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迷走神经切断、窦主动脉去传入大鼠中PaCO2变化的局部血流动力学效应

Regional hemodynamic effects of changes in PaCO2 in the vagotomized, sino-aortic de-afferented rat.

作者信息

Lioy F, Blinkhorn M T, Garneau C

出版信息

J Auton Nerv Syst. 1985 Apr;12(4):301-13. doi: 10.1016/0165-1838(85)90045-1.

Abstract

Rats were anesthetized with urethane (1.5 g/kg i.p.) paralyzed with gallamine (3 mg/kg, i.v.), artificially ventilated and the vagi, carotid sinus and aortic nerves were cut. PaCO2 levels of 16.4 +/- 0.8, 23.3 +/- 1.6, 32.3 +/- 1.8 and 51.9 +/- 2.2 mm Hg were obtained by hyperventilation in 0%, 3%, 5% and 8% CO2 in O2, respectively. Radioactive microspheres labelled with 57Co or 113Sn were injected into the left ventricle and cardiac output and regional blood flows were determined by the 'arterial reference sample' method. Increasing PaCO2 induced an increase in systemic arterial pressure which was predominantly due to a significant increase in total peripheral resistance, while the increase in cardiac output was much less pronounced and no changes in heart rate were observed. The effect of increasing PaCO2 on regional vascular resistance (VR) was not uniformly distributed. CO2 induced a dilatation in the cerebral, bronchial and hepatic artery vascular beds. Coronary VR was not affected while vasoconstriction was induced by CO2 in the other vascular territories. This vasoconstriction was most significant in skeletal muscle, skin, pancreas, large intestine and kidneys. In most of these territories the vasoconstrictor effect of CO2 was observed at PaCO2 levels above 23.3 mm Hg, while between 16.4 and 23.3 mm Hg there was either no change or a decrease in VR. Propranolol and phentolamine (1 mg/kg and 10 mg/kg, i.v., respectively), which caused a 78% +/- 2% adrenergic blockade, significantly reduced the CO2 pressor and vasoconstrictor effects. Our experiments show that, after peripheral chemoreceptor denervation in the rat: (a) there is a direct relationship between PaCO2 and VR mediated by the sympathetic nervous system over the whole range of PaCO2 values from hypocapnia to hypercapnia, and (b) the various vascular territories contribute to a different extent to the CO2-induced changes in total peripheral resistance.

摘要

用氨基甲酸乙酯(1.5 g/kg腹腔注射)对大鼠进行麻醉,用加拉明(3 mg/kg,静脉注射)使其麻痹,进行人工通气,并切断迷走神经、颈动脉窦神经和主动脉神经。分别通过在含0%、3%、5%和8%二氧化碳的氧气中进行过度通气,使动脉血二氧化碳分压(PaCO2)水平达到16.4±0.8、23.3±1.6、32.3±1.8和51.9±2.2 mmHg。将标记有57Co或113Sn的放射性微球注入左心室,并通过“动脉参考样本”法测定心输出量和局部血流。PaCO2升高导致体循环动脉压升高,这主要是由于总外周阻力显著增加,而心输出量的增加则不太明显,且未观察到心率变化。PaCO2升高对局部血管阻力(VR)的影响并非均匀分布。二氧化碳可使脑、支气管和肝动脉血管床扩张。冠状动脉VR不受影响,而在其他血管区域二氧化碳可诱导血管收缩。这种血管收缩在骨骼肌、皮肤、胰腺、大肠和肾脏中最为显著。在大多数这些区域,在PaCO2水平高于23.3 mmHg时观察到二氧化碳的血管收缩作用,而在16.4至23.3 mmHg之间,VR要么没有变化,要么降低。普萘洛尔和酚妥拉明(分别为1 mg/kg和10 mg/kg,静脉注射)可导致78%±2%的肾上腺素能阻滞,显著降低二氧化碳的升压和血管收缩作用。我们的实验表明,在大鼠外周化学感受器去神经支配后:(a)在从低碳酸血症到高碳酸血症的整个PaCO2值范围内,PaCO2与VR之间存在由交感神经系统介导的直接关系,(b)不同的血管区域对二氧化碳诱导的总外周阻力变化的贡献程度不同。

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