Though hypercapnia is a naturally occurring physiological state, it is generally accompanied by hypoxic conditions (Venkataraman et al., 2008). The convolution associated with concurrent changes in carbon dioxide and oxygen volumes offer unclear results to researchers investigating the effects of arterial gas changes (Brogan et al., 2003; Cinar et al., 2012). Researchers at the University of Toronto have developed a computer-controlled gas blender (RespirAct<sup>TM</sup>, Thornhill Research, Toronto, Ontario, CA) capable of measuring and altering end-tidal gas volumes, which are indicative of arterial blood gas changes (Brogan et al., 2003; Cinar et al., 2012). Researchers have utilized this technology to investigate cerebral vascular reactivity (Kassner et al., 2010; Mandell et al., 2008; Mark et al., 2011; Prisman et al., 2008), but differing methodologies and a lack of reproducibility studies raise questions about the validity of the findings. In addition, the peripheral response to a hypercapnic, normoxic environment is not well documented. This dissertation will investigate the effects of a hypercapnic environment on the cerebral and peripheral vascular beds. We hypothesize that the vascular changes associated with a hypercapnic environment are repeatable in both the cerebral and peripheral beds. We further hypothesize that the cerebral vascular changes will occur more quickly than the peripheral changes. Lastly, we hypothesize that a comparison between hypercapnia-induced vasodilation of the brachial artery will provide a similar, but slower dilatory response than reactive hyperemia. The results of this dissertation may provide further insight into the mechanisms responsible for hypercapnia-induced vasodilation of the cerebral and peripheral blood vessels, and may provide repeatable methodologies to be utilized in future research.
University of Minnesota Ph.D. dissertation. March 2015. Major: Kinesiology. Advisor: Donald R. Dengel. 1 computer file (PDF); viii, 108 pages.
Geijer, Justin Robert.
Cerebral and peripheral hemodynamic responses to increased end-tidal carbon dioxide volumes.
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