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窒息后未成熟仔猪的体感诱发电位和脑含水量

Somatosensory evoked potential and brain water content in post-asphyxic immature piglets.

作者信息

Rose V C, Shaffner D H, Gleason C A, Koehler R C, Traystman R J

机构信息

Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-4961, USA.

出版信息

Pediatr Res. 1995 May;37(5):661-6. doi: 10.1203/00006450-199505000-00018.

DOI:10.1203/00006450-199505000-00018
PMID:7603787
Abstract

Depression of somatosensory evoked potentials (SEP) after a single episode of complete asphyxia with near cardiac arrest was evaluated to determine whether persistent SEP depression is related to postresuscitation edema in cortical gray matter or subcortical white matter. Piglets (< 7 d of age) were anesthetized with sodium pentobarbital and fentanyl. Asphyxia was produced by occlusion of the endotracheal tube for 7 min. Arterial O2 saturation fell to 5%. Resuscitation was achieved in < 2 min with ventilation, epinephrine, and chest compressions. Regional brain water content was determined from the difference between wet and dry weight. Two control groups were also analyzed; one immediately after (n = 5) and one 6 h after induction (n = 7) of anesthesia. SEP amplitude became isoelectric during asphyxia and recovered to 50 +/- 13% (n = 7) of baseline 6 h after resuscitation. In the 6-h control group, SEP amplitude remained above baseline. The percent water content (mean +/- SEM) among the three groups (asphyxia versus time control versus brief anesthesia control) was not different in the cortical gray matter (83.0 +/- 0.7% versus 82.4 +/- 0.4% versus 83.2 +/- 0.3%) or subcortical white matter (75.6 +/- 0.8% versus 74.8 +/- 0.9% versus 75.6 +/- 0.5%). In seven other piglets, cerebral blood flow and O2 consumption recovered to baseline by 1 h after asphyxia. Therefore, we found that the sustained depression of SEP amplitude, after 7 min of asphyxia in immature piglets, is not related to brain edema or persistent decreases in global cerebral O2 consumption.

摘要

对经历单次伴有近乎心脏骤停的完全性窒息发作后的体感诱发电位(SEP)进行评估,以确定SEP持续降低是否与复苏后皮质灰质或皮质下白质水肿有关。用戊巴比妥钠和芬太尼对小于7日龄的仔猪进行麻醉。通过堵塞气管导管7分钟造成窒息。动脉血氧饱和度降至5%。在不到2分钟内通过通气、肾上腺素和胸外按压实现复苏。根据湿重和干重的差值确定局部脑含水量。还分析了两个对照组;一组在麻醉诱导后立即(n = 5),另一组在麻醉诱导后6小时(n = 7)。SEP振幅在窒息期间变为等电位,并在复苏后6小时恢复至基线的50±13%(n = 7)。在6小时对照组中,SEP振幅保持在基线以上。三组(窒息组与时间对照组与短暂麻醉对照组)的皮质灰质(83.0±0.7%对82.4±0.4%对83.2±0.3%)或皮质下白质(75.6±0.8%对74.8±0.9%对75.6±0.5%)的含水量百分比(平均值±标准误)无差异。在另外七只仔猪中,窒息后1小时脑血流量和氧消耗恢复至基线水平。因此,我们发现,未成熟仔猪窒息7分钟后SEP振幅的持续降低与脑水肿或全脑氧消耗的持续减少无关。

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