CEREBRAL ENERGY METABOLISM AND BLOOD FLOW IN THE RAT

体液和神经因子在脑血流控制中的作用 流动和新陈代谢是有争议的。我们研究了大脑的控制 在正常和压力条件下的血流和新陈代谢。我们的 最初的工作是用高碳酸血症模型来应对压力，但 研究可以扩展到其他应激模型，例如，缺氧， 低血糖和长期饮酒戒断。我们最初的 观察表明，肾上腺髓质是 控制脑血流对高碳酸血症反应的因素 压力。进一步的研究表明，其中一个因素是三角洲- 阿片肽。此外，最近的研究表明， 高碳酸血症应激的脑血流量是通过一氧化氮调节的 氧化物合成系统。然而，这些研究表明， 涉及一氧化氮合酶的通路，这些通路负责 高碳酸血症增加脑血流量和耗氧量 不涉及NMDA受体。最近的研究表明，至少有一部分 高碳酸血症患者脑血流量的增加与 脑氧耗增加。

The role of humoral and neuronal factors in the control of cerebral blood flow and metabolism is controversial. We studied the control of cerebral blood flow and metabolism under normal and stressful conditions. Our initial work was done with the hypercapnic models for stress, but the studies may be extended to other models of stress, e.g., hypoxia, hypoglycemia and withdrawal from chronic alcohol consumption. Our initial observations demonstrated that the adrenal medulla was the source of factors that controlled the response of cerebral blood flow to hypercapnic stress. Further work indicated that one of these factors was a delta- opioid peptide. Also, recent work demonstrated that the response of cerebral blood flow to hypercapnic stress is mediated through the nitric oxide synthesizing system. These studies showed, however, that the pathways involving nitric oxide synthetase that are responsible for the hypercapnic increases in cerebral blood flow and oxygen consumptions do not involve NMDA receptors. Recent studies have shown that at least part of the increase in cerebral blood flow in hypercapnia is coupled to an increase in cerebral oxygen consumption.