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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Nitric oxide, prostaglandins, and impaired cerebral blood flow autoregulation in group B streptococcal neonatal meningitis.
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Nitric oxide, prostaglandins, and impaired cerebral blood flow autoregulation in group B streptococcal neonatal meningitis.

机译：B组链球菌新生儿脑膜炎中一氧化氮，前列腺素和脑血流量自动调节受损。

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摘要

Impaired autoregulation of cerebral blood flow (CBF) contributes to CNS damage during neonatal meningitis. We tested (i) the hypothesis that cerebrovascular autoregulation is impaired during early onset group B streptococcal (GBS) meningitis, (ii) whether this impairment is regulated by vasoactive mediators such as prostaglandins and (or) nitric oxide (NO), and (iii) whether this impairment is preventable by specific and (or) nonspecific inhibitors: dexamethasone, ibuprofen, and Nomega-nitro-L-arginine, a NO inhibitor. Sterile saline or 10(9) colony-forming units (cfu) of heat-killed GBS was injected into the cerebral ventricle of newborn piglets. CBF autoregulation was determined by altering cerebral perfusion pressure (CPP) with balloon-tipped catheters placed in the aorta. GBS produced a narrow range of CBF autoregulation due to an impairment at the upper limit of CPP. We report that in vivo in the early stages (first 2 h) of induced GBS inflammation (i) GBS impairs the upper limit of cerebrovascular autoregulation; (ii) ibuprofen, dexamethasone, and Nomega-nitro-L-arginine not only prevent this GBS-induced autoregulatory impairment but improve the range of cerebrovascular autoregulation; (iii) these autoregulatory changes do not involve circulating cerebral prostanoids; and (iv) the observed changes correlate with the induction of NO synthase gene expression. Thus, acute early onset GBS-induced impairment of the upper limit of CBF autoregulation can be correlated with increases of NO synthase production, suggesting that NO is a vasoactive mediator of CBF.
机译：新生儿脑膜炎期间，脑血流量（CBF）的自动调节受损会导致中枢神经系统损害。我们测试了（i）早发B组链球菌（GBS）脑膜炎期间脑血管自动调节受到损害的假设，（ii）这种损害是否受血管活性介质如前列腺素和（或）一氧化氮（NO）的调节，以及（iii ）是否可以通过特异性和（或）非特异性抑制剂（地塞米松，布洛芬和NO抑制剂Nomega-nitro-L-精氨酸）预防这种损害。将无菌盐水或10（9）个热杀死的GBS菌落形成单位（cfu）注入新生仔猪的脑室。通过使用放置在主动脉中的气球尖端导管改变脑灌注压力（CPP）来确定CBF自动调节。由于CPP上限受到损害，GBS产生了狭窄的CBF自动调节范围。我们报告在体内诱导的GBS炎症的早期阶段（头2小时）（i）GBS损害了脑血管自动调节的上限; （ii）布洛芬，地塞米松和Nomega-硝基-L-精氨酸不仅可以预防这种由GBS引起的自动调节障碍，而且可以改善脑血管自动调节的范围; （iii）这些自动调节的变化不涉及循环的脑前列腺素; （iv）观察到的变化与诱导NO合酶基因表达有关。因此，急性早期GBS诱导的CBF自动调节上限受损可能与NO合酶产生的增加相关，表明NO是CBF的血管活性介质。

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