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Toxic effects of catecholamines on skin
R W Burk1, D Serafin, B Klitzman
1Plastic Surgery Research Laboratories, Duke University Medical Center, Durham, N.C.
Plastic and Reconstructive Surgery
|January 1, 1990
Summary
Catecholamines like epinephrine can accelerate skin death in ischemic tissue by activating beta 2 receptors. This skin necrosis effect, independent of vasoconstriction, can be reversed with beta-blocker medication.
Area of Science:
- Biochemistry
- Dermatology
- Pharmacology
Background:
- Catecholamines are known for their vasoactive properties.
- Their direct toxic effects on skin tissue, independent of blood flow changes, are less understood.
- Investigating these direct effects is crucial for understanding skin necrosis.
Purpose of the Study:
- To investigate the direct cytotoxic effects of catecholamines on skin.
- To determine the specific receptors involved in catecholamine-induced skin necrosis.
- To assess the potential for reversal of this toxicity with beta-blockade.
Main Methods:
- Excised rat and human breast skin were incubated with various catecholamines.
- Lactate dehydrogenase (LDH) release was measured as an indicator of cell death.
- Effects of adrenergic receptor blockers (propranolol, selective beta 2, alpha, beta 1) were assessed.
Main Results:
- Epinephrine and norepinephrine significantly increased LDH release in rat skin at specific concentrations.
- Similar toxicity was observed in human breast skin with epinephrine.
- The toxic effects were mediated by beta 2 receptors and reversed by propranolol and beta 2 blockade.
Conclusions:
- Catecholamines, particularly epinephrine, can directly cause skin cell death (necrosis) in ischemic skin.
- This toxicity is primarily mediated through beta 2 adrenergic receptors.
- Beta-blockade is effective in reversing catecholamine-induced skin necrosis, suggesting a therapeutic potential.