Neuronal Control of Cerebrovascular Bed : Role of Basal Forebrain

脑血管床的神经元控制：基底前脑的作用

基本信息

批准号：
09671449
负责人：
MAEDA Minoru
金额：
$ 2.37万
依托单位：
JUNTENDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671449/
关键词：
Cerebrovascular Bed Cholinergic Basal Forebrain Nitric Oxide NOS inhibitor Basalocortical Neurovascular Pathway Cerebral Hypothermia Cerebral Perfusion Pressure Relative Ischemia ICP CBV Intracortical NO neuron NO Hypothermia CBF

项目摘要

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

I]胆碱能基底前脑对ICP和脑血管床的控制-通过皮质内一氧化氮神经元的基底皮质神经血管通路的作用-之前，我们报道了中枢去甲肾上腺素能细胞群、胆碱感受性桥脑区和胆碱能基底前脑（BF）的功能）在平台波的产生中本研究调查了基底皮质神经血管通路和皮质内硝酸的参与。实验采用氯醛糖麻醉、高岭土诱发脑积水的猫20只，连续监测脑组织中的ICP、BP和ETCO_2。还分别使用 Laserflo 和电化学 NO 电极连续测量。将谷氨酸或 Ach 显微注射到背侧猫的下丘脑核 (DMH) 产生持续增加的 ICP 和 CBF 以及下降的 BP。ETCO_2 浓度变化不大。随着 ICP.NO 浓度和 CBV 的增加，DMH 单神经元放电的带来率增加。在自发的“A”波期间，NO 和 CBV 也随着 ICP 的上升阶段或下降阶段而增加或减少，如引起的 ICP 变化。通过将谷氨酸微注射到 DMH 中，同侧额叶和顶叶中的 NO 浓度显着增加，并与 ICP 增加和 CBV 增加相关，以响应将 Ach 微注射到 DMH 中。一氧化氮合成的有效抑制剂 (L-NAME) 减少了这些Ach-在 ICY、圆锥形 CBV 和 NO 中引起。胆碱能 BF 可能有助于脑血管床的调节，目前的观察表明NO 在 BF 介导中的肠道参与引起了 ICP 和 CBV 的增加，并表明至少有一个 NO 神经元来源的参与，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。II] Misery Perfusion由脑低温引起-脑血管床和NO浓度-。治疗性脑低温广泛用于治疗严重颅脑损伤和脑缺血。研究了脑低温对24只麻醉猫脑血流量（CBF）和代谢以及正常脑血管系统的影响。脑低温可能导致血管收缩。，NO浓度低，脑部灌注痛苦31℃，可以避免相对缺血的潜在风险。复温期间还评估了脑缺血参数，以确定临界脑灌注压（CPP）阈值，以避免缺血恶化。复温期间CPP达到60mmHg会导致不可逆性缺血，这表明脑灌注压的持续存在因此，复温期需要较高的CPP（>90mmHg）以避免脑缺血。