Hepatic vascular response to anaphylaxis in isolated canine liver

Abstract

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.

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

“…The hepatic sinusoidal pressure was measured by the doubleocclusion method (22,32). Both the inflow and outflow lines were simultaneously and instantaneously occluded for 13 s using the solenoid valves, after which P pv and Phv rapidly equilibrated to a similar or identical pressure, which was Pdo.…”

“…Moreover, CO is released in the hepatic circulation in response to various stressful stimuli (2, 3). However, there are no studies that determined the role of CO in the hepatic anaphylaxis.To clarify the anaphylactic disturbance of hepatic circulation, we herein established anaphylactic models of isolated portally perfused guinea pig livers, in which the sinusoidal pressure was measured using the double-occlusion method (22,32). The first purpose of the present study was to determine effects of anaphylaxis on hepatic vascular resistance distribution and liver weight changes.…”

“…Canine anaphylactic hepatic congestion is caused by constriction of postsinusoidal hepatic veins. Yamaguchi et al (32), using the vascular occlusion method in isolated perfused livers derived from naturally sensitized dogs, demonstrated that selective postsinusoidal constriction occurs during hepatic anaphylaxis induced by injection of the Ascaris suum antigen in the perfusing blood. On the other hand, it has not been known so far whether in other species than dogs anaphylactic reaction causes constriction of postsinusoidal hepatic veins, resulting in hepatic congestion and pooling of circulating blood.…”

NG-Nitro-L-arginine Methyl Ester, but Not Methylene Blue, Attenuates Anaphylactic Hypotension in Anesthetized Mice

“…We have proposed that the liver and splanchnic vascular beds are involved in anaphylactic hypotension (3 -6). Indeed, the liver plays a crucial role in the pathogenesis of circulatory collapse in canine anaphylactic shock (3,7). Anaphylaxis-induced hepatic venous constriction induces pooling of blood in the liver, as well as in upstream splanchnic organs.…”

Acute Liver Injury That Followed Food-Dependent Exercise-Induced Anaphylaxis.

“…However, the exact mechanismresponsible for anaphylactic hepatic congestion and portal hypertension remains obscure, although various chemical mediators of anaphylaxis have been shown to increase the portal pressure (20)(21)(22)(23)(24). Recently Yamaguchi et al proposed that an increase in sinusoidal pressure caused by hepatic venoconstriction mayplay an important role in the develop* ment of portal hypertension and hepatic congestion associated with anaphylactic shock (25). But anaphylactic shock including FDEIAn rarely induces liver injury: In our case alcohol intake mayhave caused acute liver injury, but alcohol intake of this amount alone could not cause acute liver injury.…”