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Canadian Journal of Anesthesia, Vol 13, 328-341, Copyright © 1966 by Canadian Anesthesiologists' Society
1 Department of Neurology and Neurosurgery, McGill University and the Montreal Neurological Institute and Hospital, Montreal, Quebec
2 Department of Neurology and Neurosurgery, McGill University and The Montreal Neurological Institute and Hospital, Montreal, Quebec
The circulation of the liver was studied in dogs by means of electromagnetic blood flow meters. Halothane anaesthesia reduces hepatic blood flow under normal conditions. Inhalation of CO2 during halothane anaesthesia increases blood flow in both the hepatic artery and the portal vein. A lesser effect is produced by the inhalation of CO2 immediately after haemorrhage. However, when this gas is administered with chloroform anaesthesia, further decrease in hepatic blood flow occurs.
Metabolic acidosis plays an important role in the reduction of hepatic blood flow in all experimental conditions. Moreover, the blood flow changes produced by chloroform anaesthesia are reversed upon correction of the chloroform induced metabolic acidosis. However, centro-lobular necrosis occurs in all chloroform animals despite correction of the circulatory impairment.
Some degree of hepatic damage was observed following halothane anaesthesia provided a state of metabolic acidosis existed during its administration. The artificial metabolic acidosis induced in these experiments coexisted with a prolonged period of arterial hypotension before death ("agonal period"). Similar liver pathology was observed in control experiments with haemorrhagic hypotension and metabolic acidosis, without halothane. Hepatic hypoxia is suggested as the common cause of these findings.
There is a correlation between the histological findings and liver function as reflected in the BSP test and SGOT levels.
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