Type of Document	Master's Thesis
Author	Baruffaldi, Joan Marie
URN	etd-02072013-040111
Title	Adrenergic regulation of splenic functions in neonatal pigs
Degree	Master of Science
Department	Veterinary Medical Sciences
Advisory Committee	Advisor Name Title Huber, William G. Committee Chair Freeman, Larry E. Committee Member Gwazdauskas, Francis C. Committee Member Wilcke, Jeffrey R. Committee Member
Keywords	Veterinary histology
Date of Defense	1989-04-05
Availability	restricted
Abstract 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,ug/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. ln 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< 0re.spo0nses we5\re not altered by the adrenhoceptoreblockades. e
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