Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Abstract

The previous chapters have described many alterations in secreted hormones and metabolic processes that occur for weeks to months after major burn injury. Interpretation of these alterations can be bewildering; however, many of the findings can be simplified and/or unified to a certain extent if they are viewed as part of an overall alteration in central nervous system (CNS) function characterized by modified control settings. The Neuroendocrine Reflex ArcEarly work with acute surgical trauma provided the conceptual framework of the neuroendocrine reflex arc. 12 In this framework, a signal from an injured area is transmitted by an afferent limb to the brain, which integrates the formation and orchestrates a neural and hormonal output as the efferent limb.Hume and Egdahl 3 studied dogs anesthetized with ether or Nembutal and with a catheter in an adrenal vein. Upon application of a scald burn, the corticosteroid (CS) secretion rate rose promptly within minutes. This response was blocked by prior section of the medulla oblongata, the spinal cord, or the peripheral nerve innervating the area of the lesion. Subcutaneous injection of ACTH in the denervated burned area provoked a CS response, indicating that if a burn toxin were present and capable of stimulating this acute response humorally, it would likely have been detected. Thus, the acute CS response to a burn did not result from pain per se, which was blocked by the anesthesia, nor from systemic absorption of a humoral toxin from the burned area, but from afferent neural information signaling the presence of an injury. In some experiments, crude measurements of circulating ACTH indicated that the CS response was associated with a surge in endogenous ACTH release. Lesions of the anterior hypothalamus blocked the CS and ACTH responses to operative trauma. These and the cord section experiments indicated that the adrenocortical response was via brain control of ACTH secretion, not via innervation of the adrenals. Nevertheless, activation of the adrenal medullae through the neural route was indicated by observation of elevated catecholamine (CA) secretion rates in the adrenal vein after injury.