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Acidosis modifies metabolic functions but does not affect vascular resistances in perfused rat livers
1Division d'Hépatologie et de Gastroentérologie, Hĵpital Cantonal Universitaire de Genève, Switzerland. catherine.pastor@medecine.unige.ch
Background:
Few data exist concerning the consequences of acidosis on intrahepatic vascular resistances and hepatic functions.
Methods:
The consequences of pH and PCO2 changes on the intrahepatic vascular reactivity to norepinephrine (NE, 10(-9) to 3 x 10(-5) M) have been investigated in isolated rat livers perfused with solutions bubbled with 5, 10, or 15% CO2 and in solutions in which pH was decreased by replacing HCO3- with NaCl while maintaining a normal PCO2. Hepatic O2 consumption (VO2) and urea release were also measured during these experiments.
Results:
The NE-induced increase of portal pressure did not change during hypercarbic and normocarbic acidosis. In contrast, the NE-induced increase of urea release was higher when the solution of perfusion was bubbled with 10 and 15% CO2, while during normocarbic acidosis the NE-induced increase of urea release did not change with pH. In the absence of NE, acidosis decreased hepatic VO2 and urea release but portal pressure was not modified by changing % CO2 or pH in the Krebs-Henseleit-bicarbonate solution.
Conclusions:
This study clearly shows that, in the liver, the consequences of acidosis are far more important on the metabolism (VO2 and urea release) than on the intrahepatic vascular resistance.