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Canadian Anaesthetists’ Society Journal

, Volume 13, Issue 4, pp 328–341 | Cite as

Hepatic circulation and hepatic function during anaesthesia and surgery: IV. Halothane anaesthesia

  • A. Galindo
  • G. F. Brindle
  • R. G. B. Gilbert
Article

Summary

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.

Keywords

Portal Vein Halothane Metabolic Acidosis Hepatic Blood Flow Hepatic Damage 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

La circulation hépatique fut étudiée chez les chiens au moyen d’un appareil electromagnétique mesurant le débit sanguin. Sous des conditions normales, l’halothane réduit le débit sanguin du foie. L’administration de CO2 durant une anesthésie à l’halothane augmente le débit sanguin à la fois dans l’artère hepatique et la veine porte. L’administration de CO2 immédiatement apres une hemorragie produit un effet moins prononcé. Cependant, quand ce gas est administré avec une anesthésie au chloroforme, on observe une diminution encore plus marquée du débit sanguin hépatique.

L’acidose métabolique joue un rôle important en ce qui regarde la diminution du débit sanguin que Ton observe au niveau du foie et ceci quelles que soient les conditions de l’experience. De plus, les altêrations du débit sanguin produites par une anesthésie au chloroforme sont corrigées si Ton traite l’acidose métabolique produite par cet agent. Cependant une nécrose centro-lobulaire se produit chez tous les animaux anesthésiés au chloroforme en dépit du fait que la détérioration circulatoire ait été corrigée.

Un certain degré de détérioration hépatique fut observé à la suite d’une anesthésie à l’halothane quand cet agent était administré à des animaux en état d’acidose métabolique. L’état d’acidose métabolique provoque artificiellement au cours de ces expériences, coincide avec une période prolongée d’hypotension artérielle précédant la mort de l’animal (“periode d’agonie“). Une détérioration identique du foie fut observée dans des expériences de contrôle dans lesquelles on avait provoqué une hypotension hémorragique et une acidose métabolique mais sans anesthésie à l’halothane. Ainsi l’on suspecte que l’hypoxie hépatique soit la cause commune de ces lesions.

II existe une correlation entre les manifestations hépatiques et les derangements des fonctions hépatiques, comme on peut le constater avec le test BSP et le niveau sanguin du SGOT.

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Copyright information

© Canadian Anesthesiologists 1966

Authors and Affiliations

  • A. Galindo
    • 1
  • G. F. Brindle
    • 1
  • R. G. B. Gilbert
    • 1
  1. 1.Department of Neurology and NeurosurgeryMcGill University and The Montreal Neurological Institute and HospitalMontreal

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