ED50 of Verapamil Inhibiting Hypoxic Pulmonary Vasoconstriction in Rats.
10.4097/kjae.1985.18.2.204
- Author:
Seong Deok KIM
1
Author Information
1. Department of Anesthesiology, College of Medicine, Seoul National University, Seoul, Korea.
- Publication Type:In Vitro ; Original Article
- MeSH:
Animals;
Calcium Channel Blockers;
Diltiazem;
Heart Failure;
Hypertension;
Nifedipine;
Oxygen;
Pulmonary Disease, Chronic Obstructive;
Pulmonary Fibrosis;
Rats*;
Vasoconstriction*;
Verapamil*
- From:Korean Journal of Anesthesiology
1985;18(2):204-209
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypoxic pulmonary vasoconstriction(HPV) is an important homeostatic mechanism maintaining arterial oxygen tension, but chronic hypoxic pulmonary vasoconstriction seen is COPD, kyphoscoliosis, and cysic fibtosis may induce pulmonary vascular fibrosis, pulmonary hypertension and finally right heart failure. The mechanism of HPV is still unknown and controversial. Many authors documented that calcium channel blockers such as verapamil, diltiazem and nifedipine amy inhibit HPV in vivo, but studies in vitro are rare. The purpose of this study was to determine DE50 of verapamil effect in HPV in vitro and to make guidelines for ongoing experimental studies about HPV. In the isolated heart-lung preperation perfused with physiologic salt-albumin-blood, ED50 of verapamil inhibition of HPV was 6.0X10(-4)mM/ml, perfusate and the regression equation was % Rmax=-2.49-23.32 log.ml.(verapamil).
