Hemodynamics in portal hypertension

Great progress in the study of blood circulation in portal hypertension was achieved when studying the model on animals. Such a model was created, for example, by binding the rats to a portal vein or bile duct or inducing cirrhosis by introducing carbon tetrachloride. The development of portal hypertension is due to an increase in both vascular resistance and portal blood flow. The main hemodynamic disorder is an increase in resistance to blood flow in the portal vein. It happens to be mechanical due to a violation of the hepatic architectonics and the formation of nodes in cirrhosis or with obstruction of the portal vein. In addition, it may be due to other intrahepatic factors, for example, collagenization of the dissespace, swelling of hepatocytes and increased resistance in portosystemic collaterals. Intrahepatic increase in resistance to blood flow in the portal vein can be dynamic. So, myofibroblasts can relax, and endothelial cells of sinusoids and cells that contain contractile proteins that can cause "spasm".

As portal pressure decreases due to the development of collaterals, which discharge blood from the portal vein into the central veins, portal hypertension is supported by an increase in blood flow in the portal vein system due to the hyperdynamic type of circulation. It is not clear whether such a circulatory disturbance in hyperdynamic type is the cause or effect of portal hypertension, or both. The heavier the hepatic-cell insufficiency, the more pronounced the hyperdynamic type of circulation. In addition, cardiac output increases and generalized vasodilation develops. The arterial pressure remains normal or decreases.

Expansion of the vessels of the internal organs is the most important factor supporting the hyperdynamic type of circulation. Increased blood flow in an unpaired vein. Increased blood flow to the mucous membrane of the stomach causes the expansion of its capillaries; with gastroscopy in the mucous membrane, stagnant changes are noted. The increase in blood flow in the portal vein increases the transmural pressure in the esophageal varicose veins. This increase occurs in all veins - both in portal and collaterals. But the amount of blood entering the liver, while decreasing. Hyperdynamic type of circulation in internal organs is provided by a combination of many factors; probably, it is determined by the ratio of vasodilator and vasoconstrictor factors. These substances can form in the hepatocytes, or do not destroy them sufficiently, or not reach hepatocytes at all, forming in the intestine and passing through intra- or extrahepatic venous shunts.

An important stimulating role is played by endotoxins and cytokines, which are formed mainly in the intestine. Under the influence of endotoxin, nitric oxide (NO) and endothelin-1 are synthesized in the vascular endothelium.

NO - a powerful short-lived mediator of vascular relaxation. It is formed from L-arginine by the action of the NO synthetase enzyme, which is induced by endotoxins and cytokines. This reaction is suppressed by analogues of arginine; with induced cirrhosis in rats, a significant increase in sensitivity to these substances, the introduction of which causes an increase in pressure in the portal vein.

Endothelin-1 - a vasoconstrictor, a high level of it in the blood with cirrhosis, probably plays an important role in providing normal blood pressure. Isolated liver of rats in vivo has been shown to cause a "spasm" of sinusoids and an increase in pressure in the portal vein.

Prostacyclin is a powerful vasodilator produced by the endothelium of the portal vein. Perhaps, with portal hypertension caused by chronic liver diseases, it plays a leading role in changing blood circulation.

Glucagon is secreted by the a-cells of the pancreas and is inactivated in the liver. Hyperglucagonemia in cirrhosis is probably due to shunting the portal vein. In physiological quantities, glucagon does not have vasoactive properties, but in pharmacological concentrations it can dilate blood vessels. Probably, in maintaining the hyperdynamic type of circulation in liver diseases, it is not a leading factor.

[1], [2], [3]