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 AbstractThe 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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