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Abstract
Seventeen patients with ascites due to cirrhosis underwent hepatic venous catheterization and pressure measurement in the ascitic fluid. Intraperitoneal fluid hydrostatic pressure (IFP) ranged 3.5–22, mean 11.2 mmHg, and correlated closely to the pressure in the inferior vena cava (r = 0.97, P< 0.001), which was on average 1.8 mmHg above that of ascitic fluid (P< 0.005). Wedged hepatic venous pressure (WHVP) (range 19–43, mean 32 mmHg) correlated directly to IFP (0.89, P< 0.001) and was significantly higher than that of ten cirrhotic patients without ascites (range 12–27, mean 20 mmHg, P< 0.005). After diuretic therapy WHVP decreased to an average of 20 mmHg. Mean plasma colloid osmotic pressures were 20 mmHg (range 18–24 mmHg) and 23 mmHg (range 19–29 mmHg) in patients with and without ascites, the values being significantly different (P<0.05). Colloid osmotic pressure of ascitic fluid ranged 1–14, mean 4.9 mmHg. Mean ratio between albumin concentration in ascitic fluid and plasma was 0.31 (range 0.12–0.77). In five pigs portal venous pressure (PVP) increased during infusion of fluid into the peritoneal cavity. The increase in PVP was smaller than that of IFP (P<0.02), indicating that ascitic fluid stems the pressures in the splanchnic venous vascular bed up to a higher level, but that the transmural hydrostatic pressure difference decreases simultaneously. The results are discussed in relation to the local ‘oedema-preventing’ mechanisms: (a) increased interstitial hydrostatic fluid pressure, (b) decreased interstitial fluidcolloid osmotic pressure, (c) increased lymph flow, and it is concluded that the peritoneal space can be considered as a special part of the interstitium in which IFP is considered to play an important role in regulation of ascitic fluid.