Susmano A, Passovoy M, Carleton R A
Cardiovasc Res. 1977 Sep;11(5):440-5. doi: 10.1093/cvr/11.5.440.
The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
高碳酸血症性肺动脉高压的机制和潜在介质尚未完全明确。我们对18只犬进行了研究，这些犬在吸入含有10%二氧化碳、20.9%氧气和69.1%氮气的混合气体前后，均处于麻醉状态且自主呼吸，以确定组胺、5-羟色胺和酸血症在高碳酸血症所致肺动脉高压中的作用。高碳酸血症使平均肺动脉压升高0.33千帕（2.5毫米汞柱），而楔压和肺小动脉阻力未发生变化。心输出量显著增加，表明高碳酸血症的肺动脉高压效应主要与血流相关。氯苯那敏和甲基麦角新碱对高碳酸血症性肺动脉高压均无显著影响。输注碳酸氢钠可纠正pH值；肺动脉压和心输出量增加，而肺小动脉阻力下降，提示心输出量增加掩盖了pH值对肺小动脉阻力的影响。氯苯那敏或甲基麦角新碱对肺阻力无影响，表明高碳酸血症时伴随的氢离子浓度升高的血管收缩作用既不归因于组胺释放，也不归因于5-羟色胺释放。
