Date Approved

12-2013

Graduate Degree Type

Thesis

Degree Name

Health Sciences (M.H.S.)

Degree Program

Biomedical Sciences

First Advisor

Frank Sylvester

Second Advisor

Doug Graham

Third Advisor

Dawn Richiert

Abstract

The objective of this study was to evaluate the changes in vascular reactivity of mesenteric arteries resulting from hyperbaric oxygen treatment. It was hypothesized that hyperbaric oxygen treatment alters vascular reactivity in mesenteric arteries due to enhanced production of ATP resulting in significantly larger responses to vasoactive stimuli. All arteries were dissected from porcine mesenteries and placed in Krebs- Henseleit solution. Arteries were initially mounted in isolated organ baths and passively loaded with tensions ranging from 1 to 25 grams at odd intervals to ascertain the optimal passive tension for studying mesenteric arteries. Following a 1-hour equilibration in Krebs-Henseleit solution, arteries were treated with potassium chloride (a nonreceptormediated vasoconstrictor; KCl; 15 – 60 mM) to assess vascular reactivity. Following determination of the optimal passive tension, additional arteries were dissected and tested for viability with KCl. Viable arteries were then subjected to a 2-hour hyperbaric treatment in 100% oxygen, 100% nitrogen, or ambient air at 1.00 or 1.75 ATA. Immediately following treatments, arteries were again mounted in isolated organ baths and passively loaded with 7 grams of tension. Following a 1-hour equilibration in Krebs- Henseleit solution, arteries were treated with KCl (15 – 60 mM). Arteries were then treated with increasing concentrations of phenylephrine (a receptor-mediated vasoconstrictor; 10-7 – 10-4 M) followed by increasing concentrations of sodium nitroprusside (a potent vasodilator; 10-7 – 10-4 M) to measure changes in vascular reactivity. Additional arteries were subjected to the 2-hour hyperbaric regiment involving 5 different gas/ pressure exposures. Arteries were then processed for determination of protein concentration and measurement of ATP concentration using commercially available assay kits. When compared to the 1 ATA room air control, KCl-induced constriction was significantly increased for the hyperbaric oxygen exposure. Treatment with hyperbaric oxygen also augmented vascular responses to phenylephrine and sodium nitroprusside relative to nitrogen, but not ambient air. There was no significant difference in ATP concentrations found among treatments. The results from these studies provide insight into the vascular effects of hyperbaric oxygen treatment.

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