The purpose of this study was to assess adrenergic control of splenic hemodynamic function and oxygen metabolism in neonatal pigs (NP). Seventeen piglets, 28-45 days of age, were anesthetized with pentobarbitol (30 mg/kg, i.p.) and prepared for measurement of splenic venous outflow. Simultaneous arterial and venous blood samples were analyzed for O₂ content and hematocrlt (Hct). Splenic oxygen consumption and extraction were calculated. The effects of adrenergic stimulation on splenic leukocyte migration and proliferation were also assessed. Fluorescence histochemistry of the spleen from NP revealed noradrenergic innervation of the vasculature taken from the hilar portions of the spleen. Norepinephrine (NE) Infusion, (2,μg/kg/min) caused a significant decrease in splenic venous outflow (P< 0.01) with a concomitant significant increase in splenic resistance (P< 0.005). Splenic leukocyte migration and proliferation did not change significantly during NE infusion, but the splenic venous Hct was significantly increased (P< 0.001). Similar changes were observed with electrical stimulation of the splenic nerve. Pretreating the NP with beta-adrenoceptor blocker, propranolol (1 mg/kg), had no significant effect on these responses. In contrast, these responses were abolished with the addition of alpha-adrenoceptor blocker, phentolamine (1 mg/kg). Splenic O₂ metabolism did not change significantly during nerve stimulation, but splenic venous Hct was significantly increased (P<0.05) These responses were not altered by the adrenhoceptore blockade.

lt is concluded that activation of the adrenergic system of the spleen causes a significant decrease in splenic venous outflow with a concomitant increase in splenic vascular resistance and this is largely mediated by the activation of the alpha-adrenoceptor system. Adrenergic stimulation of the spleen did not influence splenic oxygen metabolism in piglets. This may relate to the high red blood cell storage and O₂ availability of the spleen and the low oxygen demand of the organ.