An experimental study of therapeutic effect of ACEI on chemical-induced ARDS in rats.
- Author:
Heliang LIU
1
;
Jinyuan ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Acute Disease; Angiotensin-Converting Enzyme Inhibitors; therapeutic use; Animals; Captopril; therapeutic use; Disease Models, Animal; Endothelium, Vascular; drug effects; physiopathology; Hypertension, Pulmonary; complications; drug therapy; Male; Oleic Acid; Rats; Rats, Wistar; Respiratory Distress Syndrome, Adult; chemically induced; etiology; prevention & control
- From: Chinese Journal of Preventive Medicine 2002;36(2):93-96
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the role of angiotensin converting enzyme inhibitor (ACEI) in the treatment of acute respiratory distress syndrome (ARDS).
METHODSChanges in physiological and biochemical indexes, and circulating endothelial cells (CEC) were observed in rats of oleic acid-induced ARDS with ACEI-Captopril (Cap) therapy and controls, respectively.
RESULTSUnder the normal systemic blood pressure, Captopril therapy showed good effect on ARDS in rats. Two hours after administration of Captopril, their pulmonary arterial pressure reduced to (14.43 +/- 1.51) mm Hg (1 mm Hg = 0.133 kPa), approximating to normal level, from (23.50 +/- 5.79) mm Hg. The number of CEC, which reflected injuries in pulmonary capillaries, decreased to (4.25 +/- 0.20)/0.9 micro l from (6.88 +/- 1.90)/0.9 micro l. Value of oxygen pressure in arterial blood (PaO(2)) increased to (70.48 +/- 9.54) mm Hg from (35.08 +/- 4.59) mm Hg. In the mean time, ratio of wet to dry lung weight was returned to nearly normal. So, it indicated that high-dose of oleic acid could only induce mild lung injury, and the development of ARDS was obviously inhibited by ACEI.
CONCLUSIONSACEI may effectively depress pulmonary arterial hypertension, block the development of ARDS, and have certain good protective effect on pulmonary capillary endothelia.
