Abstract

Accurate and practical assessment of the brain circulation is needed to adequately estimate the viability of cerebral blood flow regulatory mechanisms in various physiological conditions. The objective of our study was to examine feasibility of the contactless green-light imaging photoplethysmography (PPG) for assessing cerebral autoregulation by revealing the dynamic relationships between cortical microcirculation assessed by PPG and changes in systemic blood pressure caused by visceral and somatic peripheral stimuli. In anesthetized male Wistar rats, the PPG video images of the open parietal cortex (either with unimpaired or dissected dura mater), electrocardiogram, and systemic arterial blood pressure (ABP) in the femoral artery were continuously recorded before, during and after visceral (colorectal distension) or somatic (tail squeezing) stimulation. In the vast majority of experiments with intact and removed dura mater, both spontaneous and peripheral stimulation-evoked changes in ABP negatively correlated with the accompanying alterations in the amplitude of pulsatile PPG component (APC), i.e., an increase of ABP resulted in a decrease of APC and vice versa. The most pronounced ABP and APC alterations were induced by noxious stimuli. Visceral painful stimulation in all cases caused short-term hypotension with simultaneous increase in cortical APC, whereas somatic noxious stimuli in 8 of 21 trials produced hypertensive effect with decreased APC. Animals with pressure 50-70 mmHg possessed higher negative cerebrovascular response rate of ABP-APC gradients than rats with either lower or higher pressure. Severe hypotension reversed the negative ratio to positive one, which was especially evident under visceral pain stimulation. Amplitude of the pulsatile PPG component probably reflects the regulation of vascular tone of cerebral cortex in response to systemic blood pressure fluctuations. When combined with different kinds of peripheral stimuli, the technique is capable for evaluation of normal and elucidation of impaired cerebrovascular system reactivity to particular physiological events, for example pain. The reported contactless PPG monitoring of cortical circulatory dynamics during neurosurgical interventions in combination with recordings of changes in other physiological parameters, such as systemic blood pressure and ECG, has the appealing potential to monitor viability of the cortex vessels and determine the state of patient’s cerebrovascular autoregulation.

Highlights

  • Adequate assessment of cerebral hemodynamics is an important task needed to be solved to estimate viability of the cortex and regulatory mechanism

  • As seen, pulsating arteries are clearly distinguished from the veins because of much higher amplitude of the pulsatile component synchronized with cardiac activity

  • Big regions of interest (ROI) in which the amplitude of the pulsatile component (APC) dynamics was monitored were selected on the location of arteries since these areas are characterized with larger amplitude of pulsations

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Summary

Introduction

Adequate assessment of cerebral hemodynamics is an important task needed to be solved to estimate viability of the cortex and regulatory mechanism. At the level of the brain vessels themselves, CBF is controlled by active changes in vascular tone occurring at the level of the cerebral arterioles, a process referred to as cerebral autoregulation. This is an ability of the brain to maintain relatively constant blood flow despite changes in blood pressure (Paulson et al, 1990; Cipolla, 2009; Fantini et al, 2016). Cerebral autoregulation is a negative feedback loop mechanism that counteracts the mean ABP increase by increasing vascular tone and narrowing the vessels diameter ( increasing resistance of vessels) that brings CBF to the original level. Physiological origin of cerebral autoregulation is still unclear, with proposed mechanisms invoking myogenic (Ozol et al, 2002; Cipolla, 2009), metabolic (Paulson et al, 1990; Ainslie and Brassard, 2014), and neurogenic processes (Hamel, 2006; Drake and Iadecola, 2007; Donnelly et al, 2016)

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