ABSTRACT
The effect of catecholamines and adrenergic receptor blocking drugs on mortality and body temperature was studied in mice subjected to burn, tourniquet, and endotoxin shock at an environmental temperature of 25 degrees C. Epinephrine and norepinephrine (0.5 mg/kg) injected intraperitoneally postburn increased shock mortality significantly (p less than 0.05); pretreatment with these catecholamines had no effect. Pretreatment of burn- and tourniquet-traumatized mice with propranolol (25 mg/kg) significantly decreased shock mortality, while pretreatment with dibenamine (25 mg/kg) significantly lowered early mortality after endotoxin. None of the catecholamines or their blocking drugs significantly prevented the characteristic immediate fall in core temperature after the three types of shock. At 6 days postburn, however, a combination of propranolol and dibenamine caused a marked fall in core temperature (p less than 0.05). These results indicate that beta-catecholamine agonists could play an important role in acute burn mortality and that both alpha- and beta-catecholamine agonists could significantly influence body temperature regulation and metabolic rate during the late postburn period.
Subject(s)
Body Temperature Regulation/drug effects , Burns/mortality , Dibenzylchlorethamine/pharmacology , Epinephrine/pharmacology , Norepinephrine/pharmacology , Propranolol/pharmacology , Animals , Blood Circulation/drug effects , Body Fluids/drug effects , Burns/physiopathology , Female , Hematocrit , Hemorrhage/physiopathology , Mice , Shock, Septic/mortality , Shock, Septic/physiopathology , Shock, Traumatic/mortality , Shock, Traumatic/physiopathology , TourniquetsABSTRACT
Swiss-Webster female mice were given a moderately severe burn, and studies were carried out on the number and function of T and B cells from the spleens of burned and normal mice. The results showed a significant decrease (p less than 0.05) in the number of T and B cells for 2-3 days after burning with a rapid return to normal and a subsequent rise above normal at 14 and 21 days postburn (p less than 0.05). In the test for function, burned mice had a significant decrease in spontaneous mitotic activity of both T and B cells during the 21-day postburn period. When spleen lymphocytes were incubated with purified mitogens, both T and B cells showed a significantly diminished mitotic response in most of the burned animals.
Subject(s)
B-Lymphocytes/immunology , Burns/immunology , Spleen/immunology , T-Lymphocytes/immunology , Animals , Female , Lectins/pharmacology , Leukocyte Count , Lipopolysaccharides/pharmacology , Lymphocyte Activation , MiceABSTRACT
The release of histamine and mortality was studied in mice after various types of experimental shock. In burn shock, serum histamine rose significantly after injury, but there was no correlation between increased serum histamine and high mortality as a consequence of several therapy regimens. For example, after treatment with histamine or Compound 48/80 before burning, there was a rise of serum histamine, yet shock mortality fell significantly. Although separate administration of antagonists of H1 - or H2 - histamine receptors had no effect on mortality, pretreatment with both diphenhydramine and burimamide significantly increased shock mortality. In tourniquet shock, serum histamine rose significantly, and treatment with both antagonists before trauma produced a significant elevation of shock mortality. In endotoxin shock, prior treatment with one or both drugs did not change mortality. These results suggest that endogenous histamine is not a lethal factor in burn and tourniquet trauma, but rather it appears to have a compensatory, beneficial effect.