Effects of cholecystokinin-octapeptide on the tension of pulmonary artery in rabbits with endotoxic shock.
- Author:
Guo-Chen DUAN
1
;
Yi-Ling LING
;
Zhen-Yong GU
;
Peng WEI
;
Zhi-Yun NIU
;
Shi-Fang YANG
Author Information
1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang, PR China.
- Publication Type:Journal Article
- MeSH:
Animals;
Hypertension, Pulmonary;
etiology;
physiopathology;
Male;
Pulmonary Artery;
drug effects;
physiology;
Rabbits;
Shock, Septic;
complications;
physiopathology;
Sincalide;
pharmacology;
Vasodilation;
drug effects
- From:
Acta Physiologica Sinica
2003;55(2):201-205
- CountryChina
- Language:Chinese
-
Abstract:
For investigation of the regulatory mechanism of cholecystokinin-octapeptide (CCK-8) on pulmonary circulation in rabbits with endotoxic shock (ES) induced by lipopolysaccharides (LPS), mean arterial pressure (MAP) and pulmonary arterial pressure (PAP) were evaluated for 5 h in five groups of rabbits: group of LPS (8 mg/kg, i.v.)-induced ES, group of CCK-8 pretreatment (15 microg/kg, i.v.) 15 min before LPS administration (8 mg/kg, i.v.), group of proglumide pretreatment (1 mg/kg, i.v.) 15 min before LPS administration (8 mg/kg, i.v.), group of CCK (15 microg/kg, i.v.) only, and normal saline (control) group. The pulmonary arterial tension was measured with isolated vascular ring technique. The results showed that LPS-induced pulmonary arterial hypertension was abolished by CCK-8. In contrast, proglumide, a nonspecific antagonist of CCK-8 receptor, potentiated the deleterious effect of LPS. The contractile response of isolated pulmonary artery to alpha-adrenoceptor agonist phenylephrine (PE) was enhanced and the relaxation response to acetylcholine (ACh) was depressed significantly after LPS was injected, but the effect could be reversed by CCK-8. These results suggest that pulmonary circulation is improved by CCK-8 in ES, and the regulatory effects of CCK-8 may be brought about by modulating the pulmonary arterial tension.
