Ganjoo P, Farber N E, Hudetz A, Smith J J, Samso E, Kampine J P, Schmeling W T
Department of Anesthesiology, The Medical College of Wisconsin, and the Zablocki Veterans Affairs Medical Center, Milwaukee 53226, USA.
Anesthesiology. 1998 Feb;88(2):429-39. doi: 10.1097/00000542-199802000-00022.
The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter.
Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min).
Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored.
These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.
α2肾上腺素能激动剂右美托咪定可改变全脑血流量(CBF)。然而,很少有研究探讨右美托咪定对脑微循环的作用。本研究检测了右美托咪定对(1)采用激光多普勒血流仪测量大鼠大脑皮质局部脑血流量,以及(2)软脑膜小动脉直径的影响。
用氟烷麻醉大鼠,安装仪器以测量激光多普勒血流测定的脑血流量(CBFldf),或通过制备颅骨凹陷直至保留半透明颅骨板来测量软脑膜小动脉直径,从而保持颅腔的完整性。两组均静脉注射20μg/kg右美托咪定。30分钟后,通过输注去氧肾上腺素(0.5至5μg/kg/min)将平均动脉压恢复至对照值。
给予右美托咪定与呼气末和动脉二氧化碳分压降低有关。在正常碳酸血症(控制二氧化碳)期间和右美托咪定诱导的低碳酸血症期间测量CBFldf和软脑膜小动脉直径。静脉注射右美托咪定显著降低全身动脉压,同时CBFldf降低(正常碳酸血症动物降低22%,低碳酸血症动物降低36%)。恢复平均动脉压可使正常碳酸血症动物的CBFldf增加,但低碳酸血症动物则不然。同样,右美托咪定在正常碳酸血症(9%)和低碳酸血症动物(17%)中均显著降低软脑膜血管直径。然而,恢复平均动脉压后,正常碳酸血症和低碳酸血症动物的血管直径仍保持降低。
这些结果提示右美托咪定对脑血管自动调节有调节作用,这可能部分由二氧化碳变化介导。右美托咪定可能对脑血管有直接作用,以在正常或低碳酸血症期间降低脑血流量。CBFldf和软脑膜小动脉对恢复平均动脉压的反应差异可能反映了测量技术的差异,因为激光多普勒测量反映了几个动脉节段对微血管灌注的净效应,而直径测量专门检查了单个软脑膜小动脉,提示右美托咪定在脑血管中的血管收缩可能由不同的区域介导。