Neuronal Control of Cerebrovascular Bed : Role of Basal Forebrain

通过皮质内一氧化氮神经元控制基底皮质神经血管通路中的胆碱能基底前脑对颅内压和脑血管床的控制——之前，我们报道了中枢去甲肾上腺素能细胞群、胆碱感受脑桥区和胆碱能基底前脑（BF）在平台波产生中的作用。本研究探讨了基底皮质神经血管通路和皮质内一氧化氮（NO）神经元在颅内压和脑血管床的控制中的作用。实验采用氯氯蔗糖麻醉固定高岭土致脑积水猫20只。连续监测ICP、BP、ETCO_2。用Laserflo和电化学NO电极分别连续测量脑血流和脑组织NO。将谷氨酸或乙酰胆碱微量注射到猫的下丘脑背内侧核（DMH）后，其ICP和CBF持续升高，BP持续降低。ETCO_2的浓度变化不大。DMH -单神经元放电的Bring率随ICP的增加呈阶段性增加。自发性“A”波时NO浓度和CBV随平台期呈阶段性升高。NO和CBV分别为。在重复的平台波中，根据ICP的上升或下降阶段增加或减少，如微量注射谷氨酸引起的ICP变化。在DMH内微量注射Ach后，同侧额叶和顶叶NO浓度显著升高，与颅内压升高和CBV升高有关。一种有效的一氧化氮合成抑制剂（L-NAME）减少了这些在ICY、锥形CBV和NO中引起的疼痛。胆碱能BF可能有助于脑血管床的调节，目前的观察表明，肠道参与的NO介导的BF引起了ICP和CBV的增加，并表明至少有一个神经元来源的NO参与，因为支配局部微血管的皮质内NOS神经元似乎受到BF神经元的调节。脑低温-脑血管床与NO浓度引起的痛苦灌注。治疗性脑低温被广泛应用于重型颅脑损伤和脑缺血的治疗。研究了脑低温对正常脑血流量、脑代谢及脑血管系统的影响。对24只麻醉猫进行脑低温状态下CBF、CBV、AVDO_2、cmo_2和CVR的监测。低温可引起31℃以下大鼠脑内血管收缩，一氧化氮浓度低，血流灌注不足。这种潜在的相对缺血风险可以通过联合使用血管加压剂来避免。在复温期间评估脑缺血参数，以确定临界脑灌注压（CPP）阈值，避免缺血恶化。再温期CPP为60mmHg，可引起不可逆缺血，提示脑血管持续收缩。因此，为了避免复温期脑缺血，需要较高的CPP （bb0 ~ 90mmHg）。少

I] Control of ICP and the Cerebrovascular Bed by the Cholinergic Basal Forebrain-role of basalocortical neurovascular pathway via the intracortical Nitric Oxide neurons-Previously, we reported the function of central noradrenergic cell groups, the cholinoceptive pontine area and the cholinergic basal forebrain (BF) in the generation of plateau waves. This study investigated the involvement of the basalcortical neurovascular pathway and intracortical nitric oxide (NO) neurons in the control of ICP and the cercbrovascular bed.Twenty cats anesthetized and immobilized with chloralose with kaolin-induced hydrocephalus were used for the experiments. ICP, BP and ETCO_2 were continuously monitored. CBF and NO in the brain tissue were also measured continuously using a Laserflo and electrochemical NO electrodes, respectively.Microinjection of glutamte or Ach into the dorsomedial hypothalamic nucleus (DMH) of the cats produced persistent increases in ICP and CBF and a decrease in BP.ETCO_2 conce … More ntration changed little.The Bring rate of the DMH -single neuron discharge increased in phase with increased ICP.NO concentration and CBV were increased in phase with the plateau phase during spontaneous "A" wave. NO and CBV were. also increased or decreased depending on the rising phase or the falling phase of ICP during repeated plateau wave like ICP variations elicited by microinjection of glutamate into the DMH.NO concentration increased considerably in the ipsilateral frontal and parietal lobes associated with increased ICP and increased CBV in response to microinjection of Ach into the DMH.A potent inhibitor of nitric oxide syntheses (L-NAME) reduced these Ach-elicited in ICY, conical CBV and NO.The cholinergic BF might contribute to he regulation of the cerebrovascular bed, The present observations suggest gut participation of NO in the mediation of the BF elicited increased ICP and CBV, and indicate the involvement of at least a neuronal source of NO, as the intracortical NOS neurons that innervate local microvessels appear to be regulated by BF neurons.II] Misery Perfusion Caused by Cerebral Hypothermic -Cerebrovascular Bed and NO Concentrations-.Therapeutic cerebral hypothermia is widely used for the treatment of severe head injury and cerebral ischemia. The effects of cerebral hypothermia on the cerebral blood flow (CBF) and metabolism, and cerebral vasculature in the normal brain were investigated. CBF, CBV, AVDO_2, CMRO_2, and CVR were momitored during cerebral hypothermia in 24 anesthetized cats.Hypothemia may cause vasoconstriction, low NO concentration, and misery perfusion in the brain blow 31℃. This potential risk of relative ischemia can be avoided by combination with vasopressor administration.The cerebral ischemic parameters were also evaluated during he rewarming period to determine the critical cerebral perfusion pressure (CPP) threshold to avoid ischemic deterioration.A CPP of 60mmHg during the rewarming period causes irreversible ischemia, which indicates continuation of cerebral vasoconstriction. Therefore, a higher CPP (>90mmHg) is required to avoid cerebral ischemia dung the rewarming period. Less