Biomedical Sciences ETDs

Publication Date

Summer 7-31-2017

Abstract

Sleep apnea, recurrent obstruction of the upper airway leads to sleep fragmentation and intermittent hypoxia (IH). In animal studies, IH causes wake-time hypertension by elevating vascular resistance due in part to decreased production of the vasodilator, hydrogen sulfide (H2S). However, much is unknown about where and how H2S acts. Inhibiting cystathionine γ-lyase (CSE) to prevent H2S synthesis augments constriction in isolated mesenteric arteries, but H2S regulation of resistance in this vascular bed in vivo is unknown. The goal of this study was to evaluate CSE regulation of blood flow and resistance in the mesenteric circulation of control rats and in rats made hypertensive by exposure to IH for 14 days. We hypothesized that inhibiting CSE would increase vascular resistance and mean arterial blood pressure (MABP) more in control than in IH exposed rats. Rats were anesthetized with inhaled isofluorane (2%) and instrumented with femoral artery and vein catheters as well as Doppler flow probes on the main mesenteric artery. Under anesthesia, CSE inhibition (β-cyanoalanine, BCA, 30 mg/kg bolus + 5 mg/kg/min infusion for 20 minutes) increased MABP in both control and IH rats compared to saline infusion (control: saline 7.2±1.2 vs. BCA −2.8±1.1; IH: saline 9.3±1.1 vs. BCA 3.3±0.7, % change from baseline, p2S is an important regulator of blood pressure and mesenteric vascular resistance and that this control is lost after IH exposure.

Keywords

Hydrogen Sulfide, Sleep Apnea, Blood Pressure, Vascular Tone, Mesenteric Vascular Resistance

Sponsors

NIH and NHLBI [Grants HL123301 and HL007736-21]​

Document Type

Thesis

Language

English

Degree Name

Biomedical Sciences

Level of Degree

Masters

Department Name

Biomedical Sciences Graduate Program

First Committee Member (Chair)

Nancy L. Kanagy

Second Committee Member

Laura Gonzalez Bosc

Third Committee Member

Nikki Jernigan

Fourth Committee Member

Heather Ward

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