SNP improves cerebral hemodynamics during normotension but fails to prevent sex dependent impaired cerebral autoregulation during hypotension after brain injury.

SNP improves cerebral hemodynamics during normotension but fails to prevent sex dependent impaired cerebral autoregulation during hypotension after brain injury.
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DOI:
10.1016/j.brainres.2010.03.024
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发表时间:
2010-05-12
期刊:
影响因子:
2.9
通讯作者:
Vavilala, Monica S.
Vavilala, Monica S.
中科院分区:
医学3区
文献类型:
--
作者:
Armstead, William M.;Kiessling, J. Willis;Kofke, W. Andrew;Vavilala, Monica S.

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创伤性脑损伤(TBI)是儿童发病的主要原因,男孩的比例过高。低血压是常见的,并使TBI后的预后恶化。先前的研究表明,肾上腺髓质素是一种脑血管扩张剂,可防止仔猪液冲击脑损伤(FPI)后低血压期间的性别依赖性自调节损伤。我们假设这一概念是可推广的,并且另一种血管扩张剂硝普钠(SNP)也可能以性别依赖的方式改善FPI后的CBF和大脑自动调节。SNP在公母仔猪中产生相同百分比的脑血管舒张。在正常张力条件下,与雌性仔猪相比,雄性仔猪在FPI后颅内压(ICP)升高的同时,枕动脉直径、皮质CBF和脑灌注压(CPP)的降低更大。在低血压期间,FPI后男性的枕动脉扩张(PAD)受损程度高于女性。然而,SNP并没有改善女性FPI后的低血压PAD,反而导致男性血管收缩。无论男女,SNP都不能阻止合并低血压和FPI时CBF、CPP或自身调节指数的降低。SNP加重了FPI后ERK MAPK的上调。这些数据表明,尽管可以预防FPI后CBF的减少,但SNP并不能预防FPI后低血压期间自身调节功能的损害。这些数据表明,单纯针对血流动力学增加CPP的治疗将无法改善合并TBI和低血压的预后。
Traumatic brain injury (TBI) is a leading cause of morbidity in children and boys are disproportionately represented. Hypotension is common and worsens outcome after TBI. Previous studies show that adrenomedullin, a cerebrovasodilator, prevented sex dependent impairment of autoregulation during hypotension after piglet fluid percussion brain injury (FPI). We hypothesized that this concept was generalizable and that administration of another vasodilator, sodium nitroprusside (SNP), may equally improve CBF and cerebral autoregulation in a sex dependent manner after FPI. SNP produced equivalent percent cerebrovasodilation in male and female piglets. Reductions in pial artery diameter, cortical CBF, and cerebral perfusion pressure (CPP) concomitant with elevated intracranial pressure (ICP) after FPI were greater in male compared to female piglets during normotension which was blunted by SNP. During hypotension, pial artery dilation (PAD) was impaired more in the male than the female after FPI. However, SNP did not improve hypotensive PAD after FPI in females and paradoxically caused vasoconstriction in males. SNP did not prevent reductions in CBF, CPP or autoregulatory index during combined hypotension and FPI in either sex. SNP aggravated ERK MAPK upregulation after FPI. These data indicate that despite prevention of reductions in CBF after FPI, SNP does not prevent impairment of autoregulation during hypotension after FPI. These data suggest that therapies directed at a purely hemodynamic increase in CPP will fail to improve outcome during combined TBI and hypotension.
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