Browsing by Author "Davis, K. Austin"
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Item Carotid arterial stiffness and cerebral blood flow variability in individuals with mild cognitive impairment(2023) Bhuiyan, Nasrul; Davis, K. Austin; Vintimilla, Raul; Borzage, Matthew; Pahlevan, Niema; King, Kevin; Johnson, Leigh; O'Bryant, Sid; Rickards, CarolinePurpose: It is unclear whether cerebral blood flow variability is a sign of impaired vascular function or an adaptation to chronic cerebral hypoperfusion in individuals with cognitive dysfunction. Elevated arterial stiffness increases transmission of pulsatile pressure to the brain, but the relationship between arterial stiffness, the magnitude of cerebral blood flow variability, and cognitive dysfunction is unknown. In this pilot study, we hypothesized that carotid artery stiffness would be higher in individuals with mild cognitive impairment (MCI) compared with individuals with normal cognition (NC), resulting in higher cerebral blood flow variability. Methods: In individuals with MCI (N=5) or NC (N=7), R-wave to common carotid artery (CCA) pulse wave velocity (PWV) was assessed as an index of arterial stiffness (via tonometry). CCA velocity (CCAv) and middle cerebral artery velocity (MCAv) were measured via transcranial Doppler ultrasound, with concurrent measurements of mean arterial pressure (MAP) via finger photoplethysmography. The amplitude of MAP, CCAv, and MCAv oscillations in the low frequency range (LF; 0.07-0.15 Hz) were assessed via fast Fourier transformation, and normalized to total power (0.04-0.4 Hz) for each participant to account for high inter-individual variability. Relationships between R-wave-carotid PWV and LF variability in CCAv and MCAv were assessed via correlational analyses. Results: There were no between-group differences for R-wave-carotid PWV (MCI: 0.91±0.16 m/s vs. NC: 0.87±0.07 m/s; P=0.70), mean CCAv (MCI: 31.8±8.8 cm/s vs. NC: 29.7±2.0 cm/s; P=0.54), mean MCAv (MCI: 50.9±6.5 cm/s vs. NC: 47.9±12.7 cm/s; P=0.63), or MAP (MCI: 102.1±10.2 mmHg vs. 104.7±13.8 mmHg; P=0.73). While there was also no difference between groups for nLF power of CCAv (MCI: 0.28±0.03 au vs. NC: 0.33±0.10 au; P=0.41), nLF power for MCAv was lower in the MCI group (MCI: 0.26±0.07 au vs. 0.43±0.12; P=0.02). Overall, there was a strong positive correlation between R-wave-carotid PWV and CCAv nLF power (R=0.81, P=0.005), but a weaker relationship for MCAv nLF power (R=0.56, P=0.09). While sub-group correlational analyses are limited based on the small sample sizes, relationships between R-wave-carotid PWV and CCAv nLF power were high for both MCI (R=0.98, P=0.02) and NC (R=0.79, P=0.06) groups, but were lower for MCAv nLF power (MCI: R=-0.12, P=0.88; NC: R=0.69, P=0.13). Conclusion: Contrary to our hypothesis, there were no differences in R-wave-carotid PWV between groups, and blood flow variability was either similar between groups (for CCAv), or lower in the MCI group (for MCAv). Overall, there was a strong positive relationship between R-wave-carotid PWV and blood flow variability in the CCA, which was also observed in sub-analysis of the MCI and NC groups. Future investigations with a larger sample size are needed to definitively determine the role of arterial stiffness on cerebral blood flow variability with cognitive dysfunction.Item The Effect of 0.1 Hz Blood Flow Oscillations on Microvascular Blood Flow Responses Following Severe Ischemia(2024-03-21) Davis, K. Austin; Bhuiyan, Nasrul; McIntyre, Benjamin; Rickards, CarolineBackground: We have shown that inducing 10 second (0.1 Hz) oscillations in arterial pressure and blood flow protects against reductions in tissue oxygenation during ischemia, independent of changes in macrovascular blood flow. However, it is unknown whether 0.1 Hz hemodynamic oscillations impacts microvascular function and vasodilatory capacity following severe ischemia. To examine this question, we assessed the reactive hyperemic response following a prolonged peripheral limb ischemia protocol with and without induced 0.1 Hz hemodynamic oscillations. Hypothesis: 0.1 Hz oscillations in blood pressure and blood flow will increase microvascular blood flow, assessed via reactive hyperemia following a 10-min period of ischemia. Methods: Thirteen healthy human participants (6M, 7F; 27.3 ± 4.2 y) completed two experimental protocols separated by ≥48 h. In both conditions, ischemia of the forearm was induced with a pneumatic cuff on the upper arm to decrease brachial artery blood velocity by ~70-80% from baseline. In the oscillation condition (OSC), 0.1 Hz oscillations in mean arterial pressure (MAP) and brachial artery blood flow were induced by inflating and deflating bilateral thigh cuffs every 5-s (10-s cycles; 0.1 Hz) throughout the forearm ischemia period. In the control condition (CON), the thigh cuffs were in place, but were inactive throughout the forearm ischemia period. Beat to beat arterial pressure was measured via finger photo plethysmography, and brachial artery diameter and blood velocity were measured via duplex Doppler ultrasound during baseline, ischemia, and the reperfusion period. The maximum mean brachial artery blood velocity, and 3-min area under the curve (AUC) of mean brachial artery blood velocity were used to determine the reactive hyperemia response. Results: The magnitude of forearm ischemia, indexed by the reduction in brachial artery conductance, was matched between conditions (CON: -74.8 ± 10.4% vs. OSC: -75.6 ± 6.7%, p=0.39). Reactive hyperemia was not different between conditions as indexed by maximum mean brachial artery blood velocity (CON: 36.4 ± 12.4 cm/s vs. OSC: 39.3 ± 11.2 cm/s, p=0.53) or 3-min brachial artery blood velocity AUC (CON: 1495 ± 744 (cm/s)2 vs. OSC: 1596 ± 804 (cm/s)2, p=0.74). Conclusion: Inducing 0.1 Hz hemodynamic oscillations during severe ischemia does not affect microvascular function, indexed by reactive hyperemia following release of the ischemic stimulus. A more direct measure of microvascular blood flow is needed to examine whether 0.1 Hz hemodynamic oscillations improves microvascular perfusion during ischemia.Item Evaluating the efficacy of wireless near infrared spectroscopy sensors for detecting central hypovolemia during simulated hemorrhage in humans(2024-03-21) Muthyala, Ritika; Davis, K. Austin; Hudson, Lindsey; Dinh, Viet Q.; Roumengous, Thibault; Wallner, Josephine; Boutwell, Casey; Rickards, Caroline A.Background: Early identification of blood loss is essential to decrease mortality from hemorrhage, a major cause of death in the military and civilian trauma settings. An industry partner has created noninvasive and wireless near infrared spectroscopy (NIRS) sensors to measure somatic tissue oxygenation (StO₂) for early detection of blood loss. In this study, we investigated the efficacy of these sensors for tracking the reduction in central blood volume (indexed by stroke volume) in humans undergoing simulated hemorrhage. We hypothesized that each NIRS sensor will progressively track the reduction in central blood volume during simulated hemorrhage in humans. Methods: Eight healthy humans (3 F, 5M; 25.3 ± 2.0 y) participated in a simulated hemorrhage protocol induced via application of lower body negative pressure (LBNP) to presyncope. Following baseline, the LBNP chamber pressure was decreased every 5-min to -15, -30, -45, -60, -70, -80, -90 and -100 mmHg, or until the onset of presyncopal symptoms (defined as a systolic arterial pressure <80 mmHg or subjective symptoms). Heart rate (via lead II ECG) and arterial pressure (via finger photoplethysmography) were monitored continuously. Stroke volume was estimated from pulse contour analysis of the finger photoplethysmography waveform. A total of five NIRS sensors measured StO2 at different anatomical locations including the sternum, forearm, deltoid, thigh, and calf. Data were analyzed over the final 3-min of each LBNP stage and the 1-min immediately prior to the onset of presyncope. Correlations between the relative changes in StO₂ of each sensor and stroke volume were assessed. Results: Stroke volume decreased by 46.9± 16.3 % at presyncope. StO₂ decreased by 1.5 ± 7.8 % at the sternum, 9.6 ± 7.4 % at the forearm, 1.5 ± 3.6 % at the deltoid, 21.3 ± 15.8 % at the thigh, and 30.4 ± 27.5 % at the calf. Of all the sites, the strongest relationship between decreases in StO₂ and stroke volume was at the calf (R-value range: 0.70-0.99, R-value mean: 0.89 ± 0.11). The sensors located at each of the other sites tracked stroke volume with high inter-participant variability (sternum, R-value range: -0.71-0.99, R-value mean: 0.24 ± 0.79; forearm, R-value range: -0.09-0.99, R-value mean: 0.61 ± 0.40; deltoid, R-value range: -0.97-0.96, R-value mean: 0.26 ± 0.83; thigh, R-value range: -0.75-0.99; R-value mean: 0.68 ± 0.64). Conclusion: Unexpectedly, the NIRS sensor on the calf, which was inside the LBNP chamber, performed the best out of the five sites in tracking the progressive reduction in central blood volume in healthy human participants. This may be due to the pooling of blood volume in the lower limbs with the LBNP stimulus, which increased deoxygenated hemoglobin, resulting in an overall lower measurement of tissue oxygen saturation. This