Vasodilative action of carbon monoxide on rat pulmonary artery in vitro.
- Author:
Xue-Qin DING
1
;
Gui-Ming LIU
;
Jun-Ke WANG
;
Zhuo-Ren SHENG
Author Information
1. Department of Anesthesiology, The First Affiliated Hospital, China Medical University, Shenyang 110001, xueqinding@yahoo.com
- Publication Type:Journal Article
- MeSH:
Acetylcholine;
pharmacology;
Animals;
Carbon Monoxide;
pharmacology;
Dose-Response Relationship, Drug;
Endothelium, Vascular;
drug effects;
Heme Oxygenase (Decyclizing);
antagonists & inhibitors;
In Vitro Techniques;
NG-Nitroarginine Methyl Ester;
pharmacology;
Nitric Oxide Synthase;
antagonists & inhibitors;
Protoporphyrins;
pharmacology;
Pulmonary Artery;
drug effects;
Rats;
Rats, Wistar;
Vasodilation;
drug effects
- From:
Acta Physiologica Sinica
2002;54(1):38-42
- CountryChina
- Language:English
-
Abstract:
The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.