OBJECTIVE: Melatonin (5-methoxy-N-acetyltrypamine), a chemical naturally pr
oduced in the pineal gland, has been suggested to be a free radical scaveng
er and an antioxidant. In the present study, the effect of melatonin on col
d-induced brain edema was evaluated by determination of cerebral water cont
ent, blood-brain barrier permeability, and areas of infarct; the effects we
re also studied histopathologically.
METHODS: Brain edema was produced in rats by creating a lesion via cortical
freezing. Animals were separated into four groups: sham-operated (craniect
omy only); control (cold injury); sham-vehicle (cold injury plus saline); a
nd melatonin treatment (cold injury plus melatonin). Melatonin was administ
ered (50 mg/kg intraperitoneally) 15 minutes after the cold injury was indu
ced. Twenty-four hours later, tissue samples from the core, from the periph
ery of the cold-injured hemisphere, and from the contralateral hemisphere s
ymmetrical to the cold injury were obtained.
RESULTS: Melatonin treatment reduced edema (mean +/- standard deviation; 86
.22 +/- 1.54% in the control group versus 80.78 +/- 2.76% in the melatonin
treatment group, P < 0.001) and blood-brain barrier permeability (45.34 +/-
2.75% in the control group versus 38.26 +/- 3.40% in the melatonin treatme
nt group, P < 0.001) at the periphery of cold injury. Area of infarct reduc
ed from 5.84 +/- 0.58% in the control group to 3.30 +/- 0.89% in the melato
nin treatment group (P < 0.001). The effect of melatonin was also confirmed
histopathologically.
CONCLUSION: Melatonin was found to be neuroprotective in instances of cold-
induced brain edema. Thus, melatonin may be a valuable therapeutic agent in
the treatment of cerebral edema.