thiamylal and Hypoxia

Hepatic oxygen metabolism and the hepatic energy charge were assessed in 21 mongrel dogs receiving 1 to 1.5 MAC of halothane or thiamylal (20-30 mg.kg-1.hr-1) intravenously while inhaling graded hypoxic mixtures (FIO2 0.21-0.08). Hepatic blood flow was measured using electromagnetic flowmetry: hepatic oxygen delivery and consumption were calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous blood and hepatic venous blood. In the hypoxia-halothane group, portal venous blood flow (FIO2 0.15-0.10), portal venous oxygen content (FIO2 0.10-0.08) and hepatic oxygen consumption (FIO2 0.08) significantly decreased compared with the hypoxia-thiamylal group. Arterial ketone body ratio (AKBR), which indicates the mitochondrial energy charge level, decreased with the development of hypoxia, and in the hypoxia-halothane group, the decrease of AKBR was significantly greater than in the hypoxia-thiamylal group at FIO2 0.08. The serum catecholamine levels, epinephrine and norepinephrine, increased in both groups at FIO2 0.08. In the hypoxia-halothane group, however, the increase of norepinephrine was significantly higher than in the hypoxia-thiamylal group at FIO2 0.08. These results suggest that, compared with halothane, thiamylal could suppress the exaggerated reaction to hypoxic hypoxemia, maintain hepatic circulation and hepatic oxygen metabolism and therefore maintain the hepatic mitochondrial redox state in better condition.

Topics: Animals; Dogs; Halothane; Hypoxia; Liver; Liver Circulation; Oxygen; Thiamylal

Cortisol is secreted as part of the stress response and has been shown to be potentially beneficial to protect against acute stress. Etomidate specifically suppresses endogenous cortisol production. The author studied cardiopulmonary and metabolic effects of hypoxia in dogs during acute adrenocortical suppression by etomidate. Six chronically tracheotomized dogs were induced with either etomidate or thiamylal. Spontaneous ventilation with constant enflurane concentration was maintained. Two hours after induction of anesthesia, isocarbic hypoxia was induced for 20 minutes. Cardiopulmonary and metabolic variables were recorded at specific intervals. The exact sequence was repeated after 1 hour. Cortisol was measured before, during the experiment, and 24 hours later. The experimental protocol was repeated 6 weeks later on the same dog using the other induction agent (thiamylal group versus etomidate group). Two-factor analysis of variance with contrasts tests was used for statistical analysis. The thiamylal group had a significant decrease in minute ventilation, respiratory rate, partial pressure of oxygen in arterial blood, with increases in partial pressure of carbon dioxide in arterial blood, heart rate and cortisol as compared to the etomidate group. Cardiopulmonary and metabolic responses to hypoxia were comparable in both groups. Therefore, acute suppression of cortisol secretion by etomidate did not adversely alter the responses to hypoxia under enflurane anesthesia in dogs.

Topics: Adrenal Cortex; Animals; Dogs; Drug Evaluation, Preclinical; Etomidate; Female; Hemodynamics; Humans; Hydrocortisone; Hypoxia; Injections, Intravenous; Male; Thiamylal

Topics: Abdomen; Anesthesia; Auscultation; Carbon Dioxide; Embolism; Endoscopy; Female; Humans; Hypercapnia; Hypoxia; Intubation, Intratracheal; Laparoscopy; Muscle Relaxants, Central; Nitrous Oxide; Pneumoperitoneum, Artificial; Premedication; Respiration; Stomach Rupture; Thiamylal