287 REVERSAL OF ADRENALINE EFFECT ON AZYGOS BLOOD FLOW AFTER B-ADRENERGIC BLOCKADE IN PATIENTS WITH CIRRHOSIS

D. Valla, D. Gaudy, C. Gaudin, P. Geoffroy, A. Braillon, D. Lebrec

INSERM U 24, H~pital Beaujon, Clichy and INSERM U 27, H6pital Foch, Suresnes, France

In patients with cirrhosis, during stress, release of adrenaline might increase porto- systemic collateral blood flow and thereby precipitate rupture of esophageal varices. This study aimed to evaluate the effects of small doses of exogenous adrenaline on the central and portosystemic circulation and to determine if propranolol may Counteract these effects.

In 6 patients with cirrhosis and esophageal varices, we assessed systemic hemodynamics and azygos blood flow at the end to the following consecutive periods: (A) a 20 min rest, (B) a 20 min adrenaline infusion (50 ng/kg/min), (C) a 20 min rest, (D) a 15 min period after IV injection of 15 mg of propranolol, (E) a 20 min adrenaline infusion (50 ng/kg/min).

Results are presented in the table (percent of period A value, mean ± SD).

Period A B C D E Cardiac index lO0 147z20 a I02± 5 83±13 a 83±13 a H e a r t r a t e 100 1 2 4 ± 1 3 a 110± 9 a 89± 7 a 8 8 ± 8 a Mean a r t e r i a l p r e s s u r e lO0 1 0 0 ± 1 3 1 0 3 ± 1 2 9 9 Z 1 2 I l l ± 7 a b S y s t e m i c v a s c u l a r r e s i s t a n c e 100 6 6 ± 1 7 a 1 0 0 ± 1 4 1 1 8 ± 2 5 1 3 6 ± 2 2 a b A z y g o s b l o o d f l o w 100 1 5 6 ± 2 4 a 1 1 4 ± 2 7 8 1 ± 1 4 a 6 8 ± 1 9 a b aSignificantly different from period A value; bSignificantly different from period D value

In conclusion, adrenaline increases azygos blood flow. After 8-adrenergic blocked% however, adrenaline decreases azygos blood flow. This reversion of adrenaline effect after 8-adrenergic blockade might explain part of the preventing action of propranolol on recurrent bleeding from esophageal varices in patients with cirrhosis.

288ADMINISTRATION OF VASOPRESSIN DOES NOT AFFECT SPLANCHNIC CIRCULATORY CHANGES INDUCED BY BLEEDING IN RATS WITH PORTAL HYPERTENSION

D. Valla, C. Girod, D. Lebrec INSERM U-24, HSpital Beaujon, Clichy, France

In stable patients with portal hypertension, vasopressin has well documented effects on the splanchnic circulation; however, the efficacy of vasopressin in controlling bleeding from oesophageal varices is controversial. We studied rats with portal hypertension to determine if vasopressin may influence the changes in splanchnic circulation associated with bleeding.

We studied 4 groups of 7 rats with portal vein stenosis. Saline (group A and B) or vaso- • --2 .

presszn (lO IU/kg/m~n; group C and D) was znfused from the 10th to the 35th min. Group B and D rats were bled from the mesenteric vein (7ml/kg for 5 min) at the 20th min. Portal venous pressure (PVP) and blood flow (microsphere method) through hepatic artery (HABF) and portal tributaries (pTBF) were determined at the 35th min. Results are in the table (mean±SEM). Group A B C D PVP (m~g) ll.4±l.l 8.7±O.6 ab 10.3±0.5 7.2±0.4 abc HABF (ml/g liver wt) 0.65±0.07 0.92±0.II a 1.06±0.O3 a 1.23±0.I0 abc PTBF (ml/lO0g body wt) 6.1±0.5 4.0±0.3 a 4.3±0.3 a 4.1±0.3 c significantly different fromagroupA and bgroup C; cnot significantly different from groupB.

In conclusion, in rats with portal hypertension, (I) hemorrhage alone induces a sustained decrease in portal venous pressure and portal tributary blood flow, and (2) administration of vasopressin does not significantly affect the splanchnic circulatory changes associated with bleeding. These observations might he explained by the release of large amounts of endogenous vasoconstrictor substmlces during bleeding. Our findings may explain the discrepancy between the results of therapeutic studies and the results of hemodynamic studies in stable patients.

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