[The effect of captopril on hemodynamics in patients of chronic obstructive pulmonary disease with pulmonary hypertension].
One of the main causes of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) is considered to be hypoxic pulmonary vasoconstriction, which may partly be mediated by angiotensin II. Ten patients with COPD were administered with captopril (25mg sublingually). Hemodynamics blood gases renin activity inducing angiotensin II and angiotension converting enzyme (ACE) and TXB2/6-ketone-PGF1 alpha were studied through Swan-Ganz catheter before and after administration of the drug. Captopril reduced mean pulmonary artery pressure and pulmonary vascular resistance by 22% and 30% respectively. Levels of ACE angiotension II and TXB2/6-ketone-PGF1 alpha were reduced. There was no significant change in blood gases. Heart rate and systemic arterial pressure did not change significantly. These results suggest that captopril is of value in reducing pulmonary artery pressure and pulmonary vascular resistance.
Wang
S
S
Affiliated Central Hospital, Shen Yang Medical College, Shenyang.
D000804:Angiotensin II / Q000097:blood; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D013929:Thromboxane B2 / Q000097:blood
D000804:Angiotensin II; D013929:Thromboxane B2; D002216:Captopril; D007703:Peptidyl-Dipeptidase A