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Long‐term octreotide treatment prevents vascular hyporeactivity in portal‐hypertensive rats
Author(s) -
Sieber C C,
Lee F,
Groszmann R J
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510230541
Subject(s) - octreotide , medicine , perfusion , portal hypertension , vasodilation , nitric oxide , endocrinology , mesenteric arteries , portal venous pressure , blood pressure , endothelium , artery , somatostatin , cirrhosis
Chronically portal‐hypertensive rats show in vitro vascular hyporeactivity in large part mediated by the endothelium‐derived vasodilator nitric oxide. We tested whether long‐term octreotide treatment (15 micrograms/kg subcutaneously in 5% D/W, 8‐hourly) corrects the in vitro vascular hyporeactivity. Increases in perfusion pressures (delta mm Hg) to potassium chloride (30‐300 mmol/L) of in vitro perfused superior mesenteric arterial vascular beds of partial portal vein‐ligated (PVL) rats were significantly ( P < .05) higher in octreotide (n = 9) compared with placebo (n = 10, 5% D/W) treated animals. Octreotide significantly ( P < .05) increased mean arterial pressure compared with placebo, the values being 129 ± 3 and 117 ± 4 mm Hg, respectively. Furthermore, a significant ( P < .001) correlation was observed between in vitro vascular reactivity and mean arterial pressure. Incubation of separate vascular beds (n = 7 for both PVL and sham‐operated rats) with octreotide (10 ‐6 mol/L) did not enhance pressure responses to 125 mmol/L potassium chloride, and failed to increase perfusion pressures in preconstricted vessel preparations (n = 6), excluding a direct inhibitory effect on NO. In summary, long‐term octreotide treatment prevents in vitro vascular hyporeactivity in prehepatic portal‐hypertensive rats, and octreotide does not exert its action through direct effects on endothelium‐derived NO.