B-vitamin supplementation of diets for 144 shipping-stressed crossbred calves (116 kg) at levels up to 10 times that recommended for growing pigs did not influence (P greater than .20) weight gain or feed conversion during a 56-d receiving trial. However, vitamin supplementation tended (P less than .10) to reduce morbidity. In a second trial, supplemental B-vitamins had no effect (P greater than .20) on efficiency of microbial growth or site and extent of digestion of organic matter, acid detergent fiber and N. Supplemental dietary riboflavin, niacin, folic acid, B12 and ascorbic acid were largely metabolized [degraded and (or) absorbed] anterior to the small intestine, with escape values of 1, 3, 10 and 0% of added vitamins, respectively, while dietary B6 and biotin largely escaped the rumen. Thiamine and pantothenic acid were intermediate in ruminal escape (52 and 22%, respectively). Small intestinal absorption of thiamine, niacin, riboflavin, B6 and B12 averaged 75, 79, 25, 79 and 48%, respectively. Coefficients for ruminal escape and microbial synthesis for each B-vitamin were calculated using the slope-ratio technique. Measured flows for thiamine, riboflavin and B12 in a third experiment were similar to flows predicted from escape and synthesis equations, though flow of niacin and B6 were under-predicted by 37 and 44%, respectively. Results are interpreted to indicate that intestinal B-vitamin supply can be predicted based on dietary composition and intake.
Background and Purpose— Long-term outcome after subarachnoid hemorrhage (SAH) is potentially linked to cytotoxic heme. Free heme is bound by hemopexin and rapidly scavenged by CD91. We hypothesized that heme scavenging in the brain would be associated with outcome after hemorrhage. Methods— Using cerebrospinal fluid and tissue from patients with SAH and control individuals, the activity of the intracranial CD91–hemopexin system was examined using ELISA, ultrahigh performance liquid chromatography, and immunohistochemistry. Results— In control individuals, cerebrospinal fluid hemopexin was mainly synthesized intrathecally. After SAH, cerebrospinal fluid hemopexin was high in one third of cases, and these patients had a higher probability of delayed cerebral ischemia and poorer neurological outcome. The intracranial CD91–hemopexin system was active after SAH because CD91 positively correlated with iron deposition in brain tissue. Heme–hemopexin uptake saturated rapidly after SAH because bound heme accumulated early in the cerebrospinal fluid. When the blood–brain barrier was compromised after SAH, serum hemopexin level was lower, suggesting heme transfer to the circulation for peripheral CD91 scavenging. Conclusions— The CD91–heme–hemopexin scavenging system is important after SAH and merits further study as a potential prognostic marker and therapeutic target.
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