Hare G M T, Worrall J M A, Baker A J, Liu E, Sikich N, Mazer C D
Department of Anaesthesia and the Cara Phelan Centre for Trauma Research, University of Toronto, St Michael's Hospital 30 Bond Street, Toronto, Ontario M5B 1W8, Canada.
Br J Anaesth. 2006 Nov;97(5):617-23. doi: 10.1093/bja/ael238. Epub 2006 Sep 6.
Haemodilution has been associated with neurological morbidity in surgical patients. This study tests the hypothesis that inhibition of cerebral vasodilatation by systemic beta2 adrenergic blockade would impair cerebral oxygen delivery leading to tissue hypoxia in severely haemodiluted rats.
Under general anaesthesia, cerebral tissue probes were placed to measure temperature, regional cerebral blood flow (rCBF) and tissue oxygen tension (P(Br)O2) in the parietal cerebral cortex or hippocampus. Baseline measurements were established before and after systemic administration of either a beta2 antagonist (10 mg kg(-1) i.v., ICI 118, 551) or saline vehicle. Acute haemodilution was then performed by simultaneously exchanging 50% of the estimated blood volume (30 ml kg(-1)) with pentastarch. Arterial blood gases (ABGs), haemoglobin concentration (co-oximetry), mean arterial blood pressure (MAP) and heart rate (HR) were also measured. Data were analysed using a two-way anova and post hoc Tukey's test [mean (sd)].
Haemodilution reduced the haemoglobin concentration comparably in all groups [71 (9) g litre(-1)]. There were no differences in ABGs, co-oximetry, HR and MAP measurements between control and beta2 blocked rats, either before or 60 min after drug or vehicle administration. In rats treated with the beta2 antagonist there was a significant reduction in parietal cerebral cortical temperature, regional blood flow and tissue oxygen tension, relative to control rats, 60 min after haemodilution (P<0.05 for each). These differences were not observed when probes were placed in the hippocampus.
Systemic beta2 adrenergic blockade inhibited the compensatory increase in parietal cerebral cortical oxygen delivery after haemodilution thereby reducing cerebral cortical tissue oxygen tension.
血液稀释与外科手术患者的神经功能并发症有关。本研究检验了这样一个假设，即全身β2肾上腺素能阻滞剂抑制脑血管扩张会损害脑氧输送，导致严重血液稀释大鼠出现组织缺氧。
在全身麻醉下，将脑组织探头置于顶叶大脑皮质或海马体中，以测量温度、局部脑血流量（rCBF）和组织氧分压（P(Br)O2）。在全身给予β2拮抗剂（10 mg kg(-1)静脉注射，ICI 118,551）或生理盐水载体之前和之后进行基线测量。然后通过同时用羟乙基淀粉置换估计血容量的50%（30 ml kg(-1)）来进行急性血液稀释。还测量了动脉血气（ABG）、血红蛋白浓度（共血氧测定法）、平均动脉血压（MAP）和心率（HR）。使用双向方差分析和事后Tukey检验[均值（标准差）]对数据进行分析。
所有组的血液稀释均使血红蛋白浓度降低程度相当[71（9）g/l]。在给予药物或载体之前或之后60分钟，对照组和β2阻滞剂处理的大鼠在ABG、共血氧测定法、HR和MAP测量方面均无差异。在血液稀释60分钟后，与对照组大鼠相比，用β2拮抗剂处理的大鼠顶叶大脑皮质温度、局部血流量和组织氧分压显著降低（每项P<0.05）。当探头置于海马体中时未观察到这些差异。
全身β2肾上腺素能阻滞剂抑制了血液稀释后顶叶大脑皮质氧输送的代偿性增加，从而降低了大脑皮质组织氧分压。
