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 illness. Design: Randomized experiment in traumatized and septic piglets. Materials and Methods: Hemodynamics 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 Results: Sustained 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). Conclusion: GH promoted metabolic acidosis in traumatized sepsis and impaired compensation of a subsequent hemorrhage.