| Research Abstract |
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
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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
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