Department of Respiratory Therapy, Kaohsiung Medical University, Taiwan.
Kaohsiung J Med Sci. 2011 Aug;27(8):336-43. doi: 10.1016/j.kjms.2011.03.007. Epub 2011 May 11.
There is now increasing evidence from the experimental and clinical setting that therapeutic hypercapnia from intentionally inspired carbon dioxide (CO(2)) or lower tidal volume might be a beneficial adjunct to the strategies of mechanical ventilation in critical illness. Although previous reports indicate that CO(2) exerts a beneficial effect in the lungs, the pulmonary vascular response to hypercapnia under various conditions remains to be clarified. The purpose of the present study is to characterize the pulmonary vascular response to CO(2) under the different conditions of pulmonary hypertension secondary to increased pulmonary blood flow and secondary to hypoxic pulmonary vasoconstriction. Isolated rat lung (n = 32) was used to study (1) the vasoactive action of 5% CO(2) in either N(2) (hypoxic-hypercapnia) or air (normoxic-hypercapnia) at different pulmonary arterial pressure levels induced by graded speed of perfusion flow and (2) the role of nitric oxide (NO) in mediating the pulmonary vascular response to hypercapnia, hypoxia, and flow-associated pulmonary hypertension. The results indicated that inhaled CO(2) reversed pulmonary hypertension induced by hypoxia but not by flow alteration. Endogenous NO attenuates hypoxic pulmonary vasoconstriction but does not augment the CO(2)-induced vasodilatation. Acute change in blood flow does not alter the endogenous NO production.
现在有越来越多的实验和临床证据表明，通过有意地吸入二氧化碳（CO2）或降低潮气量来实现治疗性高碳酸血症，可能是机械通气在危重病中策略的有益辅助手段。尽管先前的报告表明 CO2 在肺部发挥有益作用，但在各种条件下高碳酸血症对肺血管的反应仍有待阐明。本研究的目的是描述在肺动脉高压继发于肺血流量增加和低氧性肺血管收缩的不同情况下，CO2 对肺血管的作用。采用离体大鼠肺（n=32）来研究（1）在不同肺动脉压水平下，用不同的灌流速度产生的 N2（低氧高碳酸血症）或空气（常氧高碳酸血症）中，5%CO2 的血管活性作用；（2）一氧化氮（NO）在介导高碳酸血症、低氧和血流相关性肺动脉高压对肺血管的反应中的作用。结果表明，吸入 CO2 可逆转低氧引起的肺动脉高压，但不能逆转血流改变引起的肺动脉高压。内源性 NO 可减轻低氧性肺血管收缩，但不能增强 CO2 引起的血管舒张。急性血流变化不会改变内源性 NO 的产生。
