| Objective The neuroprotective effect of hypothermia has long been recognized. The aim of this work was to compare the neuroprotective effect of systemic, head and local vascular cooling hypothermia procedures in ischemic rats.Methods Stroke in Sprague–Dawley rats (n=64) was induced by a 3 hour right middle cerebral artery occlusion using an intraluminal filament. Before reperfusion, ischemic animals (n=16 in each group) received hypothermia (systemic, head or local vascular) or no treatment. Brain temperature, infarction volume (n=8 in each group) and functional outcome (n=8 in each group) were compared.Results Regarding brain temperature, vascular cooling significantly reduced the temperature of ischemic territory in cortex from 37.2±0.1 to 33.4±0.4℃and in striatum from 37.5±0.2 to 33.9±0.4℃within 5 minutes. This hypothermic condition remained for up to 60 minutes after reperfusion. However, systemic cooling reduced brain temperature at a similar level for six times longer. In the head cooling group, the target temperature was reached in 15 minutes, but returned to normal within 5 minutes. Although all hypothermia procedures induced neuroprotection, ischemic rats with vascular cooling showed significantly (p<0.001) better neuroprotection with 10.7±2.6% infarction, compared to 54.2±1.9% (no treatment), 37.1±1.0% (head cooling) and 29.1±3.4% (systemic cooling). Significantly (p<0.001) better effects on motor function were also detected in vascular cooling groups at 14 and 28 days. Conclusion Vascular cooling appears to be the most effective in reducing infarct volume and improving functional outcome than the other two hypothermia methods in a rat ischemia/reperfusion model.Test2: Neuroprotective Effect Of Acute Ethanol Administration In Rat With Transient Cerebral IschemiaObjective Numerous studies have shown that mild to moderate alcohol consumption is inversely associated with risk of ischemic stroke, suggesting ethanol may have a neuroprotective effect. We test the hypothesis in a rat transient cerebral ischemia model, and further characterize the properties of ethanol as a possible treatment for acute ischemic stroke.Methods Sprague-Dawley rats were subjected to 2 hours middle cerebral artery occlusion. Three sets of experiments were conducted (1) to test whether various doses of ethanol (0.5g/kg, 1.0 g/kg, 1.5 g/kg) has neuroprotective effect; (2) to test whether the protective effect of ethanol can be improved by pairing it with hypothermia; and (3) to test whether ethanol affects intracranial hemorrhage after administration of recombinant tissue plasminogen activator (rtPA) or urokinase (UK) in ischemic rats.Results Ischemic rats with dose of 1.5g/kg ethanol showed significantly (p<0.001) better neuroprotection with 29.2±1.8%infarction, compared to 53.9±2.3% (no treatment), 42.0±1.1% (1.0g/kg) and 49.7±2.8% (0.5g/kg). The neuroprotective effect of ethanol seemed to be further improved combining with hypothermia. To testing intracerebral hemorrhage, ethanol did not increase cerebral hemorrhage when given in combination with rt-PA or UK.Conclusions Our study suggests that a dose of 1.5g/kg ethanol administrated after the onset of reperfusion has neuroprotective effect, can be added to hypothermia therapy, and do not interfere with or complicate rt-PA or UK therapy. |
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