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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. / Master of Science

To study the effects of feeding and diet on postnatal development of the small intestine in newborn piglets during the time 0 - 24 hours after birth, three studies were conducted: 1. Unsuckled newborn piglets were fed from a bottle with colostrum or milk from either sows or cows, infant formula, or water. After 24 hours intestinal development was compared with that in piglets at birth and others naturally suckled. Sow colostrum caused greater increases in weight and length of the small intestine than did any of the other diets. The increases were due to mucosal cell swelling caused by cellular protein accumulation, hyperplasia and, in the duodenum, hypertrophy. Feeding sow colostrum increased mucosal lactase activity. Cow colostrum caused decreases in mucosal RNA levels. Increases in the DNA content of the intestinal mucosa occurred in all groups, including the water fed group. Colostrum feeding also enhanced pancreatic growth and feeding infant formula increased liver weight. 2. The effects of enteral feeding on small intestinal development were investigated by feeding nutrient solution to unsuckled newborn piglets by orogastric tube or parenterally. Both groups after 24 hours had greater intestinal development than did the piglets at birth. The development was most pronounced in the duodenum and lower ileum. Apart from a greater small intestinal length in the orogastrically fed piglets there were no significant differences between the orogastrically and parenterally fed groups. 3. To investigate the effects of sucking per se on small intestinal development, groups of unsuckled piglets were fed for 24 hours with either sow colostrum or infant formula by orogastric tube or being allowed to suck from a bottle. Sucking did not affect intestinal development whereas colostrum, regardless of how it was fed, had significantly greater effects on intestinal development than did infant formula. For the colostrum fed piglets the intestinal length, tissue weight, circumference, wall thickness, villous height and width, RNA content, protein:DNA ratio and RNA:DNA ratio were all significantly greater than for those fed infant formula. In the duodenum the estimated cell migration rate was faster and mucosal cell replacement time was shorter than in other parts of the small intestine, regardless of the diet fed. The greater villous height in the piglets fed sow colostrum was most likely due to the combined effects of cellular swelling and an increase in the number of villous cells. These results indicate that (a) sow colostrum causes cellular swelling related to colostral protein accumulation, cell hyperplasia and, in the duodenum, hypertrophy, (b) there is a basal rate of mucosal cell division which contributes to mucosal growth regardless of diet and method of feeding, (c) the duodenum exhibits a greater growth and sensitivity to the trophic effects of colostrum compared to other parts of the small intestine, (d) feeding cow colostrum to newborn piglets causes a pronounced decrease in mucosal RNA content and (e) diets affect postnatal development of the small intestine whereas the route or method of feeding has no significant effects on small intestinal development in piglets during the first 24 hours after birth.