Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia
Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia
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DOI：
10.1161/01.str.27.9.1578
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发表时间：
1996-09-01
期刊：
影响因子：
8.3
通讯作者：
Wieloch, T
中科院分区：
文献类型：
--
作者：
Coimbra, C;Drake, M;Wieloch, T
背景和目的缺血后药物干预可能延缓神经元损伤的发展，而不是提供持久的神经保护。此外，发烧使人类中风后的恢复复杂化。在这里，我们报告的影响后期postischic治疗与低温和解热/抗炎药，安乃近，在1周和2个月的survival.Methods大鼠的细胞损伤进行了10分钟的前脑缺血。在恢复2小时时诱导低温（33 ℃）并维持7小时。安乃近（100 mg . kg（-1）IP），从14至72小时恢复期每3小时给药一次。每6小时测量一次体温，持续60天。在7天和2个月的recovery.Results神经元损伤进行了评估，从17至72小时的恢复，观察到一段时间的高温，安乃近废除，但缺血后低温治疗没有。安乃近治疗在第7天减少了43%的神经元损伤，在存活2个月时，观察到轻微（168）保护。缺血后单纯低温治疗可延迟神经元损伤。相比之下，联合治疗的低温，其次是安乃近显着减少超过50%的神经元损伤，在7天和2个月的recovery.Conclusions神经元变性可能会持续数月后，短暂性脑缺血的侮辱，和长期的保护措施，需要制定持久的神经保护作用。恢复期间的高热会导致缺血性损伤，与炎症相关的过程可能有助于神经元损伤的发展。如果随后用抗炎/解热药物治疗，早期和延长的缺血后低温提供了强大和持久的保护。
Background and Purpose It has been recognized that post ischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival.Methods Rats were subjected to 10 minutes of forebrain ischemia. Hypothermia (33 degrees C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg . kg(-1)IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery.Results From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (168) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damage. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery.Conclusions Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammation may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti-inflammatory/antipyretic drugs.