[Effects of cholecystokinin-octapeptide on the tension of pulmonary artery in rabbits with endotoxic shock].
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.
Duan
Guo-Chen
GC
Department of Pathophysiology, Hebei Medical University, Shijiazhuang, PR China.
Ling
Yi-Ling
YL
Gu
Zhen-Yong
ZY
Wei
Peng
P
Niu
Zhi-Yun
ZY
Yang
Shi-Fang
SF
D000818:Animals; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology*; D011817:Rabbits; D012772:Shock, Septic / Q000150:complications / Q000503:physiopathology*; D012844:Sincalide / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects
D012844:Sincalide