Int. J. Exp. Path. (2007), 88, 1–7 doi: 10.1111/j.1365-2613.2006.00509.x
ORIGINAL ARTICLE
Motor impairment and neuronal damage following hypothermia in tropical amphibians Nelson L. Dalo´, Gustavo A. Bracho and Juan C. Pin˜a-Crespo Faculty of Veterinary Medicine, Research Unit Haity Moussatche´, Universidad Centroccidental Lisandro Alvarado, Barquisimeto, Venezuela
INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
Received for publication: 2 May 2006 Accepted for publication: 21 September 2006 Correspondence: Nelson L. Dalo´ PO Box 722 Barquisimeto 3001A Venezuela Tel.: +58-251-2592409 Fax: +58-251-2592404 E-mail:
[email protected]
Summary Although the induction of mild to moderate cerebral hypothermia in mammals can have neuroprotective activity, some deleterious effects have been described when inducing deep hypothermia during cooling of the brain. In the spinal cord, rapid deep cooling can induce seizure activity accompanied by release of the excitatory neurotransmitters, glutamate and aspartate. We used cold-sensitive tropical amphibians as a model to determine (a) the critical temperature inside the central nervous system necessary to induce seizures during rapid cooling; (b) the survival rate during slow deep cooling of the whole animal; and (c) whether deep cooling can cause neuronal cell damage. Seizures induced by deep rapid (£3 min) cooling of the spinal cord began when a critical temperature of 10.4 C was reached. During slow (‡30 min) deep cooling of the whole animal (12 h at 2–3 C), around 70% of animals died. Spinal reflexes were enhanced when temperatures within the spinal cord reached between 9.0 C and 11.6 C. A fivefold increase in blood glucose level was observed during slow deep cooling. Recovery after slow deep cooling was accompanied by motor impairment and the main histological findings were condensation of the cytoplasm and nuclear pyknosis. Severe neuronal cell damage was characterized by swelling, vacuolated cytoplasm with distended neuronal bodies. These results indicate that deep cooling can easily induce neuronal cell damage in the central nervous system of cold-sensitive animals. They also warn us to the potential sequels associated with the use of deep brain cooling as a neuroprotective strategy. Key words brain cooling, cold exposure, cold injury, hypothermia, neuronal damage
Cooling of the brain has been shown to be an effective way of protecting the brain against damage associated with traumatic brain injury (McLean & Wong 1996; Dalton & Perez-Pinzon 2003). Additional evidence also suggests that during cardiac arrest, brain injury can be prevented by deep cooling of the brain to
