Medicine and Health Sciences


Francis Sylvester


Acute hyperbaric oxygen treatment (HBOT) alters vascular reactivity, yet the underlying mechanism requires further clariJication. As Furchgott and Zawadzki previously demonstrated the obligatory role of the endothelium in regulating blood vessel tone, our lab seeks to determine if the simple squamous epithelium of the tunica intima mediates the observed changes in vascular reactivity following HBOT. Intact or chemically denuded porcine, mesenteric arterial rings were exposed to one of three treatments: 100% oxygen at 1.75 atm, room air at 1.75 atm, and room air at 1.00 atm. Additionally, a separate series of experiments utilized a Clark-type electrode to measure the oxygen concentrations observed in the hyperbaric chamber. These recordings demonstrated signiJicant differences among the three treatment groups. Following two hours of exposure to hyperbaric treatment, vessels were mounted in isolated organ baths and coupled to force transducers so that changes in arterial force were recorded in response to multiple agonists. The vasoconstrictors, potassium chloride (6x10-2 M) and phenylephrine (10-7-3x10-6 M), were used to record increases in tension. The vasodilators, acetylcholine (10-7-10-4 M) and sodium nitroprusside (10-7-10-4 M), were used to record decreases in tension. Lack of a dilator response to acetylcholine, an endothelial-dependent vasodilator, was used as validation for denudation. Potassium chloride and phenylephrine induced signiJicant increases in tension in all treatments. Nitroprusside induced signiJicant decreases in tension in all treatments. Comparison of the intact arteries to the denuded arteries following HBOT indicated that the endothelium did not account for the changes in vascular reactivity. Further investigation of the acute effects of HBOT on vascular reactivity is needed to better understand the potential beneJits of hyperbaric oxygen therapy for treating cardiovascular disease.