Integrative Physiology
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12503/32551
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Browsing Integrative Physiology by Author "Davis, Austin"
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Item Evaluating the Role of Arterial Stiffness on Amplitude of Cerebral Blood Flow Oscillations(2024-03-21) Lal, Kevin; Davis, Austin; Anderson, Garen; Bhuiyan, Nasrul; Rickards, CarolineBackground: Changing the pattern of cerebral blood flow by forcing oscillations in arterial pressure and blood flow at 0.1 Hz (10-second cycle) can limit reductions in cerebral tissue oxygenation during a condition of reduced cerebral perfusion. This method of inducing 0.1 Hz hemodynamic oscillations is called Pulsatile Perfusion Therapy (PPT). Sympathetic activation can increase the amplitude of 0.1 Hz hemodynamic oscillations, and acutely increase arterial stiffness. The impact of increasing carotid arterial stiffness on the magnitude of 0.1 Hz cerebral blood flow oscillations has not been examined. We hypothesize that the with application of 0.1 Hz PPT during a condition of cerebral hypoperfusion, 1) the subsequent increase in sympathetic activity will acutely increase carotid arterial stiffness, and; 2) greater carotid artery stiffness will result in a higher amplitude of oscillations in cerebral blood flow. Methods: 10 healthy participants (8 males, 2 females) were exposed to 10-min of oscillatory lower body negative pressure (OLBNP) at 0.1 Hz, which induced both a state of cerebral hypoperfusion, and 0.1 Hz hemodynamic oscillations. Middle cerebral artery velocity (MCAv), internal carotid artery (ICA) diameter, and beat-to-beat arterial pressure were measured. ICA stiffness was determined using the beta-stiffness index, incorporating ICA diameter and arterial pressure measurements. The amplitude of 0.1 Hz MCAv oscillations was assessed via fast Fourier transformation. Results: While OLBNP increased MCAv 0.1 Hz oscillations (36.1 ± 24.2 cm/s2 vs. 812.4 ± 668.0 cm/s2; P=0.01), ICA beta stiffness was not different between the baseline and OLBNP conditions (12.3 ± 4.9 au vs. 13.2 ± 5.7 au; P=0.56). There was no relationship between ICA stiffness and the amplitude of MCAv oscillations during OLBNP (r=0.17, P=0.68). Conclusions: Contrary to our hypothesis, ICA stiffness did not increase during 0.1 Hz OLBNP, and there was no correlation between ICA stiffness and the magnitude of MCAv oscillations induced at 0.1 Hz. These data suggest that ICA stiffness may not determine the magnitude of induced oscillations in cerebral blood flow. Future studies will examine these effects in older adults to determine the potential beneficial application of PPT for the treatment of low cerebral perfusion conditions (e.g., Alzheimer’s disease, stroke).Item Interactions Between Carotid Arterial Stiffness, Amplitude of Cerebral Blood Flow Oscillations, and Cerebral Tissue Oxygenation During Simulated Hemorrhage in Humans(2024-03-21) Hudson, Lindsey; Davis, Austin; Anderson, Garen; Rosenberg, Alexander; McKeefer, Haley; Bird, Jordan; Pentz, Brandon; Byman, Britta; Jendzjowsky, Nicholas; Wilson, Richard; Day, Trevor; Rickards, CarolineIntroduction: Inducing 0.1 Hz (10-s cycle) oscillations in cerebral blood flow attenuates the reduction in cerebral tissue oxygenation during simulated hemorrhage in humans. It is unknown, however, how stiffness of the cerebral feed arteries influences the magnitude of cerebral blood flow oscillations, and/or the protection of cerebral tissue oxygenation. When 0.1 Hz oscillations are induced during simulated hemorrhage, we hypothesize that: 1) arterial stiffness of the internal carotid artery (ICA) will increase from rest; 2) the amplitude of 0.1 Hz oscillations in cerebral blood flow will be higher in individuals with stiffer arteries, and; 3) the reduction in cerebral tissue oxygenation will be smaller with higher amplitude of cerebral blood flow oscillations. Methods: 8 healthy human participants (age: 30.1±7.6 y) underwent a 10-min hypovolemic oscillatory lower body negative pressure (OLBNP) protocol, where chamber pressure oscillated every 5-s between -30 mmHg and -90 mmHg (i.e., 0.1 Hz). ICA beta stiffness index was calculated from measurements of ICA diameter (via ultrasound imaging), and arterial pressure (via finger photoplethysmography). Middle cerebral artery velocity (MCAv) was measured using transcranial doppler ultrasound, and cerebral tissue oxygenation (ScO2) was measured with near infrared spectroscopy. Fast Fourier transformation was used to quantify oscillations in mean MCAv at ~0.1 Hz. Results: While Mean MCAv 0.1 Hz oscillations increased from baseline to OLBNP (N=8, 34.0±33.9 (cm/s)2vs. 104.7±58.1(cm/s)2, p=0.01), ICA beta stiffness did not increase (N=5, 6.1±0.7 au vs. 8.2±2.7 au, p=0.21). There was no relationship between baseline ICA beta stiffness and the percent change in mean MCAv 0.1 Hz oscillations (N=5; r=0.44, p=0.46). ScO2 decreased from baseline to OLBNP (N=8, 66.5±2.9 % vs. 64.8±2.9%,p=0.03), but there was also no relationship between the percent change in mean MCAv 0.1 Hz oscillations and the decrease in ScO2(r=0.28, p=0.50). Conclusions: Based on these data, 0.1 Hz OLBNP does not affect ICA stiffness, and there is no relationship between ICA stiffness, amplitude of induced 0.1 Hz cerebral blood flow oscillations, and the reduction in cerebral tissue oxygenation during simulated hemorrhage. However, as this analysis was performed retrospectively, and arterial stiffness was not initially an outcome measure, there was limited data available for analysis. This limitation will be addressed in a project currently in progress in our laboratory.