ABSTRACT
A statistical correlationl was made between adrenocorticotropin (ACTH) and four elements in rats under control, stress, and stress-recovery conditions. Blood serum zinc showed a strong positive correlation with the rise in ACTH during stress and its decline in stress recovery. Serum calcium, copper, and magnesium demonstrated little correlation with ACTH changes. The strong ACTH-zinc correlation points to an as yet undefined interaction between ACTH and zinc
Subject(s)
Adrenocorticotropic Hormone/blood , Minerals/blood , Stress, Physiological/blood , Adrenal Glands/physiopathology , Animals , Calcium/blood , Copper/blood , Corticosterone/blood , Fluorometry , Hypotension/blood , Magnesium/blood , Male , Pituitary Gland/physiopathology , Rats , Spectrum Analysis , Stress, Physiological/physiopathology , Zinc/bloodABSTRACT
Serum cortisol levels are increased in patients after thermal injury. Lymphocyte function is altered in these patients, which renders them susceptible to infections. Elevated cortisol levels may contribute to this compromised state. In this study, we have demonstrated that cortisol directly affects lymphocyte membrane fluidity as measured by the polarization of fluorescence from the membrane-associated probe diphenylhexatriene in peripheral blood lymphocytes. Membrane fluidity increased in vitro with short- or long-term cortisol exposure. However, membranes of control peripheral blood lymphocytes that were previously exposed to cortisol became resistant to the fluidizing effect of cortisol, which implies membrane adaptation to long-term cortisol exposure. Cortisol effects were similar to those associated with ethanol, a known membrane-fluidizing agent, in peripheral blood lymphocytes and cytotoxic T lymphocytes. Membrane fluidity was compared in peripheral blood lymphocytes from thermally injured patients and peripheral blood lymphocytes from normal (control) subjects. Peripheral blood lymphocyte membrane fluidity increased in major thermal injury. Our data suggest that cortisol affects lymphocyte membrane fluidity in vitro in a manner similar to the membrane fluidity alterations that are observed in vivo after thermal injury. These observations reflect a direct membrane effect of cortisol, which may explain, in part, the cellular dysfunction and immunologic suppression that is observed after thermal injury.
Subject(s)
Burns/metabolism , Hydrocortisone/physiology , Lymphocytes/metabolism , Membrane Fluidity/physiology , Adult , Burns/immunology , Ethanol/pharmacology , Female , Fluorescence Polarization , Humans , In Vitro Techniques , Male , Membrane Fluidity/drug effects , Time FactorsABSTRACT
Arterial-venous magnesium differences were examined in mongrel dogs stressed with reversible and lethal hypovolemia. Increases in serum Mg with hemorrhage have long been known to occur in both humans and animals, yet, increased blood Mg levels have not been viewed as an indicator of the irreversible shock state. The magnesium gradient was shown to be a good indicator of cell destruction which is consistent with lethal shock.