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Hemodynamic studies in long‐ and short‐term portal hypertensive rats: The relation to systemic glucagon levels
Author(s) -
Sikuler Emanuel,
Groszmann Roberto J.
Publication year - 1986
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.1840060315
Subject(s) - medicine , hyperdynamic circulation , portal hypertension , portal venous pressure , hemodynamics , cardiology , constriction , blood pressure , vasodilation , cardiac output , endocrinology , vascular resistance , cirrhosis
It is not known whether the hyperdynamic state which has been observed in several experimental models and in patients with portal hypertension reflects a temporary phase during the evolution of the portal hypertensive syndrome or is an expression of a permanent steady state. A hemodynamic study was performed in a group of rats with long‐standing portal hypertension induced by portal vein constriction performed 6.2 ± 0.1 months earlier. A group of rats matched by age and weight with short‐term (20.7 ± 0.9 days) portal hypertension and a group of long‐term (6.2 ± 0.1 months) sham‐operated rats were used as controls. Cardiac output and regional blood flows were measured using a radioactive microsphere technique. Arterial blood levels of glucagon, a known vasodilator that was implicated in the etiology of the hyperdynamic circulation, were also measured. Portal pressure in long‐ and short‐term portal hypertensive groups (12.3 ± 0.4 and 13.7 ± 0.4 mm Hg; not statistically significant) was higher than in the sham group (9.0 ± 0.3 mm Hg; p<0.01). Cardiac output in the long‐term portal hypertensive rats was similar to the sham‐operated group and lower than in the short‐term portal hypertensive group (19.4 ± 1.0 and 20.6 ± 1.5 vs. 32.7 ± 2.0 ml·min −1 . 100 gm body weight −1 ; p<0.01). Portal venous inflow in the long‐term portal hypertensive group was also similar to the sham group and lower than in the short‐term portal hypertensive group (4.51 ± 0.36 and 4.58 ± 0.39 vs. 6.72 ± 0.48 ml·min −1 100 gm body weight −1 ; p<0.01). Systemic glucagon levels were 244 ± 17 and 297 ± 33 pg·ml −1 in long‐ and short‐term portal hypertensive groups, respectively (not statistically significant). Glucagon level in the sham group was lower (181 ± 22 pg·ml −1 ; p<0.05) compared to the other two groups. These results indicate that after long‐term portal vein constriction, the hyperdynamic circulation disappears while the portal hypertension persists. Whether this is unique to this model or is a universal phenomenon in portal hypertension has yet to be established. High glucagon blood levels do not induce a hyperdynamic circulation in chronic portal hypertension.