finding is interesting, and further modifications and testing of these sensors are required to reliably track blood volume loss in patient populations.Item Hemodynamic Responses to Oscillatory Thigh Cuff Inflations(2023) McIntyre, Benjamin; Davis, K. Austin; Bhuiyan, Nasrul; Rickards, CarolineBackground. In the clinical setting, individuals have varying tolerance to hypovolemia induced by blood loss. Experimental generation of 0.1 Hz oscillations (~10-s cycle) in arterial pressure and cerebral blood flow via oscillatory lower body negative pressure (OLBNP) increases tolerance to this simulated hemorrhage, and protects cerebral tissue oxygenation. However, use of OLBNP as a method of inducing hemodynamic oscillations in the clinical setting is limited as: 1) it is a large and cumbersome technique, and; 2) it induces central hypovolemia, which would only worsen the magnitude of hemorrhage. In this study we evaluated a more clinically applicable method of inducing 0.1 Hz oscillations in arterial pressure and cerebral blood flow, using intermittent inflation of bilateral thigh cuffs. We hypothesized that the amplitude of arterial pressure and cerebral blood flow oscillations at 0.1 Hz would increase in response to repeated thigh cuff inflations at 0.1 Hz when compared with a baseline control condition. Methods. Ten healthy human subjects were tested (6 male, 4 female; 26.8 ± 4.1 y). Middle cerebral artery velocity (MCAv) was measured via transcranial doppler ultrasound, arterial pressure was measured via finger photoplethysmography, and end tidal CO2 (etCO2) was measured via capnography. Following a 10-min baseline period, intermittent thigh cuff inflations at 0.1 Hz and 230 mmHg (5-s inflation, 5-s deflation) were performed for 10-min ("oscillations”). 0.1 Hz oscillatory amplitude of mean arterial pressure and mean MCAv were quantified using Fast Fourier transformation during the last 5-min of baseline and the oscillatory period, and compared via two-tailed paired t-tests. Results. The amplitude of 0.1 Hz oscillations increased during the oscillatory period vs. baseline for mean arterial pressure (baseline: 1.7 ± 1.0 mmHg2 vs. oscillations: 9.0 ± 6.2 mmHg2; P = 0.004) and mean MCAv (baseline: 1.1 ± 0.6 (cm/s)2 vs. oscillations: 3.4 ± 3.1 (cm/s)2; P = 0.04). Absolute mean arterial pressure was similar between baseline and the oscillatory period (baseline: 97.2 ± 8.1 mmHg vs. oscillations: 99.1 ± 15.0 mmHg; P = 0.54), but absolute mean MCAv was lower during the oscillatory period (baseline: 61.7 ± 14.6 cm/s vs. oscillations: 53.2 ± 13.1 cm/s; P = 0.02). This reduction in mean MCAv was most likely due to hypocapnia (indexed by etCO2) induced by pacing the breathing of all subjects at ≥10 breaths/min (baseline: 33.2 ± 4.8 mmHg vs. oscillations 27.2 ± 4.5 mmHg; P = 0.005). Conclusions. Intermittent thigh cuff inflations at 0.1 Hz induced 0.1 Hz oscillations in both arterial pressure and cerebral blood flow when compared to baseline. These findings indicate that intermittent thigh cuff inflations could be developed as a method to induce pulsatile perfusion as a potential new therapy for individuals experiencing major blood loss.Item Induced Blood Flow Oscillations at 0.1 Hz Protects Oxygenation of Severely Ischemic Tissue(2023) Davis, K. Austin; Bhuiyan, Nasrul; McIntyre, Benjamin; Rickards, CarolinePurpose: Early interventions that improve vital organ perfusion will reduce the number of lives lost from blood loss injuries. We have shown that generating 10 second (~0.1 Hz) fluctuations or "oscillations” in arterial pressure and blood flow during simulated hemorrhage protects cerebral tissue oxygenation. Lower body negative pressure (LBNP) was used to both simulate hemorrhage, and induce the hemodynamic oscillations in these previous studies. However, the magnitude of cerebral tissue ischemia is limited to 20-30% with LBNP due to the onset of pre-syncopal symptoms. To examine the effect of 0.1 Hz hemodynamic oscillations on blood flow delivery and tissue oxygenation of severely ischemic tissues, we developed a limb ischemia model. Hypothesis: Oscillatory arterial pressure and blood flow will attenuate reductions in brachial artery blood flow and forearm tissue oxygenation in a severely ischemic limb. Methods: Nine healthy human subjects (5M, 4F; 27.2 ± 4.1 y) completed two experimental protocols separated by ≥48 h. In both conditions, ischemia of the forearm was induced with a pneumatic cuff on the upper arm to decrease brachial artery (BA) blood velocity by ~70-80% from baseline. In the oscillation condition (OSC), 0.1 Hz oscillations in mean arterial pressure (MAP) and BA blood flow