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At least 253 records · Page 14Linked to original sources
PubMed1996

The NO donor sodium nitroprusside reverses the negative effects on hepatic arterial flow induced by endotoxin and the NO synthase inhibitor L-NAME.

In previous studies we have observed that the nitric oxide synthase inhibitor L-NAME induces a profound deterioration of liver circulation in experimental endotoxemia. Using the same porcine model we now have evaluated the possibility of modulating these effects with the nitric oxide donor sodium nitroprusside. Infusion of endotoxin led to a gradual deterioration of hemodynamic parameters, including liver blood flow. The decreases in portal blood flow paralleled and matched the decreases in cardiac output, and no compensatory increase in hepatic arterial flow occurred. L-NAME had detrimental effects on hemodynamics, including the liver circulation. The latter effects could, however, partially be reversed by sodium nitroprusside. Hepatic arterial flow increased from 1.9 to 7.2 ml/kg/min, with a concomitant decrease in hepatic arterial resistance from 5,364 to 1,746 dyn s/cm5 kg. A control group exhibited no significant change in either flow or resistance. The response to sodium nitroprusside was rapid and vigorous, and probably largely due to relaxation of the hepatic arterioles, and not to abatement of intrahepatic edema or plugging of the sinusoids. Furthermore, we conclude that the endotoxin-induced dysfunction of the hepatic arterial buffer response may be due to a selective inhibition of vascular endothelial function.

Animals↗
PubMed2003

A model of dual circulation in liver acini with hypoxia regulated adenosine secretion.

It was postulated by W.W. Lautt that the hepatic artery flow compensation for changes in portal vein flow (the 'hepatic arterial buffer response') is regulated through the portal blood washout of adenosine from the small fluid compartment that surrounds the hepatic arterial resistance vessels. It is presumed that the adenosine secretion there is constant and independent of oxygen supply or liver demand. It was reported by others that liver secretes variable quantities of adenosine and that secretion is related to the level of liver hypoxia. This paper is an attempt to describe a model of acinar circulation without sources of constant adenosine secretion. The presented model is based on the fact that portal blood enters acinar space near the vascular stalk in the zone 1, while most of the arterial branches empty one-third from the interlobular septa, at the beginning of the zone 2, just downstream from the zone 1. Another important characteristic of liver architecture is that near 5/9 of lobular volume is in the zone 1. Liver cells in zone 1 are well oxygenated by the portal blood and they have low adenosine secretion that might seem almost constant. Since most arterial branches empty more peripherally, the zone 1 normally does not depend on the arterial circuit and most of arterial branches are governed by the adenosine secretion from the upstream zone 1. Low portal flow, would increase adenosine secretion from the zone 1 and thus dilate numerous downstream arterial resistance vessels. An increased flow from these arterial vessels would compensate any decrease in the portal flow. Zones 2 and 3 probably have higher adenosine secretion rates since the oxygenation depends on the amount of added arterial blood and on the liver cell metabolism. Some of the arterial branches in those zones are probably open all the time, preserving them zones from hypoxic injury. Since the main point for arterial inflow is concentrated downstream from the zone 1, in cases of low portal pressures, or elevated upstream resistance, some of the arterial blood might leave the acinus in retrograde direction via the portal branch and enter some other acinus as a part of portal blood. These arterio-portal communications might be important in cases of low or none portal flow when zone 1 is in hypoxia. In the 3D liver space with tightly packed acini, very complex and ever-changing patterns of combined antegrade and retrograde flows can be expected.

Adenosine↗
PubMedDate not supplied

Hypothermic machine perfusion of the liver and the critical balance between perfusion pressures and endothelial injury.

Hypothermic machine perfusion (HMP) provides better protection against cold ischemic injury than cold storage in marginal donor kidneys. Also, in liver transplantation a switch from static cold storage to HMP could be beneficial as it would allow longer preservation times and the use of marginal donors. A critical question concerning application of HMP in liver preservation is the crucial balance between perfusion pressure and occurrence of endothelial injury. Rat livers were cold-perfused for 24 hours to study perfusion pressures for both hepatic artery and portal vein. Cold storage served as control and was compared to HMP-preserved livers using a mean arterial perfusion pressure of 25 mm Hg and a portal perfusion pressure of 4 mm Hg (25% of normothermic liver circulation) and to HMP at 50 mm Hg and 8 mm Hg perfusion, respectively (50% of normothermic liver circulation). UW solution was enriched with 14.9 micromol/L propidium iodide (PI) to stain for dead cells and with an additional 13.5 micromol/L acridine orange to stain for viable hepatocytes. A low PI-positive cell count was found using HMP at 25% of normal circulation compared to cold storage. The PI count was high for the HMP group perfused at just 50% of normal circulation compared to HMP at 25% and compared to cold storage. In summary, for liver HMP, perfusion at 25% showed complete perfusion with minimal cellular injury. HMP using perfusion pressures of 25 mm Hg for the hepatic artery and 4 mm Hg for the portal vein is feasible without induction of endothelial injury.

Animals↗