Experimentally-induced subclinical hyperammonemia in dairy goats

Two experiments were conducted to investigate metabolic responses to induce d subclinical (subacute) hyperammonemia in goats. In Experiment I Alpine we thers (n = 6, mean BW 44 +/- 1.3 kg) were fed one of two isonitrogenous (11 .2% CP on DM basis) and isoenergetic (70% TDN) diets that contained 0 (CON) or 10% (NPN) of the total dietary N as urea, and administered an oral urea load test (OULT 0, 100, 200, and 300 mg urea/kg BW) in a balanced incomple te block design. Live weight gain and DM intake were not affected (P > 0.10 ) by diet. Ruminal ammonia N was 30%, higher in CON wethers (P < 0.091), wh ereas whole blood ammonia N was 8% higher (P < 0.061) in NPN wethers. There were no consistent diet-related differences in ruminal pH or plasma urea N , glucose, and nonesterified fatty acid (NEFA) concentrations (P > 0.10). A dministration of the OULT increased (P < 0.0001) ruminal ammonia N, free, n onionized ammonia N, and pH, whole blood ammonia N, and plasma urea N, gluc ose, and NEFA concentrations. At 60 min after OULT, ruminal fluid total vol atile fatty acids (VFA) concentration was 16.5% greater in CON wethers (P < 0.011) as a result of greater levels (0.018 < P < 0.093) of acetate, propi onate, butyrate, and valerate. Ruminal ammonia N (P < 0.063), total VFA (P < 0.081), and plasma urea N (P < 0.0001) exhibited a diet X OULT interactio n. In Experiment 2, Alpine wethers (n = 8, mean BW 46 <plus/minus> 1.2 kg) were placed in metabolism crates and fed a diet that contained 10.5% CP and 69% TDN. Goats were fitted with chronic indwelling catheters in the right and left jugular veins. The experimental design consisted of a replicated 4 X 4 Latin square arrangement with four treatment days and four levels of c ontinuous intravenous infusions (via the left venous catheter) of ammonium chloride (NH4Cl)-saline solutions: 0 (SAL), 4.7 (LOAC), 9.5 (MEAC), and 14 mu mol (HIAC) NH4Cl/kg BW/min. The 240 min treatment infusions were precede d and followed by infusions of physiological saline of 60 and 240 min, resp ectively. Plasma ammonia N concentrations increased (P < 0.0001) during the infusion of NH4Cl solution, peaking at 65.3, 135.4, 210.5, and 330.7 mug/d l, for SAL, LOAC, MEAC, and HIAC, respectively, but returned to pre-infusio n levels within minutes following cessation of NH4Cl infusion. Plasma urea N (P < 0.074), glucose (P < 0.0087), and L-lactate (P < 0.012) responded si milarly to plasma ammonia N. Compared with the SAL group, infusion of NH4Cl increased total urine output (P < 0.0005) and urinary nitrogen output (P < 0.05) over a 12 h collection period. In goats, subclinical hyperammonemia could be experimentally induced using an OULT (100-300 mg urea/kg BW) and i ntravenous NH4Cl infusion (4.7-14 mu nol NH4Cl/kg BW) without reaching the clinical or lethal stages of ammonia toxicity. (C) 2001 Elsevier Science B. V. All rights reserved.