Hemorrhagic shock induces an S100Bincrease associated with shock severity
Hemorrhagic shock induces an S100Bincrease associated with shock severity
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DOI：
10.1097/01.shk.0000055345.58165.52
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发表时间：
2003-05-01
期刊：
影响因子：
3.1
通讯作者：
Redl, H
中科院分区：
文献类型：
--
作者：
Pelinka, LE;Bahrami, S;Redl, H
S 100 B是脑损伤的胶质细胞标志物。在以前的临床研究中，我们发现在多发性创伤和失血性休克但无脑外伤的患者中，S 100 B在最初24小时内升高。我们目前实验研究的目的是确定这种创伤后S 100 B增加是由脑外软组织损伤还是失血性休克引起的，以及它是否与失血性休克的严重程度有关。通过股动脉导管将麻醉大鼠放血至30-35 mmHg的平均动脉压（MAP），并维持该MAP直至早期失代偿，从而实现失血性休克。在失代偿初期，MAP要么立即升高至40-45 mmHg（中度休克），要么维持至40%的失血量回流（重度休克），然后升高至40-45 mmHg。复苏后提供40-45毫米汞柱的MAP已维持40分钟。软组织损伤是通过中线剖腹手术在失血性休克或无休克发作时进行，并维持30分钟。失血性休克引起早期S 100 B增加在失代偿发作。S100 B在24 h内仍保持升高，且重度休克后显著高于中度休克后.相反，无失血性休克的软组织损伤不引起S100 B升高.本研究首次证实S 100 B升高是由失血性休克引起的，并与休克的严重程度有关。
S 100 B is a glial marker of cerebral injury. In a previous clinical study, we found an S 100 B increase within the first 24 h in patients with multiple trauma and hemorrhagic shock but without cerebral trauma. The aim of our current experimental study was to determine whether this posttraumatic S 100 B increase is caused by extracerebral soft tissue injury or by hemorrhagic shock and whether it is associated with the severity of hemorrhagic shock. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter and maintaining this MAP until incipient decompensation. At incipient decompensation, MAP was either increased immediately to 40-45 mmHg (moderate shock) or was maintained until 40% of shed blood had been returned (severe shock), and then increased to 40-45 mmHg. Resuscitation was provided after 40-45 mmHg MAP had been maintained for 40 min. Soft tissue injury was achieved by midline laparotomy performed at the onset of hemorrhagic shock or without shock and was maintained for 30 min. Hemorrhagic shock caused an early S 100 B increase at the onset of decompensation. S 100 B remained increased for 24 h and was significantly higher after severe than after moderate shock. In contrast, soft tissue injury without hemorrhagic shock caused no S 100 B increase. The data presented demonstrate for the first time that the S 100 B increase is induced by hemorrhagic shock and is associated with the severity of shock.