Morphological changes of the neural cells after blast injury of spinal cord and neuroprotective effects of sodium beta-aescinate in rabbits.

OBJECTIVE: Explosive blast neurotrauma is becoming more and more common not only in the military population but also in civilian life due to the ever-present threat of terrorism and accidents. However, little attention has been offered to the studies associated with blast wave-induced spinal cord injury in the literatures. The purpose of this study is to report a rabbit model of explosive blast injury to the spinal cord, to investigate the histological changes, focusing especially on apoptosis, and to reveal whether beta-aescinate (SA) has the neuroprotective effects against the blast injury. METHODS: Adult male New Zealand white rabbits were randomly divided into sham group, experimental group and SA group. All rabbits except the sham group were exposed to the detonation, produced by the blast tube containing 0.7 g cyclotrimethylene trinitramine, with the mean peak overpressure of 50.4 MP focused on the dorsal surface of T9-T10 level. After evaluation of the neurologic function, spinal cord of the rabbits was removed at 8 h, 1, 3, 7, 14 or 30 days and the H&E staining, EM examination, DNA gel electrophoresis and TUNEL were progressively performed. RESULTS: The study demonstrated the occurrence of both necrosis and apoptosis at the lesion site. Moreover, the SA therapy could not only improve the neurologic outcomes (P<0.05) but also reduce the loss of motoneuron and TUNEL-positive rate (P<0.05). CONCLUSIONS: In the rabbit model of explosive blast injury to the spinal cord, the coexistent apoptotic and necrotic changes in cells was confirmed and the SA had neuroprotective effects to the blast injury of the spinal cord in rabbits. This is the first report in which the histological characteristics and drug treatment of the blast injury to the spinal cord is demonstrated.

Oral iodine toxicity in chicks can be reversed by supplemental bromine.

Four chick bioassays were conducted to quantify iodine (I) toxicity and its amelioration in young chicks. A supplemental I level from KI of 600 mg/kg depressed growth in chicks fed methionine-deficient diets but not in those fed methionine-adequate diets. An I dose level >or= 900 mg/kg was required to cause growth depression in chicks fed a methionine-adequate corn-soybean meal diet. Iodine intoxicated chicks also displayed neurological symptoms and extreme malaise, but dose levels up to 1200 mg I/kg had no effect on blood hemoglobin or hematocrit. Supplemental I levels of 1000-1500 mg/kg caused severe growth depressions that could be totally reversed by dietary addition of 50 or 100 mg/kg bromine provided as NaBr. Nuclear accidents or terrorist actions that result in I toxicity and thyroid cancer or goiter may benefit from use of NaBr as a therapeutic agent.