EFFECT OF FORAGE QUALITY AND MONENSIN ON THE RUMINAL FERMENTATION OF FISTULATED COWS FED CONTINUOUSLY AT A CONSTANT INTAKE

Citation
Rp. Lana et Jb. Russell, EFFECT OF FORAGE QUALITY AND MONENSIN ON THE RUMINAL FERMENTATION OF FISTULATED COWS FED CONTINUOUSLY AT A CONSTANT INTAKE, Journal of animal science, 75(1), 1997, pp. 224-229
Citations number
30
Categorie Soggetti
Agriculture Dairy & AnumalScience
Journal title
ISSN journal
00218812
Volume
75
Issue
1
Year of publication
1997
Pages
224 - 229
Database
ISI
SICI code
0021-8812(1997)75:1<224:EOFQAM>2.0.ZU;2-4
Abstract
A ruminal fermentation study was used to investigate the relationship between forage quality and monensin-dependent amino acid-sparing. Two fistulated cows were fed three combinations of chopped (2.5 to 5.0 cm in length) timothy and alfalfa hays (100:0, 50:50, and 0:100) and two levels of monensin (0 and 350 mg . cow(-1). d(-1)). The diets were off ered 12 times per day (9 kg of DM/d), and the rumen reached a steady-s tate, reducing animal and day variation. Alfalfa hay had 1.4 times mor e CP and 1.4 times less NDF than timothy hay, and the substitution of timothy with alfalfa increased (P < .05) ruminal ammonia. Monensin had no effect on total ruminal ammonia when timothy hay was present in th e diet, and it increased total ruminal ammonia with the 100% alfalfa d iet. Effects on ruminal ammonia were, however, confounded by monensin- dependent decreases in ruminal pH (P < .05). Dissociated ammonia, the species most likely to be absorbed from the rumen, declined when monen sin was added to the 100% timothy diet (P < .05). Monensin had no effe ct on dissociated ammonia if alfalfa was 50 or 100% of the forage, but it counter-acted alfalfa-dependent decreases in bacterial protein (P < .05). The idea that monensin could spare amino acids was supported b y the observation that monensin decreased (P < .001) the specific acti vity of deamination and increased bacterial protein at all combination s of alfalfa and timothy. Increases in bacterial protein could be expl ained by monensin-dependent increases in total VFA.