Most patients with severe traumatic shock exhibit hyperglucagonemia, usually without a commensurate increase in insulin, within the first few hours after injury. Hyperglucagonemia was not observed in three patients during major surgery unaccompanied by hypotension. Hyperglucagonemia can be produced in dogs by inducing hypovolemic shock through exsanguination. Exsanguination hyperglucagonemia can be significantly reduced by beta adrenergic blockage with propranolol but not by alpha adrenergic blockade with phentolamine. It is concluded that hyperglucagonemia and lowering of the insulin glucagon ratio are part of the endocrine response to injury and are at least partially mediated via beta adrenergic stimulation. It has been reported by Marco, Valverde and co workers and more recently by Wise et al. that corticosteroids also known to be elevated in trauma, increase basal and stimulated glucagon secretion and could, therefore, contribute to the hyperglucagonemia in these studies. The presence of a reduced insulin glucagon ratio results in increased hepatic glucose production and thus contributes to the elevation of plasma glucose levels that accompany shock. The hyperglycemia of shock may well constitute an important and appropriate survival response by helping to maintain glucose delivery to the brain in the face of a declining cerebral blood flow. However, if inappropriately long continued, the low insulin glucagon ratio would promote increased use of amino acids for new glucose production at the expense of protein synthesis and thus contribute to or perhaps mediate the catabolic state associated with injury and other stressful illness.
|Original language||English (US)|
|Title of host publication||Transactions of the Association of American Physicians|
|Number of pages||8|
|State||Published - 1973|
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