ABSTRACT
The ability of ascorbic acid (AA) as an antioxidant to suppress the inflammatory reaction was investigated. Carrageenan-induced foot pad edema was produced in the right hind foot of anesthetized mice (n = 22). Subsequently, Group A (n = 11) received 25 mg AA in saline (IP) and Group B, an equal volume of saline. After 2 1/2 hrs the animals were sacrificed and increase in weight of the amputated right paw over the amputated left paw was expressed as percentage edema (PE). The PE in Group A was 43.8 +/- 5.9, and in Group B was 59.3 +/- 3.9 (p less than 0.05, unpaired t-test). The same experiment was repeated with the AA administered 10 minutes prior to injury. The change in edema was not statistically significant. It is concluded that high dose AA suppresses edema if given after but not before injury.
Subject(s)
Ascorbic Acid/therapeutic use , Edema/drug therapy , Animals , Carrageenan , Edema/chemically induced , Edema/prevention & control , Female , Male , MiceABSTRACT
Head injury is a major factor in the mortality of traumatized patients, accounting for about 50 percent of the resulting fatalities. Alcohol intoxication is frequently (25 to 50 percent) associated with head injuries. This study was undertaken to investigate the effects of alcohol on head trauma in a standardized animal model. Swiss Webster mice (25 ± 2 g) were given intraperitoneally 0.2 mL of either saline or 50 percent ethanol in saline. Thirty minutes later, under light ether anesthesia, severe concussion was produced by dropping a 39.5-g lead weight from a height of 30 cm. The trauma was centered on the midskull by channeling the weight through a vertical tube, 1.2 cm in diameter. Animals were observed daily for eight days. Among the controls, 12 of 12 mice, (100 percent) survived for four days and 8 of 12 (67 percent) survived eight days. In the alcohol recipients, there were 10 of 21 survivors (48 percent) at four days and only one survivor (5 percent) at eight days. This study clearly demonstrates that alcohol increases the lethality of standardized head trauma in mice. The mechanism by which alcohol modifies the effects of craniocerebral trauma remains to be elucidated.