title: [Cholecystokinin-octapeptide alleviates tumor necrosis factor-alpha induced changes in rabbit pulmonary arterial reactivity and injuries of endothelium in vitro].
abstract: To explore the mechanism underlying cholecystokinin-octapeptide (CCK-8) induced attenuation of pulmonary arterial hypertension (PAH) in endotoxic shock, the effects of CCK-8 on the changes in rabbit pulmonary arterial reactivity induced by tumor necrosis factor-alpha (TNF-alpha) were observed with the isolated arterial ring technique, and the ultrastructure of pulmonary arterial endothelium was observed under a scanning electron microscope. The contractile response to -adrenoceptor agonist phenylephrine (PE), the endothelium-dependent relaxation response to acetylcholine (ACh) and the endothelium-independent relaxation response to sodium nitroprusside (SNP) were not affected by TNF-alpha (4000 U/ml) after incubation for 2 h, while, if the incubation time was prolonged to 7 or 14 h, the relaxation response of pulmonary artery to ACh was depressed significantly, which, however, could be reversed by concomitant exposure to CCK-8 (0.5 microgram/ml). Incubation of pulmonary artery with CCK-8 (0.5 microgram/ml) alone did not bring out any contractile responses. Moreover, CCK-8 (0.5 microgram/ml) alleviated the ultrastructural lesions induced by TNF-alpha (4000 U/ml). These results suggest that CCK could protect pulmonary arterial endothelium against the detrimental effects by TNF-alpha.
authors.affiliation: Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: A H
authors.initials: AH
authors.lastname: Meng
authors.forename: Y L
authors.initials: YL
authors.lastname: Ling
authors.forename: D H
authors.initials: DH
authors.lastname: Wang
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Gu
authors.forename: S J
authors.initials: SJ
authors.lastname: Li
authors.forename: T N
authors.initials: TN
authors.lastname: Zhu
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000648:ultrastructure*; D005260:Female; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D011651:Pulmonary Artery / Q000502:physiology* / Q000648:ultrastructure; D011817:Rabbits; D012844:Sincalide / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D014409:Tumor Necrosis Factor-alpha; D012844:Sincalide