• Maggy Riad, Marianna Mogos, Duraiyah Thangathurai, and Philip D Lumb.
• Department of Anesthesiology, Keck School of Medicine of the University of Southern California, Los Angeles, California 90033, USA.
• Curr Opin Crit Care. 2002 Aug 1; 8 (4): 281-4.

AbstractCorticosteroids are considered to be essential stress hormones. They are secreted together with adrenocorticotropic hormone (ACTH) in response to the pulsatile secretion of corticotropin-releasing hormone from the paraventricular nucleus of the hypothalamus. Changes in pulse amplitude are responsible for the diurnal rhythm in circulating ACTH and cortisol levels. Steroid levels increase immediately after injury, pain, fever, and hypovolemia in response to the stimulation of corticotropin-releasing hormone secretion by various cytokines. The increase in steroid levels is typically proportional to the magnitude of stress, with serum cortisol values being highest in moribund patients and shortly before death. With severe and prolonged stress, steroid levels are increased for weeks to months and may be associated with hypertrophy of the adrenal cortex. Cortisol acts in concert with catecholamines to maintain the vascular tone, endothelial integrity, vascular permeability, and the distribution of total body water within the vascular compartment. It also potentiates the vasoconstrictor effects of catecholamines. Cortisol helps to stimulate lipolysis, inhibit protein synthesis, facilitate amino acid mobilization from muscle, induce the enzymes of gluconeogenesis, enhance secretion of glucagon, inhibit insulin secretion, and stimulate conversion of lactic acid to glycogen. Because of their anti-inflammatory properties, steroids have been proposed as therapeutic adjuvants in systemic inflammation and may protect the host against overshooting defense reactions by reducing the migration of leukocytes to the inflammatory sites and the incidence of neutrophil-mediated tissue injury and organ dysfunction.

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