Hemodynamic studies in long- and short-term portal hypertensive rats: The relation to systemic glucagon levels

Abstract

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−1. 100 gm body weight⁻¹; p−1 100 gm body weight⁻¹; p−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.