GROWTH-HORMONE IMPAIRED COMPENSATION OF HEMORRHAGIC-SHOCK AFTER TRAUMA AND SEPSIS IN SWINE

Objective: To study hemodynamic effects of growth hormone (GH) and its main mediator, insulin-like growth factor-1, in a model of critical i llness. Design: Randomized experiment in traumatized and septic piglet s. Materials and Methods: Hemodynamics and blood gases before and sust ained 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 Results: Sustained volume loss before cardiac arrest was lower in the GH group , The GH group was characterized by metabolic acidosis, During the hem orrhage, visceral blood flow (portal and renal) as a fraction of cardi ac output (fractional flow) was lower and peripheral fractional flow h igher in the GH group, Fractional renal artery flow was higher in the insulin-like growth factor-1 group (p < 0.05 for the comparisons state d). Conclusion: GH promoted metabolic acidosis in traumatized sepsis a nd impaired compensation of a subsequent hemorrhage.