侧和静脉侧阻力的变化高度相关。因此,似乎升高的PCSF主要导致肺静脉收缩。用去甲肾上腺素和肾上腺素输注也得到了类似的结果。这与先前的研究一致,表明在该制剂中,肾上腺儿茶酚胺是导致Pa-v升高以响应PCSF的原因。