High-voltage electrical injury: chronic wound evolution.

A chronic electrical burn model employing documentary and diagnostic techniques was designed in the primate for investigating wound evolution up to 10 days after injury. A standardized 40-kJ, 3500-V, 4.2-A, 2.5-s bilateral, symmetrical upper extremity electrical injury was performed. Gross observation studies documented tissue injury extending more proximally on the deep surfaces of individual muscles and between muscle layers. Specific regions, or "choke" points, in the forearm exist in which decreased cross-sectional areas and highly resistant tissue composition resulted in increased heat production and more severe tissue damage. Muscle injury was analyzed using light microscopy, revealing patchy cellular necrosis intermixed with viable cells. Digital subtraction angiography demonstrated segmental narrowing and "pruning" of large vascular trunks with a significant decrease in nutrient vessels in affected areas. Ulnar nerve conduction studies showed loss of conduction proximal to the cubital fossa with no recovery. Although characteristic patterns of injury were documented in skin, muscle, vessels, and nerves, no experimental evidence was found for progressive necrosis.

Relationship between plasma corticosterone and adrenal epinephrine after diazepam treatment in rats.

Following recent observations that diazepam treatment increases adrenal epinephrine in rats, we were interested in studying the possible mechanisms of this action of diazepam on rat adrenal glands. All diazepam treatments studied (1-25 mg . kg-1.day-1 for 10 days) led to an increase in adrenal epinephrine following a linear dose-effect relationship. Since epinephrine synthesis is under neuronal and humoral controls, we investigated their respective importance in the effect of diazepam on the adrenal gland. The denervation of the adrenal gland did not prevent the increase in adrenal epinephrine by diazepam treatment. On the hand, diazepam treatment was shown to cause an increase in plasma corticosterone in parallel with an increase in adrenal epinephrine. Administration of dexamethasone (a synthetic corticoid) and hypophysectomy prevented the increase in adrenal epinephrine and plasma corticosterone resulting from diazepam treatment. We thus conclude that the increase in adrenal epinephrine seen after diazepam treatment is parallel to the increase in plasma corticosterone. Moreover, since the action of diazepam on adrenal epinephrine is prevented by dexamethasone or hypophysectomy, we hypothesize that diazepam is acting on the adrenal cortex via the release of adrenocorticotropic hormone (ACTH). ACTH and corticosterone would be responsible for the increased activity of epinephrine-synthesizing enzymes in adrenal medulla.