Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol
Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol
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DOI：
10.1016/j.jns.2005.10.016
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发表时间：
2006-02-15
影响因子：
4.4
通讯作者：
Zausinger, S
中科院分区：
文献类型：
--
作者：
Bermueller, C;Thal, SC;Zausinger, S
目的：蛛网膜下腔出血（subarachnoid hemorrhage，SAH）后的死亡和严重并发症主要是由于颅内压（intracranial pressure，ICP）升高和脑血流量（cerebral blood flow，CBF）减少引起的全脑缺血。我们最近在SAH动物模型中证明了小体积复苏（7.5%盐水与6%右旋糖酐70组合）的神经保护作用，导致ICP升高正常化，减少形态学损伤并改善神经恢复。在本研究中，我们比较了两个临床许可的高渗高渗盐水溶液与常规使用的高渗剂甘露醇的小容量复苏的概念，并探讨其对ICP，CBF，神经恢复和SAH.Methods后的形态学损害的影响：60葡聚糖耐药的Wistar大鼠进行SAH血管内细丝。连续记录颅内压（ICP）、平均动脉压（MABP）和双侧局部脑血流（CBF）。将所有动物随机分为4组：（1）0.9% NaCl（4 ml/kg bw），（11）7.5% NaCl+6%右旋糖酐70（4 ml/kg bw），（111）7.2% NaCl+羟乙基淀粉200，000（4 ml/kg bw）和（IV）20%甘露醇（9.33 ml/kg bw），在SAH后30分钟给予。在SAH后第1、3和7天评估神经功能缺损。SAH后第7天评估形态学损害。结果：SAH的诱导导致ICP立即增加至46.6 +/- 3.2 mm Hg（平均S.E.M.）。和29.6 +/- 1.3（平均值+/- S.E.M.）SAH后90分钟min Hg。虽然用两种高渗盐水溶液（11，111）和20%甘露醇溶液治疗均可降低ICP，但只有用高渗盐水和右旋糖酐70（11）治疗的组在输注后20分钟内显示出同侧CBF增加，运动皮层和尾壳核中存活的神经元显著更多。死亡率分别从60%（1）和73%（111和IV）降低到40%，在组II中。结论：在研究的所有高渗溶液中，小容量复苏与NaCl 7.5%结合6%右旋糖酐70在减少SAH的初始有害后遗症方面发展为最有效的，导致降低ICP和SAH后大鼠的形态学损伤较少。(c)2005 Elsevier B. V.保留所有权利。
Objective: Death and severe morbidity after subarachnoid hemorrhage (SAH) are mainly caused by global cerebral ischemia through increased intracranial pressure (ICP) and decreased cerebral blood flow (CBF). We have recently demonstrated neuroprotective effects of small volume resuscitation (7.5% saline in combination with 6% dextran 70) in an animal model of SAH, leading to normalization of increased ICP, reduced morphological damage and improved neurological recovery. In the present study, we compared the concept of small volume resuscitation represented by two clinically licenced hypertonic-hyperoncotic saline solutions with the routinely used hyperosmotic agent-mannitol-and investigated their effects on ICP, CBF, neurological recovery and morphological damage after SAH in rats.Methods: 60 dextran-resistant Wistar rats were subjected to SAH by an endovascular filament. ICP, MABP (mean arterial blood pressure) and bilateral local CBF were continuously recorded. All animals were randomly assigned to four groups: (1) NaCl 0.9% (4 ml/kg bw), (11) 7.5% NaCl+6% dextran 70 (4 ml/kg bw), (111) 7.2% NaCl+HES 200,000 (4 ml/kg bw) and (IV) 20% mannitol (9.33 ml/kg bw) given 30 min after SAH. Neurological deficits were assessed on days 1, 3 and 7 after SAH. The morphological damage was evaluated on day 7 after SAH.Results: The induction of SAH resulted in an immediate ICP increase to 46.6 +/- 3.2 mm Hg (mean S.E.M.) and 29.6 +/- 1.3 (mean +/- S.E.M.) min Hg 90 min post-SAH. While a treatment with both hypertonic saline solutions (11, 111) decreased ICP as well as the 20% mannitol solution, only the group treated with hypertonic saline and dextran 70 (11) showed an increase of ipsilateral CBF for 20 min after the infusion and significantly more surviving neurons in the motorcortex and caudoputamen. Mortality was reduced from 60% (1) and 73% (111 and IV), respectively, to 40% in group II.Conclusion: Of all hypertonic solutions investigated, small volume resuscitation with NaCl 7.5% in combination with 6% dextran 70 evolved to be most effective in terms of reducing the initial harmful sequelae of SAH, leading to lowered ICP and less morphological damage after SAH in the rat. (c) 2005 Elsevier B.V. All rights reserved.