Lo E H, Steinberg G K
Department of Neurosurgery, Stanford University School of Medicine, Calif.
Stroke. 1992 Jun;23(6):889-93. doi: 10.1161/01.str.23.6.889.
Mild hypothermia has been shown to ameliorate neuronal damage due to cerebral ischemia. In our study, the influence of mild-to-moderate hypothermia was examined in a rabbit model of focal cerebral ischemia.
After 4 hours of permanent ischemia induced by occlusion of the anterior and middle cerebral and internal carotid arteries, somatosensory evoked potentials and regional cerebral blood flow were measured. Ex vivo magnetic resonance imaging scans were also obtained to determine the degree of ischemic brain injury. Three temperature (temporalis muscle) groups were studied: 37 degrees C, 33 degrees C, and 30 degrees C (n = 5 per group). An additional two animals were used to confirm that temporalis muscle temperatures were well correlated with brain temperature. Rectal temperatures were kept constant (37.5 degrees C) in all groups.
After 4 hours of focal ischemia, evoked potentials in the normothermic animals remained depressed (2.2 +/- 2.1% [mean +/- SEM] preocclusion values). Recovery of potentials was significantly enhanced in both hypothermic groups (p less than 0.05): 18.2 +/- 6.5% (33 degrees C) and 43.6 +/- 12.2% (30 degrees C). Quantitative magnetic resonance measurements showed that T1 and T2 relaxation times were increased in the core ischemic regions within the cortex (20.4 +/- 4.0% and 25.3 +/- 5.9%, respectively). These elevations in T1 and T2 were reduced by hypothermia. However, blood flow was not improved by lowered temperature; in fact, flow in the 30 degrees C group was significantly decreased compared with the other groups (p less than 0.01). There was no statistically significant correlation between specific cerebral blood flow values and T1 or T2 elevations.
These results demonstrate that hypothermia can improve evoked potentials and magnetic resonance parameters in permanent focal ischemia. However, moderate hypothermia (30 degrees C) appears to also significantly decrease blood flow in the ischemic brain.
轻度低温已被证明可改善脑缺血所致的神经元损伤。在我们的研究中,我们在局灶性脑缺血兔模型中检测了轻至中度低温的影响。
通过闭塞大脑前、中动脉及颈内动脉诱导永久性缺血4小时后,测量体感诱发电位和局部脑血流量。还进行了离体磁共振成像扫描以确定缺血性脑损伤的程度。研究了三个温度(颞肌)组:37℃、33℃和30℃(每组n = 5)。另外使用两只动物来确认颞肌温度与脑温高度相关。所有组的直肠温度保持恒定(37.5℃)。
局灶性缺血4小时后,常温动物的诱发电位仍受抑制(为闭塞前值的2.2±2.1%[平均值±标准误])。两个低温组的电位恢复均显著增强(p < 0.05):分别为18.2±6.5%(33℃)和43.6±12.2%(30℃)。定量磁共振测量显示,皮质内核心缺血区域的T1和T2弛豫时间增加(分别为20.4±4.0%和25.3±5.9%)。低温可减轻T1和T2的这些升高。然而,降低温度并未改善血流量;事实上,30℃组的血流量与其他组相比显著降低(p < 0.01)。特定脑血流量值与T1或T2升高之间无统计学显著相关性。
这些结果表明,低温可改善永久性局灶性缺血中的诱发电位和磁共振参数。然而,中度低温(30℃)似乎也会显著降低缺血脑的血流量。