肺心病患者吸入一氧化氮即刻血液动力学效应

Acute Hemodynamic Effects of Inhaled Nitric Oxide in Patients With Cor Pulmonale

目的：评价一氧化氮（ＮＯ）对肺心病肺动脉高压的急性治疗作用。方法：１３例（男９例，女４例）肺心病患者，平均年龄５２±１１岁（２１～５６岁）。检查前３天停服血管扩张药，在心导管检查时吸入ＮＯ（２０～８０ｐｐｍ）１０～１５分钟，吸入前后测右房压、肺动脉压同时取动脉及混合静脉血测血氧饱和度、血氧分压（ＰａＯ２）及混合静脉血氧饱和度（ＳｖＯ２）。结果：吸入ＮＯ后，肺动脉压下降，收缩压、舒张压及平均压分别下降３６．０％、３２．４％及２８．１％（Ｐ均＜０．００１）；肺血管阻力降低３８．５％（Ｐ＜０．０１）；肺动脉收缩压与体动脉收缩压比值从０．３９下降到０．２４，心脏指数增加１０．５％（Ｐ＜０．０１）；ＰａＯ２、ＳｖＯ２均值分别增加４．７％、８．７％（Ｐ均＜０．０５）。结论：吸入ＮＯ可使肺心病肺动脉高压患者肺血管扩张，降低肺动脉压及右室后负荷能预防或延缓心力衰竭的发生。

Objective:To evaluate the acute therapeutic effects of inhaled nitric oxide(NO) in patients of chronic cor pulmonale with pulmonary hypertension.Methods:Thirteen patients(9 males and 4 females),aged 52±11 yrs (21～56 yrs) of chronic cor pulmonale with pulmonary hypertension,inhaled NO(20-80 ppm) for 10-20 min during cardiac catheterization. All vasodilating drugs were stopped three days before the examination.Hemodynamic parameters were measured before and after inhalation. Arterial and mixed venous blood samples were taken for the measure ments Of SaO2 PaO2 and SvO2.Results:After inhalation of NO,the systolic,diastolic and mean pulmonary arterial pressure dropped by 36.0%,32.4%and 28.1%,respectively,all p<0.001,total pulmonary resistance also decreased by 38.5%(p<0.01).The ratio of pulmonary systolic pressure to systemic systolic pressure fell from 0.39 to 0.24,Cardiac index increased by 10.5%(p<0.01),PaO2, SvO2 increased by 4.7%and 8.7%,respectively(all p<0.05).Conclusions:Inhalation of NO could cause pulmonary arterial vasodilation of chronic cor pulmonale with pulmonary hypertension.Reduction of PAP lowers right ventricular after-load,which might prevent or postpone the onset of right heart failure.