The Effect of Hypertonic Saline and Mannitol against Edema Formation after Cryogenic Brain Injury in Rats / 대한마취과학회지

BACKGROUND: After experimental cryogenic cerebral injury, severe focal brain contusion develops due to blood-brain barrier breakdown and vasogenic cerebral edema formation. This study has been conducted to find out the effects of hypertonic saline against cryogenic brain edema in rats. METHODS: Thirty rats of either sex weighing 250 to 300 g underwent a 60 seconds of cryogenic brain injury. All rats were randomly divided into one of three groups; control group (n = 10), 7.5% saline group (n = 10), and 10% mannitol group (n = 10). The water contents were measured 60 minutes after cryogenic injury by using the dry-weight method. RESULTS: The water contents in the 7.5% saline and 10% mannitol groups were significantly decreased compared with the control group. The levels of edema in the 7.5% saline and 10% mannitol groups were also significantly decreased compared with the control group. Although it appeared as if that 10% mannitol might decrease edema formation more than 7.5% saline, there were no statistical differences between the 7.5% saline and 10% mannitol groups. CONCLUSIONS: Hypertonic saline (7.5%) may be as effective agent to reduce edema formation after brain trauma to the same degree as mannitol.

The Effect of Nitric Oxide on Edema Formation in Cryogenic Brain Injury Model of the Rat / 대한마취과학회지

BACKGROUND: Nitric oxide (NO) is a simple molecule with a complex involvement in a wide variety of biologic functions. However, whether NO protects or aggravates brain injury is still controversial. This study was conducted to determine the effect of nitric oxide on the formation of brain edema resulting from a focal cryogenic injury in rats. METHODS: Thirty nine Sprague-Dawley rats (200~250 gm) were allowed food and water ad libitum. Anesthesia was induced in a specially designed plastic box with 5% halothane in oxygen. In experiment I (24 rats), animals were divided randomly into eight group (3 rats in each group) according to the decapitation time in control, 15, 30, 45, 60, 90, 120, and 180 min. Cryogenic injury was made by pouring liquid nitrogen to exposed temporo-parietal area through metal funnel for 60 seconds. After cryogenic injury, brain was quickly removed and cerebral hemispheres were seperated. Separated cerebral hemispheres were dried in a drying oven for 7 days at 60 degrees C. Cerebral water content was assessed by dry-weight method. In experiment II (15 rats), one subgroup (n=8) was control group, normal saline 0.5 ml was injected intraperitoneally 30 minutes before injury. the other (n=7) was experimental group, and a competitive nitiric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), was given intraperitoneally 30 minutes before injury in a dose of 20 mg/kg. Body temperature was monitored during whole experiment. Ninety minutes after injury, brain was quickly removed and cerebral hemispheres were seperated. The cerebral water content of separated cerebral hemisphere was assessed by dry-weight method. RESULTS: In time courses of cryogenic brain edema of experiment I, the amount of brain edema was increased till 90 minutes after cryogenic brain injury and then decreased. In L-NAME group of ex-periment II, the amount of cerebral edema was not changed significantly (p<0.05). But, there was a tendency of decrease in brain edema formation in L-NAME group than control group. CONCLUSION: It was not proved that nitric oxide had a major role in the edema formation aftercryogenic brain injury, but it still seems that nitric oxide has at least partly involved in the pathogenesis of cerebral edema resulting from traumatic brain injury.