were then induced by inflating and deflating bilateral thigh cuffs every 10 seconds (0.1 Hz) throughout the forearm ischemia period. In the control condition (CON), the thigh cuffs were in place, but were inactive throughout the forearm ischemia period. BA blood flow was measured via duplex ultrasound, forearm muscle tissue oxygenation (SmO2) was measured via near infrared spectroscopy, and arterial pressure was measured via finger photoplethysmography. Results: The magnitude of forearm ischemia, indexed by the reduction in BA blood velocity, was matched between protocols (CON: -75.2 ± 8.4 % vs. OSC: -78.3 ± 7.8 %, p=0.20). Power spectral density of 0.1 Hz oscillations in MAP (CON: 19.4 ± 22.8 mmHg2 vs. OSC: 716.8 ± 514.6 mmHg2; p<0.001) and BA blood velocity (CON: 0.7 ± 1.0 cm/s2 vs. OSC: 10.6 ± 7.1 cm/s2, p=0.02) were greater with oscillatory thigh cuff compression compared with the control condition. While oscillatory thigh cuff compression during forearm ischemia had no effect on absolute MAP (CON: 94.3 ± 6.6 mmHg vs. OSC: 94.4 ± 10.8 mmHg, p=0.99), BA blood flow (CON: 9.7 ± 5.8 ml/min vs. OSC: 9.5 ± 7.3 ml/min, p=0.82), or BA conductance (CON: 0.10 ± 0.06 ml/min/mmHg vs. OSC: 0.09 ± 0.06 ml/min/mmHg, p=0.39), the reduction in SmO2 was attenuated (CON: -38.7 ± 8.3 % vs. OSC: -28.4 ± 9.7 %; p=0.04). These data provide further evidence for the use of 0.1 Hz hemodynamic oscillations as a therapeutic intervention for conditions associated with severe vital organ ischemia such as hemorrhage, stroke, myocardial infarction, and sepsis.Item Peripheral Vascular Function is Not Correlated to Subjective Sleep Quality in Young Healthy Humans(2023) Stanteen, Chandler; Davis, K. Austin; Bhuiyan, Nasrul; McIntyre, Benjamin; Rickards, CarolineBackground: Peripheral vascular dysfunction (including endothelial dysfunction) may be an early biomarker of cardiovascular disease. Prior studies have shown a relationship between poor sleep quality and impaired vascular function, indexed by flow-mediated dilation (FMD) of the brachial artery. However, these investigations did not allometrically scale for baseline artery diameter, nor control for shear stress, which both affect the magnitude of flow-mediated vasodilation. Without scaling for baseline artery diameter, FMD may overestimate the magnitude of dilation in individuals with small baseline diameters. Additionally, greater shear stress will elicit a greater magnitude of vasodilation via release of vasoactive mediators from the endothelium, such as nitric oxide. With the quality of sleep declining in the United States, and cardiovascular disease remaining a leading cause of mortality, we sought to further explore the relationship between sleep quality and peripheral vascular function corrected for both baseline artery diameter and the magnitude of shear stress. Hypothesis: Poor sleep quality is associated with impaired peripheral vascular function indexed by "corrected” brachial artery FMD. Methods: Thirteen young and healthy human participants (7M, 6F) completed the Pittsburgh Sleep Quality Index (PSQI) survey prior to assessment of brachial artery FMD. PSQI scores range from 0-21, with higher scores indicating worse sleep quality. Brachial artery diameter and blood velocity were then obtained via duplex Doppler ultrasound during a 2-min baseline, a 5-min occlusion of the brachial artery, and a 3-min reactive hyperemia period. FMD of the brachial artery was calculated as the percent change from baseline diameter to the maximum diameter induced by reactive hyperemia. Shear stress was estimated as shear rate, calculated as eight times the ratio of brachial artery blood velocity to diameter. FMD was corrected for baseline diameter, and the shear stress area under the curve up to maximum diameter via ANCOVA (i.e., "corrected FMD”). Pearson correlations were calculated between PSQI score and uncorrected FMD, and between PSQI score and ANCOVA corrected FMD. Results: The mean PSQI score was 5.3 ± 4.5 (range, 0-17), and mean FMD was 5.0 ± 2.2 % (range, 2.7-9.4 %). While an unexpected modest positive correlation was observed between uncorrected FMD and PSQI score (r=0.51, p=0.08), corrected FMD and PSQI score were not correlated (r=0.38, p=0.25). Conclusion: There was no relationship between subjective sleep quality and peripheral vascular function as measured by corrected FMD in this cohort of young and healthy participants. These findings likely reflect the multivariate nature of vascular function in young healthy adults with lower cardiovascular risk, and the subsequent narrow range of both flow-mediated dilation and subjective sleep quality.