Integrative Physiology
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12503/29932
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Browsing Integrative Physiology by Author "Anderson, Garen"
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Item Visit-to-Visit Reproducibility of Cerebral Vascular Reactivity to CO2 in Healthy Young Humans(2020) Anderson, Garen; Rickards, Caroline; Rosenberg, Alexander; Barnes, Haley; Hua, VincentPartial pressure of arterial CO2 (PaCO2) is an important regulator of cerebral blood flow. The magnitude of change in cerebral blood flow per unit change in PaCO2 represents the cerebral vascular responsiveness to a CO2 stimulus, and is used as an index of cerebrovascular health. Accordingly, it is important to assess the reproducibility of this technique for clinical diagnoses. Purpose: To assess visit-to-visit reproducibility of a cerebral vascular reactivity to CO2 test in healthy young humans. Methods: Healthy adults (n=6, 25±2 y) performed a 5-min cerebral vascular reactivity to CO2 protocol (+5 mmHg end-tidal CO2 (etCO2) above eucapnic baseline) on two separate visits (7-234 days between visits). EtCO2 and middle cerebral artery velocity (MCAv) were measured continuously. Coefficient of variation (CV) was calculated for cerebral vascular reactivity to CO2 ((%Δ MCAv)/Δ etCO2), etCO2, and mean MCAv responses between the two visits. Results: While the CO2 stimulus between visits was similar (Visit 1: 5.3±0.2 mmHg vs. Visit 2: 5.1±0.3 mmHg, p=0.54) with a CV of 2.8%, there was a difference in the MCAv response to this stimulus (Visit 1: +15±1 cm/s vs. Visit 2: +12±2 cm/s, p=0.09; CV=19%). This resulted in a large variation in cerebral vascular reactivity to CO2 between visits (Visit 1: 4.6±0.3 %/mmHg vs. Visit 2: 3.6±0.5 %/mmHg, p=0.06; CV=18%). Conclusion: These findings suggest that despite a similar magnitude of change in the CO2 stimulus, physiological variations in cerebral vascular reactivity to CO2 occur in young healthy adults between two experimental visits.Item White Mountain Expedition 2019: The Impact of Sustained Hypoxia on Cerebral Blood Flow Responses and Tolerance to Simulated Hemorrhage(2020) Anderson, Garen; Rickards, Caroline; Barnes, Haley; Bird, Jordan; Pentz, Brandon; Byman, Britta; Jendzjowsky, Nicholas; Wilson, Richard; Day, Trevor; Rosenberg, AlexanderTrauma-induced hemorrhage can occur at high altitude (HA) from a variety of causes, including battlefield injuries, motor vehicle/air accidents, and major falls. Based on the known compensatory increases in cerebral blood flow that occur with exposure to hypoxia, we hypothesized that tolerance to simulated hemorrhage (via application of lower body negative pressure, LBNP) at HA would be similar compared to low altitude (LA) due to increased cerebral blood flow and oxygen delivery, and the subsequent preservation of cerebral tissue oxygenation. Healthy human subjects (N=8; 4F/4M) participated in LBNP protocols to presyncope at LA (1045 m) and at HA (3800 m) following 4-5 days of acclimatization. Arterial pressure, heart rate, stroke volume, internal carotid artery (ICA) blood flow, and cerebral oxygen saturation were measured continuously. Time to presyncope was similar between conditions (LA: 1276±108s vs. HA: 1208±108s; P=0.58). Similar responses to LBNP were observed at LA and HA in mean arterial pressure (LA: -16±2% vs. HA: -16±2%; P=0.85), stroke volume (LA: -57±5% vs. HA: -60±5%; P=0.39), and heart rate (LA: +69±12% vs. HA: +65±8%; P=0.71). ICA blood flow was higher at HA vs. LA (P=0.01), and decreased with LBNP under both conditions (P≤0.005), with no effect of altitude on cerebral oxygen saturation (P=0.73). These findings suggest that hypoxia with ascent to 3800 m does not affect tolerance to simulated hemorrhage in young healthy adults, which may be due to 1) similar cardiovascular reflex responses, and/or 2) compensatory increases in cerebral blood flow and subsequent preservation of cerebral tissue oxygenation.