Sørensen H R, Husum B, Waaben J, Andersen K, Andersen L I, Gefke K, Kaarsen A L, Gjedde A
Department of Cardiothoracic Surgery, Copenhagen University, Denmark.
J Thorac Cardiovasc Surg. 1987 Nov;94(5):727-32.
Emboli in the brain microvasculature may inhibit brain activity during cardiopulmonary bypass. Such hypothetical blockade, if confirmed, may be responsible for the reduction of cerebral metabolic rate for glucose observed in animals subjected to cardiopulmonary bypass. In previous studies of cerebral blood flow during bypass, brain microcirculation was not evaluated. In the present study in animals (pigs), reduction of the number of perfused capillaries was estimated by measurements of the capillary diffusion capacity for hydrophilic tracers of low permeability. Capillary diffusion capacity, cerebral blood flow, and cerebral metabolic rate for glucose were measured simultaneously by the integral method, different tracers being used with different circulation times. In eight animals subjected to normothermic cardiopulmonary bypass, and seven subjected to hypothermic bypass, cerebral blood flow, cerebral metabolic rate for glucose, and capillary diffusion capacity decreased significantly: cerebral blood flow from 63 to 43 ml/100 gm/min in normothermia and to 34 ml/100 gm/min in hypothermia and cerebral metabolic rate for glucose from 43.0 to 23.0 mumol/100 gm/min in normothermia and to 14.1 mumol/100 gm/min in hypothermia. The capillary diffusion capacity declined markedly from 0.15 to 0.03 ml/100 gm/min in normothermia but only to 0.08 ml/100 gm/min in hypothermia. We conclude that the decrease of cerebral metabolic rate for glucose during normothermic cardiopulmonary bypass is caused by interruption of blood flow through a part of the capillary bed, possibly by microemboli, and that cerebral blood flow is an inadequate indicator of capillary blood flow. Further studies must clarify why normal microvascular function appears to be preserved during hypothermic cardiopulmonary bypass.
脑微血管中的栓子可能会在体外循环期间抑制脑活动。这种假设的阻塞如果得到证实，可能是在接受体外循环的动物中观察到的脑葡萄糖代谢率降低的原因。在先前关于体外循环期间脑血流量的研究中，未对脑微循环进行评估。在本动物（猪）研究中，通过测量低渗透性亲水性示踪剂的毛细血管扩散能力来估计灌注毛细血管数量的减少。通过积分法同时测量毛细血管扩散能力、脑血流量和脑葡萄糖代谢率，使用不同的示踪剂并设置不同的循环时间。在八只接受常温体外循环的动物和七只接受低温体外循环的动物中，脑血流量、脑葡萄糖代谢率和毛细血管扩散能力均显著下降：常温下脑血流量从63降至43 ml/100 gm/min，低温下降至34 ml/100 gm/min；常温下脑葡萄糖代谢率从43.0降至23.0 μmol/100 gm/min，低温下降至14.1 μmol/100 gm/min。常温下毛细血管扩散能力从0.15显著降至0.03 ml/100 gm/min，但低温下仅降至0.08 ml/100 gm/min。我们得出结论，常温体外循环期间脑葡萄糖代谢率的降低是由于部分毛细血管床血流中断，可能是由微栓子引起的，并且脑血流量不是毛细血管血流的充分指标。进一步的研究必须阐明为什么在低温体外循环期间正常的微血管功能似乎得以保留。
