MILD CEREBRAL HYPOTHERMIA DURING AND AFTER CARDIAC-ARREST IMPROVES NEUROLOGIC OUTCOME IN DOGS

被引:289
作者
LEONOV, Y
STERZ, F
SAFAR, P
RADOVSKY, A
OKU, K
TISHERMAN, S
STEZOSKI, SW
机构
[1] UNIV PITTSBURGH,PRESBYTERIAN HOSP,INT RESUSCITAT RES CTR,3434 5TH AVE,PITTSBURGH,PA 15260
[2] UNIV PITTSBURGH,PRESBYTERIAN HOSP,DEPT ANESTHESIOL CRIT CARE MED,PITTSBURGH,PA 15213
[3] UNIV PITTSBURGH,PRESBYTERIAN HOSP,DEPT PATHOL,PITTSBURGH,PA 15213
[4] UNIV PITTSBURGH,PRESBYTERIAN HOSP,DEPT SURG,PITTSBURGH,PA 15213
[5] UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261
关键词
Anoxia; Brain cooling; Cardiopulmonary resuscitation; Cerebral resuscitation; Global brain ischemia; Hemodilution;
D O I
10.1038/jcbfm.1990.8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We previously found mild hypothermia (34-36°C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34°C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5°C was reversed with cardiopulmonary bypass and defibrillation in ≤5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p < 0.01), OPC 2 in 4 (p < 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p < 0.01), OPC 2 in 4 (p < 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.
引用
收藏
页码:57 / 70
页数:14
相关论文
共 61 条
[1]   INHIBITION OF CEREBRAL OXYGEN AND GLUCOSE CONSUMPTION IN THE DOG BY HYPOTHERMIA, PENTOBARBITAL, AND LIDOCAINE [J].
ASTRUP, J ;
SORENSEN, PM ;
SORENSEN, HR .
ANESTHESIOLOGY, 1981, 55 (03) :263-268
[2]   CEREBRAL PROTECTIVE EFFECT OF LOW-GRADE HYPOTHERMIA [J].
BERNTMAN, L ;
WELSH, FA ;
HARP, JR .
ANESTHESIOLOGY, 1981, 55 (05) :495-498
[3]   HYPOTHERMIA - ITS POSSIBLE ROLE IN CARDIAC SURGERY - AN INVESTIGATION OF FACTORS GOVERNING SURVIVAL IN DOGS AT LOW BODY TEMPERATURES [J].
BIGELOW, WG ;
LINDSAY, WK ;
GREENWOOD, WF .
ANNALS OF SURGERY, 1950, 132 (05) :849-866
[4]  
BRADER EW, 1988, AM J EMERG MED, V6, P161
[5]   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
[6]  
BUSTO R, 1989, IN PRESS STROKE
[7]   PROTECTIVE EFFECT OF HYPOTHERMIA IN CEREBRAL OXYGEN DEFICIENCY CAUSED BY ARTERIAL HYPOXIA [J].
CARLSSON, C ;
HAGERDAL, M ;
SIESJO, BK .
ANESTHESIOLOGY, 1976, 44 (01) :27-35
[8]  
CHEN RYZ, 1978, AM J PHYSL, V234, pH136
[9]   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
[10]  
CONNOLLY JE, 1962, SURGERY, V52, P15