Department of Anesthesia, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 125 Paterson St., Suite 3100, New Brunswick, NJ 08901-1977, USA.
Anesth Analg. 2011 Aug;113(2):349-55. doi: 10.1213/ANE.0b013e31822071db. Epub 2011 May 19.
We performed this study to determine how dexmedetomidine would affect regional cerebral blood flow (rCBF) and microregional O(2) consumption during nonhemorrhagic normovolemia and during severe hemorrhagic hypotension in rats.
Forty-eight male rats were anesthetized with isoflurane and their lungs were mechanically ventilated. Half of the rats were bled to reach a mean arterial blood pressure of 40 to 45 mm Hg and were maintained at this level for at least 30 minutes before rCBF or microregional arterial oxygen saturation (Sao(2)) and venous oxygen saturation (Svo(2)) were determined. The other half were not bled and served as nonhemorrhagic controls. Half of each group was given dexmedetomidine 1 μg/kg/min IV for 45 minutes and the other half was given the same amount of normal saline infusion. The infusion started 10 minutes before blood withdrawal for the hemorrhagic groups. The rCBF was determined using (14)C-iodoantipyrine, and the microregional Sao(2) and Svo(2) were determined using cryomicrospectrophotometry at 45 minutes of infusion.
Dexmedetomidine decreased heart rate by 25%, but the decrease of mean arterial blood pressure was not significant. The total amount of blood withdrawn and hemoglobin were similar between the normal saline-treated and the dexmedetomidine-treated groups. In normovolemia, dexmedetomidine significantly decreased rCBF (-58%) in the lateral cortex with a similar percentage decrease (-57%) of calculated O(2) consumption. Microregional Svo(2) was similar between the normal saline-treated group (62.8% ± 1.3% [mean ± SD]) and the dexmedetomidine-treated group (60.7% ± 1.8%) despite a large difference in rCBF. Hemorrhage significantly decreased rCBF (-44%) in the lateral cortex in the normal saline-treated rats with no significant change in regional cerebrovascular resistance. In contrast, in the lateral cortex of the dexmedetomidine-treated rats, the decrease of rCBF was not significant but there was a significant decrease in regional cerebrovascular resistance. A decrease (-25%) in the O(2) consumption was observed in the lateral cortex of the normal saline-treated rats with hemorrhage, but hemorrhage did not decrease O(2) consumption in the dexmedetomidine-treated rats. Despite significantly lower rCBF (-34%) in the dexmedetomidine-treated rats, the Svo(2) was similar between the normal saline-treated (42.8% ± 2.5%) and the dexmedetomidine-treated rats (43.2% ± 2.7%).
Our data showed that in normovolemia, dexmedetomidine produced a proportionate decrease of rCBF and O(2) consumption. Hemorrhage decreased rCBF more than O(2) consumption. Dexmedetomidine prevented rCBF and O(2) consumption from decreasing after hemorrhage. Our data suggest that dexmedetomidine may help provide optimal O(2) supply and consumption balance during hemorrhage.
我们进行这项研究，以确定右美托咪定在非出血性正常血容量和严重出血性低血压期间如何影响大鼠的局部脑血流（rCBF）和微区氧消耗。
48 只雄性大鼠用异氟醚麻醉，并进行机械通气。一半的大鼠被放血以达到平均动脉血压 40 至 45mmHg，并在 rCBF 或微区动脉氧饱和度（Sao（2））和静脉氧饱和度（Svo（2））确定之前至少维持 30 分钟。另一半未被放血，作为非出血对照。每组的一半给予右美托咪定 1μg/kg/min 静脉输注 45 分钟，另一半给予等量生理盐水输注。对于出血组，输液在采血前 10 分钟开始。使用（14）C-碘安替比林测定 rCBF，使用低温显微镜分光光度法测定微区 Sao（2）和 Svo（2）在输液 45 分钟时。
右美托咪定使心率降低 25%，但平均动脉血压降低不明显。生理盐水处理组和右美托咪定处理组的总出血量和血红蛋白相似。在正常血容量状态下，右美托咪定显著降低外侧皮质的 rCBF（-58%），计算的氧消耗也有相似的百分比降低（-57%）。尽管 rCBF 差异很大，但生理盐水处理组（62.8%±1.3%[平均值±SD]）和右美托咪定处理组的微区 Svo（2）相似。出血显著降低了生理盐水处理大鼠外侧皮质的 rCBF（-44%），而区域脑血管阻力无明显变化。相比之下，在右美托咪定处理大鼠的外侧皮质中，rCBF 的降低不显著，但区域脑血管阻力显著降低。出血后，生理盐水处理大鼠外侧皮质的氧消耗下降（-25%），但右美托咪定处理大鼠的氧消耗未下降。尽管右美托咪定处理大鼠的 rCBF 明显降低（-34%），但生理盐水处理组（42.8%±2.5%）和右美托咪定处理组（43.2%±2.7%）的 Svo（2）相似。
我们的数据表明，在正常血容量状态下，右美托咪定使 rCBF 和氧消耗成比例下降。出血使 rCBF 减少超过氧消耗。右美托咪定可防止出血后 rCBF 和氧消耗减少。我们的数据表明，右美托咪定可能有助于在出血期间提供最佳的氧供应和消耗平衡。
