Hypothermia reduces cytotoxic edema and metabolic alterations during the acute phase of massive SAH: a diffusion-weighted imaging and spectroscopy study in rats.
Acute changes in cerebral perfusion and metabolism after subarachnoid hemorrhage (SAH) have been shown to contribute significantly to acute brain injury. The purpose of this study was to examine the effects of moderate hypothermia on the acute changes after massive experimental SAH as evaluated by diffusion-weighted imaging (DWI) and magnetic resonance spectroscopy (MRS). SAH in rats was induced by injection of 0.5 mL of arterial blood. Normothermic animals (NT, n = 10) were kept at 37.0 +/- 0.2 degrees C, while temperature was lowered to 32.0 +/- 0.2 degrees C in the primary hypothermia group (pHT, n = 10) prior to SAH and in the secondary hypothermia group (sHT, n = 10) immediately after SAH. DWI and MRS were performed from 30 min prior up to 3 h after injury. The apparent diffusion coefficient (ADC) was measured in cortical and hippocampal regions of interest (ROIs). MRS included lactate, N-acetyl aspartate (NAA), and creatine in a central voxel. DWI showed a generalized, significant decline in ADC after SAH in NT. Significant change in ADC in pHT was absent, and accelerated recovery for animals in sHT was noted. MRS analysis revealed significant lactate accumulation to 204 +/- 40% from baseline only in NT, while sHT was characterized by a transient, less pronounced increase of lactate (159 +/- 11%) and lactate in pHT did not change significantly (117 +/- 11%). NAA did not change significantly when compared to baseline or between groups for NT, pHT, or sHT. Creatine rose significantly to 166 +/- 27% in NT after the insult, indicating increased metabolic stress which was absent in pHT (106 +/- 8%) and sHT (124 +/- 18%). Hypothermia can ameliorate early development of cytotoxic edema, lactate accumulation, and a general metabolic stress response after SAH, even when started after the insult. Our study indicates that a potentially beneficial influence on metabolism and cerebral perfusion in this crucial phase is practicable and might hold the key to further improve outcome in SAH.
Schubert
Gerrit Alexander
GA
Department of Neurosurgery, University Hospital Mannheim, University of Heidelberg, Mannheim, Germany. gerrit.schubert@nch.ma.uni-heidelberg.de
Poli
Sven
S
Schilling
Lothar
L
Heiland
Sabine
S
Thomé
Claudius
C
D000208:Acute Disease / Q000628:therapy; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001831:Body Temperature / Q000502:physiology; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001929:Brain Edema / Q000503:physiopathology / Q000628:therapy*; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D003401:Creatine / Q000378:metabolism; D004058:Diffusion; D038524:Diffusion Magnetic Resonance Imaging; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D007036:Hypothermia, Induced / Q000379:methods*; D019344:Lactic Acid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013345:Subarachnoid Hemorrhage / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*
D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate; D003401:Creatine