Hyperbaric oxygen therapy is a unique therapeutic regimen used primarily as adjunct therapy for a variety of debilitating and potentially lethal disease processes. This therapy is most often carried out at 2.36 atmospheres absolute with inhalation of 100 percent oxygen. Research literature discusses the potential for hyperbaric oxygen induced hypoglycemia causing a variety of clinical symptoms that may abort further treatment. The mechanisms for the regulation, metabolism and storage of glucose leading to this hypoglycemia have not been well described. The objectives for this research included determining the effects of hyperbaric oxygen in dogs on: (1) serum glucose and the glucoregulatory hormones, glucagon, cortisol and insulin, (2) aerobic and anaerobic metabolism via measurement of lactate, pyruvate, carbon dioxide and clearance of radiolabeled glucose from the circulation, and (3) the storage of radiolabeled glucose as glycogen in liver and muscle.

Results of this study did not support the previous research findings on hypoglycemia. Serum glucose patterns over the course of a 90 minute hyperbaric exposure showed a relative hyperglycemia when compared against sham animals. Statistically significant differences occurred between the hyperbaric and sham treated animals in the following parameters--glucose, glucagon, cortisol, carbon dioxide, and lactate without changes in blood clearance or storage of tritiated glucose. The addition of an enzyme inhibitor, Sorbinil, to the hyperbaric treatment caused a relative hypoglycemia when compared against hyperbaric oxygen alone or sham treated animals.

We drew the following conclusions from this study. (1) Hyperglycemia with concomitant increases in glucagon and cortisol in the treatment group showed misregulation of the glucoregulatory system under hyperbaric oxygen conditions. (2) Elevated serum carbon dioxide levels confirmed that increased dissolved carbon dioxide occurs when hemoglobin is completely saturated with oxygen under hyperbaric conditions. (3) Despite studies indicating increased uptake of glucose across cell membranes, no alteration in the blood clearance of glucose could be detected. This, in addition to the mean serum carbon dioxide and pyruvate values, suggests that no increased aerobic metabolism occurs during hyperbaric oxygen exposure. (4) Serum lactate levels indicate a rather dramatic increase in anaerobic metabolism approximately midway through the treatment. This peak in serum lactate correlates with an increase in seizure activity of animals exposed to hyperbaric oxygen. Additionally, it was found that pre-treatment with glucose decreased the seizure rate from 50 percent in the fasting animals to 10 percent in the pre-treated animals. Pre-treatment with glucose may be protective of the organism against oxygen toxicity seizures. Lactate levels were not obtained in the pre-treatment group to determine if a like decrease in anaerobic metabolism occurs with the administration of glucose. (5) Sorbinil, an aldose reductase inhibiting enzyme, caused a significant decrease in serum glucose which is unexplained by enzyme inhibition. (6) A larger sample size would be required to determine the effects of hyperbaric oxygen on the storage of glucose in liver and muscle.