Effects of hypothermia on evoked potentials, magnetic resonance imaging, and blood flow in focal ischemia in rabbits.

Abstract

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.