• K Unneberg, L Balteskard, M Mjaaland, and A Revhaug.
• Department of Surgery, University Hospital of Tromsø, Norway.
• J Trauma. 1996 Nov 1; 41 (5): 775-80.

ObjectiveTo study hemodynamic effects of growth hormone (GH) and its main mediator, insulin-like growth factor-1, in a model of critical illness.DesignRandomized experiment in traumatized and septic piglets.Materials And MethodsHemodynamics and blood gases before and sustained volume loss during a controlled, fatal hemorrhage were recorded in a GH treated group (n = 8), an insulin-like growth factor-1 treated group (n = 8), a control group with trauma and sepsis (n = 8), and a control group with trauma only (n = 6).Measurements And Main ResultsSustained volume loss before cardiac arrest was lower in the GH group. The GH group was characterized by metabolic acidosis. During the hemorrhage, visceral blood flow (portal and renal) as a fraction of cardiac output (fractional flow) was lower and peripheral fractional flow higher in the GH group. Fractional renal artery flow was higher in the insulin-like growth factor-1 group (p < 0.05 for the comparisons stated).ConclusionGH promoted metabolic acidosis in traumatized sepsis and impaired compensation of a subsequent hemorrhage.

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