The effects of feeding on the development of metabolic acidosis in the rat: Comparison between perfused liverin situ and whole animal
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Rat liver perfused in situ was charged with two concentrations of halothane. Lactate increased in a time- and dose-dependent manner in the liver of the fed rat, whereas its increase in the starved rat was much milder (1.7 → 9.2 mmol·l −1 → 1vs 0.6 → 1.4 mmol·l −1 after a 3 hr charge with 6.0% halothane). Base excess decreased also more markedly in the fed rat. Glucose increased 2.3 times the control value in the fed rat, whereas it did not change significantly in the starved rat. Changes produced by enflurane were very similar to those produced by halothane. It was inferred that in the presence of halothane and enflurane, hepatic glycogen was transformed into glucose and then to lactate by the inhibition of NADH dehydrogenase. In the liver of the starved rat, glucose, hence lactate, did not increase because of the depletion of glycogen.
When halothane (1.9%) was given to the whole animal, changes in lactate, base excess and glucose in the arterial blood were very mild. Marked disparities in these parameters between the two experimental models were inferred to be due to: 1) possible insinuation of anaerobic metabolism in the perfusion experiments, 2) a well-kept balance between the suppression of cellular metabolic activity and inhibition of energy production by halothane in the whole animal, and 3) involvement of neural and humoral factors in the intact whole animal.
Key wordsfeeding liver perfusion glucose metabolic acidosis halothane
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