Insulin and glucose levels

Insulin and G l u c o s e Levels To the Editor: Martin and coworkers demonstrated a significant fall in plasma insulin and a rise in blood glucose concentrations during CPR in a canine model [April 1985; 14:293-297]. They suggested that the cause of this decline in insulin concentration was related to a fall in pancreatic perfusion. Although this may be partly responsible, an additional possibility is that an elevated plasma epinephrine concentration supressed insulin release. Their study design used an epinephrine infusion of a 5~g/kg/min during CPR, which would be expected to produce substantial plasma epinephrine concentrations because a mean infusion of 0.07 ~g/kg/min in adults resulted in mean plasma epinephrine concentrations of 715 pg/mL. 1 In the same study, plasma epinephrine concentrations above 400 pg/mL suppressed insulin release: A canine study without epinephrine infusion (data not presented) had a similar effect on blood glucose and plasma insulin [April 1985; 14:293-297]; this does not, however, preclude epinephrine-induced inhibition of insulin secretion. W o r t s m a n and colleagues 2 measured plasma catecholamines following cardiac arrest in adults and reported mean epinephrine concentrations of approximately 10,000 pg/mL compared to normal resting concentrations of 34 _+ 2 pg/ mL. Epinephrine is a potent catecholamine, Plasma concentrations of 75 to 125 pg/mL increase systolic blood pressure a n d lipolysis; h y p e r g l y c e m i a , k e t o g e n e s i s , and glycogenolysis occur at 100 to 200 pg/mL. 1 Epinephrine has a number of additional metabolic and hemodynamic effects, s u m m a r i z e d elsewhere, a i n c l u d i n g p r o f o u n d renal and splanchnic vasoconstriction at high concentrations. Therefore observed alterations in pancreatic blood flow, 4 elevations in blood glucose, and suppression of plasma insulin may be related to epinephrine's action. These epinephrineinduced actions do not detract from Martin's conclusion that glucose-insulin-potassium may be helpful post cardiac arrest; these actions do suggest that further investigati~,n into the endocrine and metabolic effects of the massive epi-

15:4 April 1986

nephrine plasma concentrations associated with critical illness 2 may be worthwhile. Arno Zaritsky, MD Division of Critical Care Medicine Children's Hospital National Medical Center Washington, DC 1. Clutter WE, Bier DM, Shah SD, et M: Epinephrine plasma metabolic clearance rates and physiologic thresholds for metabolic and hemodynamic actions in man. J Clin Invest 1980;66:94-101. 2. Wortsman J, Frank S, Cryer PE: Adrenomedullary response to maximal stress in humans. Am ] Med 1984~77:779-784. 3. Zaritsky AL, Chernow B: Catecholamines, sympathomimetics, in Chernow B, Lake CR (eds): The Pharmacologic Approach to the Critically Ill Patient. Baltimore, Williams and Wilkins, 1983, pp 481-509. 4. Ralston SH, Voorhees WD, Babbs CF: Intrapulmonary epinephrine during prolonged cardiopulmonary resuscitation: Improved regional blood flow and resuscitation in dogs. Ann Emerg Med 1984; 13:79-86. In Reply: The authors thank Dr Zaritsky for his comments concerning our study. We agree with his concerns about the effects of epinephrine, whether exogenous or endogenous, on pancreatic blood flow, blood glucose, and insulin. Our investigations in this area are continuing in an effort to answer these questions. The effects of cardiac arrest and resuscitation on other end organs in addition to the heart and brain is a previously unstudied area that could have profound effects on successful resuscitation. The precise role of pancreatic hormonal influences during resuscitation, if any, remains speculative at the current time. Gerard B Martin, MD Department of Emergency Medicine Henry Ford Hospital Detroit, Michigan

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