The formation of ascites in cirrhosis is a consequence of a complex process, in which, along with mechanical disorders of blood circulation in the system of portal vein, play the role of hormonal and renal factors, changes in colloid-osmotic pressure.
Portal hypertension and associated stagnation in the portal vein and lymphatic vessels are serious predisposing factor to the emergence of ascites. However, by themselves, in the absence of other violations, they do not cause water retention in the abdomen. The only exception is, perhaps, the obstruction of the hepatic vein. The greatest value of the portal stagnation is that it defines the accumulation of extravascular fluid it is in the abdominal cavity. The main mechanical moment, giving rise to the formation of ascites is an increased postsynodal flow resistance in the liver. This is partly due to the obstruction of the hepatic lymph ways, partly as a result of heightened limpopoprovince on the surface of the liver into the abdominal cavity is allocated an increased number of lymph (Hyatt, 1955; Baggenstoss, Cain, 1957). Extravascular accumulation of fluid also contributes to the increased capillary permeability and hypoalbuminemia. The latter leads to decreased intravascular colloid-osmotic pressure, begins output of fluid in the tissue. Accumulated in the abdominal cavity fluid can be effectively drained by suction through a powerful lymphatic system parietal peritoneum. If fluid intake exceeds specified drainage capacity, protein-rich fluid in the abdominal cavity creates an osmotic conditions for increase of ultrafiltration of vessels parietal peritoneum.
According to Cherrick and others (1960), the accumulation of ascites depends on the ratio between the two groups of factors acting in opposite directions. The increase in the portal venous and ascitic colloid-osmotic pressure contributes to the further formation of ascites; at the same time, the increase in intra-abdominal and increase colloid-osmotic pressure in serum prevent the accumulation of ascites.
No doubt that a variety of mechanisms based on the principle Starling, play a significant role in maintaining ascites after his arrival. However, the relationship between hypoalbuminemia and a violation of the osmotic balance, on the one hand, and the formation of ascites, on the other - SAC just.
Through soaked protein and water found that ascites between vascular system and the abdominal cavity there is a movement in both directions (Prentice, 1952); infusion of albumin often does not reduce but rather increase the accumulation of fluid (Kleckner, 1960); sometimes ascites easily liquidated in severe gipoalbuminemii, it never comes back development at moderate decrease albumin in the blood (Shinaberger, Galambos, 1964). These observations suggest that the formation of ascites is not a simple consequence extravasation and its appearance is much more complex process.
A large role in maintaining the constancy of the aquatic environment of the body belongs to the kidneys engaged in the regulation of sodium and water in the body. The specified regulatory function is closely connected with the production of mineralocorticoids adrenal glands, and cardiovascular risk factors. Changing these complex physiological mechanisms underlies the vicious circle, the calling and the supporting tissue swelling, including ascites. In the States, causing swelling, but not related to kidney disease, the function of the latter may be changed in several different areas: 1) reduction of renal plasmatica; 2) reduction of glomerular filtration; 3) increased reabsorption of sodium and water in the proximal renal tubules; 4) reduced capacity to excretion water load; 5) the increase under the influence of aldosterone reabsorption of sodium and excretion of potassium in the distal renal tubules. Shinaberger and Galambos (1964) believe that education peripheral arterio-venous anastomoses cirrhosis of the liver leads to the decrease in peripheral resistance to blood flow. Despite the fact that the total volume of the circulating plasma increased, much of it comes in the developed portal systemic venous anastomoses. As a result, the effective renal plasmatica decreases owing to what may be reduced glomerular filtration. The alternating current plasma and behavior glomerular filtration are not primary in violation of the regulation of the exchange of sodium and water in liver diseases (Deming, Luetscher, 1957). However, vomiting, re-evacuation of the ascitic fluid and the use of diuretics can cause critical falling of the volume of circulating blood, and hence reduce the renal plasmatica. Crucial in the delay sodium and water is changing resorption them into the tubules of the kidneys. The exchange of electrolytes primarily regulated by hormones of adrenal cortex, of which aldosterone most actively delay sodium in the body.
At diseases of a liver, with current otern-astiticeski syndrome, there is an increased secretion of aldosterone (Deming, Luetscher, 1963; Wolff, 1958; R. G. Sprintsson, 1968, and others). Increased levels of aldosterone is increased reabsorption of sodium in the distal renal tubules and excretion of potassium or of hydrogen ions. Thus, there is a positive balance of sodium and a negative balance of potassium.
Giperaldosteronizm for liver diseases can be caused by two mechanisms: 1) the emergence of hypovolemia the fluid from the vascular bed. Gipovolemia irritating volume receptors, which sets in motion the so-called natriyureticeski reflex that stimulates aldosterone cortical layer of the adrenal gland (Smith, 1957); 2) decreasing ability of the liver to inactivate hormones, including aldosterone (Wolff and others, 1958).
Delay sodium in turn causes irritation of tissue osmoreceptors and through the so-called antidiuretic reflex stimulates the secretion of antidiuretic hormone posterior lobe of the pituitary. Raising the level of antidiuretic hormone increases reabsorbqiyu water in the renal tubules, thus water is available in the tissues until then, until the osmotic balance is restored. This leads to the release of fluid from the vascular bed, hypovolemia, the excitement of surround receptors and further delay sodium. Thus, there is a vicious circle, inducing and supporting the accumulation of fluid out of the blood vessels.
No matter how close relationship between the level of aldosterone and delay sodium and fluid, giperaldosteronizm itself does not lead to edema. It is obvious that the formation of ascites in liver diseases is the result of a complex set of mechanisms.