We determined the vascular response to anaphylaxis in isolated canine livers perfused with autologous blood at a constant pressure via the portal vein, with hepatic artery ligation to simplify the vascular system. We also studied the validity of the double occlusion pressure (Pdo) as a measure of the capillary pressure (Pc) in the isolated canine liver. Pdo was compared with Pc measured using the traditional isogravimetric method (Pc,i), and both parameters showed a strong correlation (Pdo = 0.34 + 0.90 Pc,i; r = 0.93; P < 0.01). This indicated that Pdo provided an accurate indication of Pc in the isolated liver. In livers with anaphylaxis induced by the intraportal injection of Ascaris suum antigen (5 mg; 1.0 +/- 0.03 mg/kg body wt), hepatic vascular resistance and Pc (assessed as Pdo) were increased transiently by 29-fold and 3.4 mmHg, respectively, along with a significant increase of liver weight. The ratio of presinusoidal to postsinusoidal vascular resistance decreased from 0.89 +/- 0.05 to 0.36 +/- 0.12, suggesting that hepatic venous constriction was predominant. In livers perfused in the antidromic direction from the hepatic vein to the portal vein, anaphylaxis caused marked presinusoidal vasoconstriction that was consistent with hepatic venoconstriction as well as a significant and sustained decrease of liver weight below the baseline. These results suggest that anaphylaxis produced hepatic weight gain because of an increase in sinusoidal pressure caused by hepatic venoconstriction. Such hepatic venoconstriction may play an important role in the development of portal hypertension and hepatic congestion associated with anaphylactic shock.

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In rabbit livers, it is not well known which segments of the hepatic vasculature are predominantly contracted by various vasoconstrictors. We determined effects of histamine, norepinephrine, and KCl on hepatic vascular resistance distribution in isolated rabbit livers perfused via the portal vein with 5% albumin-Krebs solution at a constant flow rate. Hepatic capillary pressure was measured by double vascular occlusion pressure (Pdo) and was used to determine portal (Rpv) and hepatic venous (Rhv) resistances. A bolus injection of either histamine or norepinephrine dose-dependently increased portal 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 perfused livers, contracted the presinusoidal vessels selectively with liver weight loss. Although KCl significantly increased Rhv in retrogradely perfused livers, the increase in Rpv by 400% of baseline predominated over the increase in Rhv by 85% of baseline. In the retrogradely perfused livers, KCl produced an initial liver weight loss followed by a profound weight gain. We conclude that histamine and norepinephrine selectively contract the presinusoidal vessels. The results on KCl effects suggest that this selective presinusoidal 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.

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