Presinusoidal vessels predominantly contract in response to norepinephrine, histamine, and KC1 in rabbit Liver

In rabbit livers, it is not well known which segments of the hepatic vascul ature are predominantly contracted by various vasoconstrictors. We determin ed effects of histamine, norepinephrine, and KCI on hepatic vascular resist ance distribution in isolated rabbit livers perfused via the portal vein wi th 5% albumin-Krebs solution at a constant flow rate. Hepatic capillary pre ssure was measured by double vascular occlusion pressure (Pdo) and was used to determine portal (Rpv) and hepatic venous (Rhv) resistances. A bolus in jection of either histamine or norepinephrine dose-dependently increased po rtal venous pressure but not Pdo, resulting in a dose-dependent increase in Rpv and no changes in Rhv. KCl (50 mM), when injected in anterogradely per fused livers, contracted the presinusoidal vessels selectively with liver w eight loss. Although KCL significantly increased Rhv in retrogradely perfus ed livers, the increase in Rpv by 400% of baseline predominated over the in crease in Rhv by 85% of baseline. In the retrogradely perfused livers, KCl produced an initial liver weight loss followed by a profound weight gain. W e conclude that histamine and norepinephrine selectively contract the presi nusoidal vessels. The results on KCl effects suggest that this selective pr esinusoidal constriction might be possibly due to predominant distribution of functionally active vascular smooth muscle in the presinusoidal vessels rather than the hepatic vein in rabbit livers.