EFFECTS OF INTRAISCHEMIC HYPOTHERMIA ON CEREBRAL-DAMAGE IN A MODEL OF REVERSIBLE FOCAL ISCHEMIA

被引:89
作者
GOTO, Y [1 ]
KASSELL, NF [1 ]
HIRAMATSU, K [1 ]
SOLEAU, SW [1 ]
LEE, KS [1 ]
SELMAN, WR [1 ]
SOLOMON, RA [1 ]
机构
[1] UNIV VIRGINIA, HLTH SCI CTR, DEPT NEUROSURG, BOX 420, CHARLOTTESVILLE, VA 22908 USA
关键词
CEREBRAL INFARCTION; CEREBRAL ISCHEMIA; HYPOTHERMIA; NEUROPROTECTION;
D O I
10.1227/00006123-199306000-00017
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
CONSIDERABLE EVIDENCE INDICATES that brain temperature during ischemia affects the extent and distribution of ischemic injury. However, only limited data have been presented concerning the influence of temperature on ischemic damage after reversible focal cerebral ischemia. Because focal ischemic events of this type resemble conditions observed in the clinic, studies were undertaken to examine the effects of mild and moderate hypothermia on the extent of cerebral infarction after focal neocortical ischemia. Under halothane anesthesia, the left middle cerebral artery and both carotid arteries were occluded reversibly for a period of 3 hours in adult Sprague-Dawley rats. The animals were killed 3 days later. Brain sections were stained with triphenyltetrazolium chloride and analyzed for infarction using a computerized image analysis system. Temporal muscle temperature and rectal temperature were monitored continuously. The following groups with different intraischemic temporal muscle temperatures were analyzed: 1) control, 35.8 to 36.2-degrees-C; 2) mild hypothermia, 33.0 to 33.5-degrees-C; and 3) moderate hypothermia, 27.5 to 29.2-degrees-C. The volumes of infarction were 214.5 +/- 17.9, 166.5 +/- 6.8, and 108.2 +/- 5.9 mm3 (mean +/- SEM) for the control, mild hypothermia, and moderate hypothermia groups, respectively. These findings demonstrate that both mild and moderate hypothermia reduce the impact of temporary focal ischemia in Sprague-Dawley rats.
引用
收藏
页码:980 / 985
页数:6
相关论文
共 21 条
[1]   A NEW MODEL OF TEMPORARY FOCAL NEOCORTICAL ISCHEMIA IN THE RAT [J].
BUCHAN, AM ;
XUE, D ;
SLIVKA, A .
STROKE, 1992, 23 (02) :273-279
[2]   THE IMPORTANCE OF BRAIN TEMPERATURE IN CEREBRAL ISCHEMIC-INJURY [J].
BUSTO, R ;
DIETRICH, WD ;
GLOBUS, MYT ;
GINSBERG, MD .
STROKE, 1989, 20 (08) :1113-1114
[3]   EFFECT OF MILD HYPOTHERMIA ON ISCHEMIA-INDUCED RELEASE OF NEUROTRANSMITTERS AND FREE FATTY-ACIDS IN RAT-BRAIN [J].
BUSTO, R ;
GLOBUS, MY ;
DIETRICH, WD ;
MARTINEZ, E ;
VALDES, I ;
GINSBERG, MD .
STROKE, 1989, 20 (07) :904-910
[4]   SMALL DIFFERENCES IN INTRAISCHEMIC BRAIN TEMPERATURE CRITICALLY DETERMINE THE EXTENT OF ISCHEMIC NEURONAL INJURY [J].
BUSTO, R ;
DIETRICH, WD ;
GLOBUS, MYT ;
VALDES, I ;
SCHEINBERG, P ;
GINSBERG, MD .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1987, 7 (06) :729-738
[5]   POSTISCHEMIC MODERATE HYPOTHERMIA INHIBITS CA1 HIPPOCAMPAL ISCHEMIC NEURONAL INJURY [J].
BUSTO, R ;
DIETRICH, WD ;
GLOBUS, MYT ;
GINSBERG, MD .
NEUROSCIENCE LETTERS, 1989, 101 (03) :299-304
[6]   THE METABOLIC EFFECTS OF MILD HYPOTHERMIA ON GLOBAL CEREBRAL-ISCHEMIA AND RECIRCULATION IN THE CAT - COMPARISON TO NORMOTHERMIA AND HYPERTHERMIA [J].
CHOPP, M ;
KNIGHT, R ;
TIDWELL, CD ;
HELPERN, JA ;
BROWN, E ;
WELCH, KMA .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1989, 9 (02) :141-148
[7]   TEMPERATURE MODULATION OF ISCHEMIC NEURONAL DEATH AND INHIBITION OF CALCIUM CALMODULIN-DEPENDENT PROTEIN KINASE-II IN GERBILS [J].
CHURN, SB ;
TAFT, WC ;
BILLINGSLEY, MS ;
BLAIR, RE ;
DELORENZO, RJ .
STROKE, 1990, 21 (12) :1715-1721
[8]   A REPRODUCIBLE MODEL OF REVERSIBLE, FOCAL, NEOCORTICAL ISCHEMIA IN SPRAGUE-DAWLEY RAT [J].
HIRAMATSU, K ;
KASSELL, NF ;
GOTO, Y ;
SOLEAU, S ;
LEE, KS .
ACTA NEUROCHIRURGICA, 1993, 120 (1-2) :66-71
[9]   THE EFFECT OF MILD HYPOTHERMIA ON PERMANENT FOCAL ISCHEMIA IN THE RAT [J].
KADER, A ;
BRISMAN, MH ;
MARAIRE, N ;
HUH, JT ;
SOLOMON, RA .
NEUROSURGERY, 1992, 31 (06) :1056-1061
[10]   PREVENTION OF POSTISCHEMIC HYPERTHERMIA PREVENTS ISCHEMIC-INJURY OF CA1 NEURONS IN GERBILS [J].
KUROIWA, T ;
BONNEKOH, P ;
HOSSMANN, KA .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1990, 10 (04) :550-556