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M Corbic

Publications and source records attributed to M Corbic.

21 records · Page 2Linked to original sources

A new method to measure portal and hepatic blood flow using taurocholate in the rat.

Hepatic artery and portal vein blood flows were assessed separately in anesthetized rats using radiolabeled taurocholate. The ratio of portal vein blood flow to total hepatic blood flow was calculated from measurements of taurocholate concentrations of portal vein, hepatic artery and hepatic vein, and of taurocholate hepatic extraction ratio. Animals were administered [14C]taurocholate intraperitoneally as a label of the taurocholate pool 24 hr before the experiments. In steady-state conditions, serum [14C]taurocholate activities were used as an index of taurocholate relative concentration and the hepatic extraction ratio of taurocholate was estimated using [3H]taurocholate infused into the systemic blood stream. Total hepatic blood flow was estimated by the Fick's principle using indocyanine green. The mean hepatic blood flow was 13.9 ml X min-1 (S.E. 1.9), and the mean ratio of portal blood flow to hepatic blood flow was 72.2% (S.E. 6.7). It is concluded that taurocholate may be used to assess separately portal venous and hepatic arterial blood flow in the rat.

Animals↗

Effect of systemic pH, PCO2 and bicarbonate concentration on biliary bicarbonate secretion in the rat.

The effect of acute metabolic or respiratory acid-base disturbances on biliary bicarbonate secretion was examined in bile fistula rats. Animals were infused with ursodeoxycholate at a rate that stimulates bicarbonate secretion (1 mumole . min-1 X 100 gm-1), in control conditions and during acute acid-base disturbances. Metabolic acidosis or alkalosis were induced by HCl or NaHCO3 infusions, and respiratory acidosis or alkalosis were created respectively by adding CO2 to the inspired gas or by hyperventilation in artificially ventilated animals. Biliary bicarbonate concentration was always higher than plasma bicarbonate concentration. During metabolic disturbances, changing the plasma bicarbonate concentration from 9.2 to 30.2 mM stimulated biliary bicarbonate secretion by 113%. During respiratory disturbances, changing the plasma PCO2 from 25.5 to 59.8 mm Hg also increased biliary bicarbonate secretion by 89%. Biliary bicarbonate output was thus independent of plasma pH. When all animals were considered, bile flow was positively correlated with biliary bicarbonate concentration (r = 0.71, p less than 0.001). Acetazolamide significantly decreased ursodeoxycholate-induced bile flow and bicarbonate secretion by 20 and 22%, respectively. These results support the hypothesis that there is a relationship between ursodeoxycholate-induced bicarbonate secretion and bile flow. They are also consistent with the view that ursodeoxycholate-stimulated biliary bicarbonate secretion in the rat is strongly affected by plasma bicarbonate and PCO2, but not by plasma pH, and involves carbonic anhydrase.

Acetazolamide↗