Christopher Wyatt (Advisor), Kathrin Engisch (Committee Member), Clintoria Williams (Committee Member)
Master of Science (MS)
The cardiorespiratory system in our bodies does not adapt to Chronic Intermittent Hypoxia (CIH) and consequently syndromes such as sleep apnea lead to pathophysiological conditions like Hypertension. It has been demonstrated that the peripheral chemoreceptors underpin the development of these conditions and at present, there are no selective drug therapies for this form of hypertension. However, evidence suggests that peripheral chemoreflex sensitivity to CO2 & hypoxia is reduced by Somatostatin (SST) in humans. Our preliminary in-vitro studies have demonstrated that SST will blunt the response of the carotid body to hypoxia and decrease the baseline activity of the carotid body. We therefore hypothesize that SST analogues given in-vivo via osmotic minipumps will attenuate the increase in BP, thereby preventing systemic hypertension from developing during CIH. Adult male Sprague-Dawley rats were implanted with Osmotic minipumps containing sterile water or SST analogue (Octreotide Acetate) and then were exposed to CIH for ≤35 days to induce hypertension. BPs were measured before, during and after IH conditioning. Each minipump administers the drug for only 28 days. It was predicted that the animals exposed to the SST analogue will be protected from CIH-induced hypertension. Data showed a sudden drop in BP post-surgery in all animals tested. This hypotension may have prevented the ability of chronic intermittent hypoxia to induce hypertension in both experimental and control animals.
Department or Program
Department of Neuroscience, Cell Biology, and Physiology
Year Degree Awarded
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