Dexmedetomidine-Induced Sedation in Volunteers Decreases Regional and Global Cerebral Blood Flow

Abstract

Dexmedetomidine-induced sedation decreased cerebral blood flow (CBF) by congruent with 33%, which could be due to direct alpha(2)-receptor cerebral smooth muscle vasoconstriction or to compensatory CBF changes caused by dexmedetomidine-induced decreases in the cerebral metabolic rate.

Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats

“…Dexmedetomidine continues to gain popularity as a sedative agent; it is also used in patients with traumatic brain injury because of its benefi cial effects on intracranial pressure (ICP) and CBF [24][25][26][27]. Dexmedetomidine has the potential to decrease blood pressure (BP) in a dose-dependent manner due to its alpha-2 agonist activity on the sympathetic ganglia and the resulting sympatholytic effects [10,28].…”

“…Among these receptors, the activation of alpha-2A receptors by dexmedetomidine exerts a neuroprotective effect [6][7][8][9]. In contrast, the activation of alpha-2B receptors by high concentrations of dexmedetomidine has been reported both to constrict cerebral vessels, thus decreasing cerebral blood fl ow (CBF) [10][11][12], and to constrict systemic vessels, resulting in increased systemic blood pressure [13]. However, the relationship between the vasoconstriction induced by high doses of dexmedetomidine and ischemic brain damage remains unclear.…”

High-dose Dexmedetomidine-induced Hypertension in a Child with Traumatic Brain Injury

“…Given its possible beneficial effects on ICP and cerebral blood flow (CBF), dexmedetomidine continues to gain popularity as an agent for sedation in patients with traumatic brain injury [5][6][7][8][9]. The effects of dexmedetomidine on ICP and CPP were evaluated by Talke et al in adult patients following transphenoidal pituitary resection [5].…”

“…There was no effect on ICP in the baseline state or in animals with intracranial hypertension (mean starting ICP of 16.8 mmHg) induced by a cryogenic lesion. Animal and human studies have also demonstrated a reduction in CBF following dexmedetomidine [7,8]. Karlsson et al demonstrated a reduction of CBF in dogs anesthetized with 0.9% halothane; however, the authors could not determine if dexmedetomidine directly constricted the cerebral vasculature or blunted the cerebral vasodilatation induced by halothane [9].…”

Evaluating the Use of Dexmedetomidine in Neurocritical Care Patients

“…Although a 2 -adrenoreceptors are located throughout the body, they are present in larger concentrations in vascular smooth muscle and in key arousal areas of the central nervous system (CNS), such as the locus ceruleus [2]. Activation of a 2 -adrenoreceptors in the CNS decreases centrally mediated sympathetic activity and induces sedation [2,3] Activation of presynaptic a 2 -adrenoreceptor on cortical blood vessels decreases norepinephrine release, whereas postsynaptic a 2 -adrenoreceptors may directly increase vascular smooth muscle tone [1][2][3].…”