Beaumont A, Hayasaki K, Marmarou A, Barzo P, Fatouros P, Corwin F
Division of Neurosurgery, Medical College of Virginia, Richmond, VA, USA.
Acta Neurochir Suppl. 2000;76:147-51. doi: 10.1007/978-3-7091-6346-7_30.
The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. Adult male rats were divided into two groups: group 1 (n = 32)--Impact Acceleration Injury (IAM) with 30 minutes hypoxia and hypotension; group 2 (n = 12)--controlled cortical impact (6.0 m/sec, 3 mm depth). Dopamine was administered 2 hours post-injury (10-60 micrograms/kg/min i.v.). Cerebral water content and apparent diffusion coefficients (ADC) values were measured at baseline and four hours post-injury using MRI. Preinjury water content was the same in each group. Group 1 was subdivided into Groups 1A & 1B based on the ADC profile. Post-injury water content in Group 1A did not differ between saline or dopamine treated animals. Water content was higher in Group 1B-dopamine (83.4 +/- 1.1%) than Group 1B-saline animals (81.4 +/- 1.3%, p = 0.006). Contusion caused significant edema formation, however there was no significant difference between the dopamine treated or untreated group when considering either ipsilateral or contralateral cortex. Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.
血管升压药加重脑水肿的风险已引起关注。此前我们报道过，在颅内压单调上升的模型中，多巴胺能够恢复脑血流量。在本研究中，我们检测了多巴胺对伴有继发性损伤的皮质挫伤和弥漫性损伤的影响。成年雄性大鼠分为两组：第1组（n = 32）——撞击加速损伤（IAM）伴30分钟缺氧和低血压；第2组（n = 12）——控制性皮质撞击（6.0米/秒，3毫米深度）。损伤后2小时给予多巴胺（静脉注射，10 - 60微克/千克/分钟）。使用磁共振成像（MRI）在基线和损伤后4小时测量脑含水量和表观扩散系数（ADC）值。每组损伤前的含水量相同。根据ADC曲线，第1组又分为1A组和1B组。1A组中，生理盐水处理组和多巴胺处理组动物损伤后的含水量没有差异。1B组中，多巴胺处理组的含水量（83.4±1.1%）高于生理盐水处理组（81.4±1.3%，p = 0.006）。挫伤导致显著的水肿形成，然而，在考虑同侧或对侧皮质时，多巴胺处理组和未处理组之间没有显著差异。然而，多巴胺显著加重了同侧和对侧海马以及双侧颞叶皮质的水肿。除对侧海马外，ADC保持不变，在对侧海马中，含水量和ADC均随多巴胺升高，提示血管源性水肿的形成。在本研究中，多巴胺在两种创伤性脑损伤模型中明显加重了水肿形成，我们得出结论，可能存在类似的临床情况；因此，对于所有脑灌注压低的患者，不应将升压药视为“通用”疗法。
