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NO, in particular NO of neuronal origin, is an important although not exclusive mediator of CO2-induced vasodilation.10 The vasodilatory response to hypercapnia is also mediated in part by prostaglandins.
Acute restoration of a normal Paco2 value will result in a significant CSF acido- sis (after hypocapnia) or alkalosis (after hypercapnia).
The response to hypoxia is synergistic with the hyperemia produced by hypercapnia and acidosis.
Interestingly, CBF in white matter increased by 22%.150 This reduction in CBF is accompanied by a parallel reduction of the cere- bral metabolic rate of glucose (CMRg) by 26%.151 Cerebral autoregulation and CO2 reactivity are preserved during xenon anesthesia in animals.152 Under background pento- barbital anesthesia in an experimental model of increased ICP, the administration of xenon did not increase ICP, and the response to both hypocapnia and hypercapnia was pre- served.153 Diffusion of xenon into air-containing spaces such as the bowel does occur, although the magnitude of air expansion is considerably less than that with N2O.154 Nonetheless, caution will have to be exercised with the use of xenon in patients with intracranial air.
CBV is considerably greater during isoflurane anesthesia than dur- ing propofol or pentobarbital anesthesia.63 In human vol- unteers, 1 MAC sevoflurane reduced regional CBF but not regional CBV; by contrast, propofol reduced both regional CBF and regional CBV (Fig. 11.16).84 In addition, CBV responds to changes in Paco2 by a reduction in CBV with hypocapnia and an increase in CBV with hypercapnia.
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