Neuronal Control of Cerebrovascular Bed : Role of Basal Forebrain

胆碱能基底前脑对ICP和脑血管床的控制--基底皮质神经血管通路通过皮质内一氧化氮神经元的作用--以前，我们报道了中枢去甲肾上腺素能细胞群、胆碱能脑桥区和胆碱能基底前脑（BF）在高原波产生中的作用。本实验用氯醛糖麻醉、制动的猫20只，观察了基底皮质神经血管通路和皮质内一氧化氮（NO）神经元对颅内压（ICP）和脑血管床的调控作用。连续监测颅内压（ICP）、血压（BP）和呼气末二氧化碳（ETCO_2）。用Laserflo和电化学NO电极连续测定脑组织中的CBF和NO，结果表明，在猫的下丘脑背内侧核（DMH）内微量注射谷氨酸或乙酰胆碱（Ach），可使ICP和CBF持续升高，BP、ETCO_2浓度持续降低，而脑组织中的NO浓度则持续升高。 关于我们 DMH单神经元放电Bring率随ICP升高而同相增加，自发A波时NO浓度和CBV随平台期升高而同相增加。NO和CBV均为阳性。在DMH内微量注射谷氨酸引起的ICP波动中，NO的浓度也随ICP的上升相或下降相而升高或降低。DMH内微量注射Ach后，与ICP升高和CBV增加有关的同侧额叶和顶叶NO浓度显著升高。胆碱能BF可能参与脑血管床的调节。本研究表明，NO参与BF的介导，引起ICP和CBV的增加，并表明NO至少涉及神经源，因为支配局部微血管的皮质内NOS神经元似乎受BF神经元调节。II]脑低温-脑血管床和NO浓度引起的痛苦灌注-治疗性脑低温广泛应用于重型颅脑损伤和脑缺血的治疗。本文观察了脑低温对正常脑血流量、代谢及脑血管的影响。在24只麻醉猫脑低温过程中，观察了脑血流（CBF）、脑血流（CBV）、AVDO_2、CMRO_2和CVR的变化。在复温期间，观察脑缺血参数，以确定避免缺血恶化的临界脑灌注压（CPP）阈值，复温期间CPP> 60 mmHg将导致不可逆的缺血，表明脑血管收缩仍在继续。因此，在复温期需要更高的CPP（> 90 mmHg）以避免脑缺血。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