SUMMARYFour lactating Friesian cows with cannulae in the rumen and in the proximal duodenum were subjected to each of four different dietary treatments. Treatments differed with respect to concentration of crude protein, supply of urea nitrogen and frequency of feeding. The rations used consisted of hay, maize silage and concentrates and were offered to the animals according to milk yield.During the last 5 days of each experimental period (5 weeks), ingesta flow at the proximal duodenum was estimated by Cr-EDTA. Samples were taken from the duodenum at 2 h intervals and were analysed for thiamin, total nitrogen and microbial nitrogen. Labelling of microbial N was achieved by continuous infusion of 16N-urea into the rumen.With treatment 2 (26% less N than with treatment 1) thiamin net synthesis in the forestomachs and total thiamin entering the duodenum were significantly reduced whereas treatment 3 (substitution of 26% plant N by urea-N) and treatment 4 (six times instead of twice feeding daily) had no effect on synthesis and flow of thiamin to the small intestines. There were significant linear regressions between flow of microbial N and flow of thiamin to the duodenum and between organic matter digested and flow of thiamin.
Six 5- to 6-month-old sheep fitted with rumen fistulas and reentrant cannulas in the duodenum and in the ileum were adapted to two dies low in thiamin and containing different percentages of urea nitrogen. The sheep were subjected to seven thiamin balance experiments, with continuous feeding and total collection of duodenal and ideal contents and feces for periods of 6 day each. Thiamin and dry matter were determined in aliquots of collected digesta and feces. Daily thiamin intake was always less than .3 mg, but average daily flow of thiamin into the duodenum was between 1.53 and 3.46 milligrams. Microbial net synthesis of thiamin in the forestomach system was between 1.44 and 3.23 mg/day, so 90 to 96% of thiamin entering the duodenum was of microbial origin. Disappearance of thiamin from the small intestines approximately equaled thiamin net synthesis in the forestomachs, indicating high absorption of microbially produced thiamin. In five experiments, thiamin balance in the large intestines was positive, but no measurements were made of thiamin breakdown within, and absorption from, the large intestines.
In vitro experiments were conducted to study the permeability to thiamin of sheep rumen wall in either direction. Isolated discs of rumen wall mucosa were used in incubation experiments over 3 hr, controlled by measurements of transmural potentials. In some experiments 14 C-labeled thiamin was used.At thiamin concentrations in the mucosal fluid ranging from .1 to 1.6/ag/ml no changes of the initial concentrations were found after incubation, whereas, at higher concentrations (3.2 to 12.8 /~g/ml) there was a slight but insignificant decrease. In no case did the initial serosal thiamin concentration change. When 2.0 /lg/ml 14 C-thiamin were applied a minor reduction of 14C-activity in the mucosal fluid was found.When .05 to .2/~g/ml thiamin were applied in the serosal bathing fluid no concentration changes measurable by chemical analysis were obtained.Experiments with taC_thiamin showed that approximately the same amount of l ac-thiamin migrated into the rumen mucosa as in the opposite direction.No accumulation of 14C-thiamin in the rumen mucosa occurred during incubation.The results indicate that the rumen wall mucosa of sheep has an extremely low permeability to thiamin and that the rumen may not be considered as a site of significant absorption or endogenous secretion of thiamin. (
Twenty pregnant cows were kept in two feeding groups. Feeding regimens were designed to induce high milk production (16 kg milk/day) in group I and low production (2 kg/day) in group II. Milk weights were corrected for fat content. After onset of lactation, each cow was fed according to actual production level. Four cows from group I and two from group II developed clinical ketosis during the first few weeks of lactation. Blood taken weekly from all animals from about 2 weeks before until an average of 7 weeks after parturition was assayed for glucocorticoids, glucose and ketone bodies. Average plasma cortisol concentration for both groups was 4.5 +/- 2.6 ng/ml (range from 0 to 13 ng/ml). Plasma cortisol levels in cows which later developed clinical ketosis were not different from those in cows that remained healthy. There was, however, a positive correlation between blood glucose and plasma cortisol, and a negative correlation between blood ketone bodies and plasma cortisol. The findings suggest that adrenal cortical activity is interrelated with onset of ketosis although plasma cortisol levels appear unsuitable for identifying ketotic cows prior to clinical manifestation of the disorder.
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