Effects of epidural hypothermic saline infusion on locomotor outcome and tissue preservation after moderate thoracic spinal cord contusion in rats.

OBJECT: Regionally delivered hypothermia has advantages over systemic hypothermia for clinical application following spinal cord injury (SCI). The effects of local hypothermia on tissue sparing, neuronal preservation, and locomotor outcome were studied in a moderate thoracic spinal cord contusion model. METHODS: Rats were randomized to four treatment groups and data were collected and analyzed in a blinded fashion. Chilled saline was perfused into the epidural space 30 minutes postcontusion to achieve the following epidural temperatures: 24 +/- 2.3 degrees C (16 rats), 30 +/- 2.4 degrees C (13 rats), and 35 +/- 0.9 degrees C (13 rats). Hypothermia was continued for 3 hours when a 45-minute period of rewarming was instituted. In a fourth group a moderate contusion only was induced in 14 animals. Rectal (core) and T9-10 (epidural) temperatures were measured continuously. Locomotor testing, using the Basso-Beattie-Bresnahan (Ba-Be-Br) scale, was performed for 6 weeks, and rats were videotaped for subsequent analysis. The lesion/preserved tissue ratio was calculated throughout the entire lesion cavity and the total lesion, spinal cord, and spared tissue volumes were determined. The rostral and caudal extent of gray matter loss was also measured. At 6 weeks locomotor recovery was similar in all groups (mean Ba-Be-Br Scale scores 14.88 +/- 3.71, 14.83 +/- 2.81, 14.50 +/- 2.24, and 14.07 +/- 2.39 [p = 0.77] for all four groups, respectively). No significant differences in spared tissue volumes were found when control and treatment groups were compared, but gray matter preservation was reduced in the infusion-treated groups. CONCLUSIONS: Regional cooling applied 30 minutes after a moderate contusive SCI was not beneficial in terms of tissue sparing, neuronal preservation, or locomotor outcome. This method of cooling may reduce blood flow in the injured spinal cord and exacerbate secondary injury.

The effects of early post-traumatic hyperthermia in female and ovariectomized rats.

Episodes of post-traumatic hyperthermia commonly occur in the head-injured patient population. Although post-traumatic hyperthermia has been shown to worsen outcome in experimental studies using male rats, the consequences of secondary hyperthermia following traumatic brain injury (TBI) have not been investigated in female animals. Thus, the purpose of this study was to examine the effects of post-traumatic hyperthermia after fluid-percussion (F-P) brain injury in intact and ovariectomized female rats. Thirty-eight female Sprague-Dawley rats were used in these experiments. Intact female rats underwent TBI followed 30 min later by a 4-h period of normothermia (37 degrees C) or brain hyperthermia (40 degrees C). Female rats that had been ovariectomized 10 days prior to TBI were also traumatized and followed by a period of normothermia or hyperthermia. At 72 h after TBI, rats were perfusion-fixed for quantitative histopathological and immunocytochemical evaluation. Following normothermic TBI, intact female rats demonstrated significantly smaller contusion volumes, decreased frequency of axonal beta-amyloid precursor protein (beta-APP) profiles, and greater numbers of NeuN-positive cortical neurons compared to traumatized ovariectomized females. Although post-traumatic hyperthermia increased contusion volume, cortical neuronal cell death and axonal damage in both intact and ovariectomized female groups, the effects of the induced hyperthermic period were more pronounced in ovariectomized animals. These findings demonstrate for the first time that post-traumatic hyperthermia worsens histopathological outcome in female rats, and that neural hormones, including estrogen and progesterone, may protect against secondary hyperthermic insults.