Critical care medicine
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Critical care medicine · Jan 1996
Burn injury alters beta-adrenergic receptor and second messenger function in rat ventricular muscle.
The molecular pharmacologic bases for the attenuated cardiovascular and metabolic responses to catecholamines, after burn injury, have not been elucidated. In the present study, myocardial tissues were used as a model of beta-adrenergic receptors to study burn injury-induced alterations in receptors and in signal transduction. ⋯ The etiology of the decreased responses in the myocardium to exogenous and endogenous beta-adrenergic receptor agonists after burn injury may be attributed to decreased affinity for ligands, and also to impaired receptor-mediated signal transduction and to decreased adenylate cyclase enzyme activity, resulting in decreased basal and stimulated second messenger (cAMP) production.
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Critical care medicine · Jan 1996
Editorial CommentLiquid breathing: stretching the technological envelope.