Wiedemann K, Weinhardt F, Hamer J, Wund G, Berlet H, Hoyer S
Anaesthesist. 1979 Jun;28(6):290-8.
The influence on total cerebral blood flow, cerebral metabolic rates for oxygen, carbon dioxide, glucose, lactate and pyruvate and on cerebral grey matter content of glucose, lactate and pyruvate and high energy phosphate compounds of combined moderate reduction in cerebral perfusion pressure (CPP) and moderate arterial hypoxaemia was studied. Individually arterial hypoxaemia and arterial hypotension of the same degree would neither impair autoregulation of cerebral blood flow nor cerebral oxygen availability. Four groups of 10 dogs each were studied under control conditions (group I), with reduction of CPP to 70 mm Hg (group II), with reduction of paO2 to 45 mm Hg (group III) or with a combination of these degrees of hypotension and hypoxaemia (group IV) after steady states of 30 min duration. Cbf was elevated by 40% in group III (p less than or equal to 0.01), CMRO2 was reduced significantly in group IV (p less than or equal to 0.01, CMR lactate was raised significantly in all three experimental groups (p less than or equal to 0.01). All other data were not significantly different from values in control animals. Cerebral tissue lactate content was elevated significantly in groups II to IV as compared to controls (less than or equal to 0.05); changes in cerebral tissue content of glucose and energy rich phosphate compounds were not statistically significant. From the seemingly normal cerebral blood flow in hypotensive-hypoxaemic dogs it is concluded that autoregulation of cerebral blood flow has become ineffective because of vasodilatation consequent upon arterial hypoxaemia. Reduction of CMRO2 in this group points to metabolic insufficiency and to relative cerebral hypoperfusion, but since changes in cerebral content of high energy phosphate compounds were not significant, severe tissue hypoxia may be excluded. The increase in cerebral tissue lactate content is attributable to increased glycolytic activity known from hypotensive and hypoxaemic states. The present investigation suggests that in patients with hypoxaemia and hypotension, brain function may be endangered by a similarly marked change of circulatory and metabolic parameters.
研究了脑灌注压（CPP）适度降低与中度动脉低氧血症联合作用对全脑血流量、脑氧、二氧化碳、葡萄糖、乳酸和丙酮酸的脑代谢率以及脑灰质中葡萄糖、乳酸、丙酮酸和高能磷酸化合物含量的影响。单独的同等程度的动脉低氧血症和动脉低血压既不会损害脑血流量的自动调节，也不会影响脑氧供应。在30分钟的稳定状态后，对四组实验犬进行研究，每组10只。分别为：对照组（I组）；CPP降至70 mmHg的组（II组）；动脉血氧分压（paO2）降至45 mmHg的组（III组）；或低血压和低氧血症达到上述程度的联合组（IV组）。III组脑血流量（Cbf）升高40%（p≤0.01），IV组脑氧代谢率（CMRO2）显著降低（p≤0.01），所有三个实验组的脑乳酸代谢率（CMR乳酸）均显著升高（p≤0.01）。所有其他数据与对照动物的值无显著差异。与对照组相比，II至IV组脑组织乳酸含量显著升高（≤0.05）；脑组织葡萄糖和富含能量的磷酸化合物含量的变化无统计学意义。从低血压-低氧血症犬看似正常的脑血流量可以得出结论，由于动脉低氧血症导致血管扩张，脑血流量的自动调节已失效。该组中CMRO2的降低表明代谢不足和相对脑灌注不足，但由于高能磷酸化合物的脑含量变化不显著，可排除严重的组织缺氧。脑组织乳酸含量的增加归因于低血压和低氧血症状态下已知的糖酵解活性增加。本研究表明，在低氧血症和低血压患者中，循环和代谢参数的类似显著变化可能危及脑功能。
