Circulatory effects of somatostatin in two conscious rat models of portal hypertension. Effects of haemorrhage

Circulatory effects of somatostatin in two conscious rat models of portal hypertension. Effects of haemorrhage

208 INFLUENCE OF ASCITES ON SYSTEMIC AND SFLANC]~IC HAEMODYNAMICS IN PATIENTS W I T H ALCOHOLIC CIRRHOSIS ACCORDING TO THE DECREE OF LIVEN FAILURE J...

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208

INFLUENCE OF ASCITES ON SYSTEMIC AND SFLANC]~IC HAEMODYNAMICS IN PATIENTS W I T H ALCOHOLIC CIRRHOSIS ACCORDING TO THE DECREE OF LIVEN FAILURE

J.M. Cereda, S.S. Lee, D. Pu~liese, A. Koshy, D. Roulot, D. Lebrec INSERM U 24, HSpital Beaujon, Clichy, France In patients with cirrhosis the relationships between the presence or absence of ascites, splanchnic and systemic haemodynamics and the severity of liver disease has not been established. Hence, we analyzed haemodynamic records of 258 patients with alcoholic cirrhosis. They were classified into 3 groups: no (0), mild (i) and severe ascites (2) and each group into 3 subgroups (A, B, C) according to a modified Pugh's classification (with ascites not taken into account). Results: mean±SD; groups with the same letter indicate significant differences (HVPG, hepatic venous pressure gradient (nm~Hg); CO, cardiac output (i/min); SVR, systemic vascular resistance (dyn.s.cm-5)). Ascites 0 (n=81) Ascites 1 (n=101) Ascites 2 (n=76) A B C A B C A B C 15.5 abe 18.3 ef 21.7 b 16.1cbg 19.4g 20.0 d 19.8 ac 19.8 f 22.3 HVPG ±5.0 ±5.6 ±3.8 ±3.5 ±5.9 ±5.8 ±6.2 ±5.0 ±4.7 6.74 a 7.68 c 9.39 a 5.84 b 6.89 d 8.61 bd 6.08 6.06 c 7.49 CO ±2.1 ±1.15 ±1.6 ±2.7 ±1.8 ±1.85 ±1.8 ±1.25 ±1.9 ii15 a 946 ef 641abe 1222cg 1008fg h 810 cdh 1195 1216 I034 bd SVR ±339 ±234 ±174 ±337 ±261 ±206 ±346 ±481 ±223 In conclusion, these results show that splanchnic and systemic haemodynamics are different between patients with and without ascites. The development of ascites is associated with a decrease in circulatory hyperkineticism, possibly by diminishing venous return. It also increases portal pressure in class A patients, but dampens the elevation in portal hypertension caused by hepatocellular insufficiency. These factors should be considered in the interpretion of haemodynamic data in cirrhotic patients.

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CIRCULATORY EFFECTS OF SONATOSTATIN IN TWO CONSCIOUS RAT MODELS OF PORTAL HYPERTENSION. EFFECTS OF HAEMORRBACE

R. Cerinij S.S. Lee, A. Haden~ue, HSpital Beaujon, Clichy, France

A. Koshy,

C. Girod, D. Lebrec INSERM U24',

Somatostatin has been reported to decrease portal pressure and thus proposed in the treatment of variceal bleeding in patients with cirrhosis. The mechanism of its haemodynamic effects is, however, not clearly understood. This study was thus undertaken to evaluate the systemic and splanchnic effects of somatostatin in 2 conscious rat models of portal hypertension: partial ligation of the portal vein (n=8) and secondary biliary cirrhosis due to bile duct ligation (n=8), and in a sham-operated group (n=8). Cardiac output and splanchnic organ blood flows were measured by the radioactive microsphere method before and 30 min after somatostatin infusion (8 ~g/kg.h). Portal pressure was measured after 8 incremental doses of somatostatin (0.25 to 16 ~g/kg.h). Moreover, the effect of somatostatin (8 ~g/kg.h) or saline (0.02 ml/min) on 5 min haemorrhage volume from the portal vein was studied in cirrhotic rats. The dose response curves showed that somatostatin significantly decreased portal pressure at a lower dose in rats with cirrhosis than in those without liver disease. Somatostatin decreased cardiac output by 20% in both groups of rats. Systemic vascular resistance increased, indicating vasoconstrictor effects of this drug. Somatostatin also significantly decreased portal tributary blood flow, by 27% in cirrhotic rats and 18% in portal vein stenosed rats. The drug had no effect in sham-operated rats. In cirrhotic rats receiving somatostatin, the amount of lost blood (2.28±0.31 ml/lO0 g) was significantly lower than in those receiving saline (2.84±0.44 ml/lO0 g). This study shows that somatostatin at a relatively high dose, decreases portal pressure principally by reducing portal tributary blood flow and may reduce the amount of haemorrhage from the portal vein.

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