Dexmedetomidine Weakens Dynamic Cerebral Autoregulation as Assessed by Transfer Function Analysis and the Thigh Cuff Method

Abstract

Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.

Dexmedetomidine Dose Dependently Decreases Oral Tissue Blood Flow During Sevoflurane and Propofol Anesthesia in Rabbits

“…The increase in the vascular resistance suggests that DEX may induce peripheral vasoconstriction caused by α2B receptor-medicated mechanisms, as in cerebral vessels. However, the relative increase in vascular resistance in the oral tissues was smaller than that in cerebral vessels when compared to the report of Ogawa et al 24 , even at the same administration rate. In addition, there is no report investigating the distribution of α2B receptors in oral tissues.…”

“…33-35 As described above, cerebral vessels are thought to contain many α2B receptors. Ogawa et al 24 administered DEX to volunteers either at low flow rate (3 μg･kg -1 ･hr -1 for 10 min, followed by 0.2 μg･ kg -1 ･hr -1 for 60 min), or at high flow rate (6 μg･kg -1 ･hr -1 for 10min, followed by 0.4…”

“…Vascular resistance for each tissue (TVR, BVR, MVR, UVR, LVR) was calculated as MAP divided by each tissue blood flow and expressed as a percent change of the respestive control value. 24 Rectal temperature was maintained at 39.0 to 39.5 throughout the experiment.…”

Static autoregulation in humans: a review and reanalysis

“…Indeed, fixing a line through several singular subject MAP/CBF relationships ignores the potential of chronic resetting, e.g., in the case with sustained hypertension [7]. Upon closer examination of the response for CBF (or a related index of CBF) to a change in MAP, recent studies have revealed that this relationship appears to be more pressure passive [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] than previously described. However, the limitations to drawing inferences from the majority of recent studies are threefold.…”

The α2-Adrenoceptor Agonist Dexmedetomidine in Current Sedation Practice

“…У больных с септическим шоком дексме детомидин уменьшает чувствительность к СО 2 в большей сте пени, чем пропофол [46]. Препарат снижает эффективность ауторегуляции мозгового кровотока при колебаниях АД [47].…”