Dataset Information

Effects of Mild Orthostatic Stimulation on Cerebral Pulsatile Hemodynamics.

ABSTRACT: The augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. To determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics, mild lower body negative pressure (LBNP, -30 mmHg) was applied to 29 men. Middle cerebral artery blood flow velocity (MCAv) was measured by transcranial Doppler technique. Stroke volume (SV) was estimated by the Modelflow method with adjustment by the Doppler ultrasound-measured SV at rest. SV, peak and pulsatile MCAv, and pulsatility index were significantly lower during the LBNP stimulation than those at the baseline (e.g., supine resting) (P < 0.05 for all), whereas mean arterial pressure and mean MCAv remained unchanged. The change in SV with the LBNP stimulation significantly correlated with corresponding changes in peak and pulsatile MCAv (r = 0.617, P < 0.001; r = 0.413, P = 0.026, respectively). These results suggest that pulsatile components of cerebrovascular hemodynamics are dampened during the transient period of orthostatic challenge (as simulated using LBNP) when compared to supine rest, and which is partly due to the modified SV.

SUBMITTER: Ninomiya Y

PROVIDER: S-EPMC6423479 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Effects of Mild Orthostatic Stimulation on Cerebral Pulsatile Hemodynamics.

Ninomiya Yuka Y Tomoto Tsubasa T Ogoh Shigehiko S Imai Tomoko T Takahashi Koki K Sugawara Jun J

Frontiers in physiology 20190312

The augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. To determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics, mild lower body negative pressure (LBNP, -30 mmHg) was applied to 29 men. Middle cerebral artery blood flow velocity (MCAv) was measured by transcranial Doppler technique. Stroke volume (SV) was estimated by the Modelflow method with adjustment by the Doppler ultrasound-measured SV a ...[more]

PMID: 30930792

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Project description:Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We analyzed hemodynamic data from 200 cardiac arrest survivors during the hypothermia period. The initial LVEF was 32.6 +/- 1.2% indicating a significantly impaired LV function. During hypothermia induction, the infusion rate of epinephrine could be significantly reduced from 9.1 +/- 1.3 microg/min [arrival intensive care unit (ICU) 35.4 degrees C] to 4.6 +/- 1.0 microg/min (34 degrees C) and 2.8 +/- 0.5 microg/min (33 degrees C). The dobutamine and norepinephrine application rates were not changed significantly. The mean arterial blood pressure remained stable. The mean heart rate significantly decreased from 91.8 +/- 1.7 bpm (arrival ICU) to 77.3 +/- 1.5 bpm (34 degrees C) and 70.3 +/- 1.4 bpm (33 degrees C). In vitro we investigated the effect of hypothermia on isolated ventricular muscle strips from explanted failing human hearts. With decreasing temperature, the contractility increased to a maximum of 168 +/- 23% at 27 degrees C (n = 16, P < 0.05). Positive inotropic response to hypothermia was accompanied by moderately increased rapid cooling contractures as a measure of sarcoplasmic reticulum (SR) Ca(2+) content, but can be elicited even when the SR Ca(2+) release is blocked in the presence of ryanodine. Contraction and relaxation kinetics are prolonged with hypothermia, indicating increased Ca(2+) sensitivity as the main mechanism responsible for inotropy. In conclusion, mild hypothermia stabilizes hemodynamics in cardiac arrest survivors which might contribute to improved survival rates in these patients. Mechanistically, we demonstrate that hypothermia improves contractility in failing human myocardium most likely by increasing Ca(2+)-sensitivity.

Project description:Objective: Cerebral autoregulation limits the variability of cerebral blood flow (CBF) in the presence of systemic arterial blood pressure (ABP) changes. Monitoring cerebral autoregulation is important in the Neurocritical Care Unit (NCCU) to assess cerebral health. Here, our goal is to identify optimal frequency-domain near-infrared spectroscopy (FD-NIRS) parameters and apply a hemodynamic model of coherent hemodynamics spectroscopy (CHS) to assess cerebral autoregulation in healthy adult subjects and NCCU patients. Methods: In five healthy subjects and three NCCU patients, ABP oscillations at a frequency around 0.065 Hz were induced by cyclic inflation-deflation of pneumatic thigh cuffs. Transfer function analysis based on wavelet transform was performed to measure dynamic relationships between ABP and oscillations in oxy- (O), deoxy- (D), and total- (T) hemoglobin concentrations measured with different FD-NIRS methods. In healthy subjects, we also obtained the dynamic CBF-ABP relationship by using FD-NIRS measurements and the CHS model. In healthy subjects, an interval of hypercapnia was performed to induce cerebral autoregulation impairment. In NCCU patients, the optical measurements of autoregulation were linked to individual clinical diagnoses. Results: In healthy subjects, hypercapnia leads to a more negative phase difference of both O and D oscillations vs. ABP oscillations, which are consistent across different FD-NIRS methods and are highly correlated with a more negative phase difference CBF vs. ABP. In the NCCU, a less negative phase difference of D vs. ABP was observed in one patient as compared to two others, indicating a better autoregulation in that patient. Conclusions: Non-invasive optical measurements of induced phase difference between D and ABP show the strongest sensitivity to cerebral autoregulation. The results from healthy subjects also show that the CHS model, in combination with FD-NIRS, can be applied to measure the CBF-ABP dynamics for a better direct measurement of cerebral autoregulation.

Dataset Information

Effects of Mild Orthostatic Stimulation on Cerebral Pulsatile Hemodynamics.

Publications

Effects of Mild Orthostatic Stimulation on Cerebral Pulsatile Hemodynamics.

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