Efficacy of Simulated, Slow Release Sodium Bicarbonate in Stabilizing Ruminal Milieu and Acid-Base Status in Lactating Dairy Cattle

Heart rate, arterial blood pressure and blood acid-base status were determined in 18 adult female mink (mean (±SEM)body weight 1052±34 g)during long-term anaesthesia with either controlled ventilation ( n=12) or spontaneous respiration ( n=6) Surgical anaesthesia was induced by intramuscular injection of ketamine hydrochloride (Ketaminol Vet®, 40.0±1.7mg/kg) and midazolam hydrochloride (Dormicum® 2.8±0.1 mg/kg) and maintained for at least 5 h by continuous intravenous infusion of this drug combination in 0.9% saline. For all animals, the mean rates of infusion of ketamine and midazolam were 48.4±1.6 and 1.61±0.12 mg/h, respectively. Following continuous infusion of the anaesthetics in isotonic saline, at a rate of 20 ml/h, a moderate 'dilution acidosis' developed, which could be corrected by replacement of part of the saline with sodium bicarbonate to a final concentration of approximately 25 mmol NaHCO3 per litre. However, when the animals were allowed to breathe spontaneously, an increase in heart rate and a combined respiratory and metabolic acidosis occurred, due to severe respiratory depression. Apart from these effects and a few cases of increased salivation, no adverse effects over time were observed on the arterial blood acid-base status and cardiovascular function of the animals during ketamine/midazolam anaesthesia. It is concluded that the procedure described for long-term anaesthesia in mink is convenient and safe for acute physiological experiments in this species, provided normal body temperature and pulmonary gas exchange is sufficiently maintained. Thus, the need for an adequately controlled artificial ventilation is strongly emphasized. Finally, a proposal for the composition of an intravenous solution, containing ketamine and midazolam hydrochloride, and sodium bicarbonate in saline, suitable for long-term anaesthesia in adult mink is presented.

Download Full-text

Evaluation of the potential protein-sparing effects of sodium bicarbonate when added to grass silage for growing steers

Canadian Journal of Animal Science ◽

10.4141/a99-029 ◽

2000 ◽

Vol 80 (1) ◽

pp. 131-136 ◽

Cited By ~ 1

Author(s):

V. Fellner ◽

L. E. Phillip ◽

H. Garino

Keyword(s):

Sodium Bicarbonate ◽

Feed Intake ◽

Fish Meal ◽

Nitrogen Retention ◽

Acid Base ◽

Urine Ph ◽

Grass Silage ◽

Voluntary Feed Intake ◽

Acid Base Status ◽

Supplemental Protein

Six Hereford-cross steers were used to determine whether or not the addition of sodium bicarbonate (NaHCO3) to grass silage (GS) would reduce the need for supplemental protein from fish meal (FM). Grass silage (31% DM; pH 4.8) was either unsupplemented or supplemented with FM (10% of silage DM); NaHCO3 was added at 0, 2, or 4% of silage DM. Supplementation with FM increased N retention (P < 0.01) but had no effects (P > 0.10) on feed intake or digestibility of organic matter (OM). Urinary N excretion decreased (P < 0.05) linearly with the addition of NaHCO3 but due to an increase in fecal N there was no significant effect (P > 0.10) of NaHCO3 on N balance. Urinary excretion of bicarbonate (HCO3) increased linearly (P < 0.01) with NaHCO3 addition, but there was no effect (P > 0.10) on urine pH or measures of blood acid-base status. Addition of NaHCO3 increased silage pH to 6.5 but had no effect (P > 0.10) on voluntary feed intake, or digestibility of OM and ADF. The results indicate that the addition of NaHCO3 to grass silage did not spare dietary protein but led to a shift in the partition of N between urine and feces. Key words: Steers, grass silage, sodium bicarbonate, nitrogen retention

Download Full-text

Effect of acid–base status on plasma phosphorus response to lactate

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-157 ◽

1984 ◽

Vol 62 (8) ◽

pp. 939-942 ◽

Cited By ~ 11

Author(s):

James R. Oster ◽

Helen C. Alpert ◽

Carlos A. Vaamonde

Keyword(s):

Lactic Acid ◽

Lactic Acidosis ◽

Sodium Bicarbonate ◽

Sodium Lactate ◽

Phosphorus Concentration ◽

Acid Anion ◽

Acid Base ◽

Phosphorus Response ◽

Acid Base Status ◽

Plasma Phosphorus

The mechanism(s) underlying the hyperphosphatemia of lactic acidosis is uncertain. We assessed the interacting influence of the acid anion and acid–base status on plasma phosphorus concentration by administering lactic acid alone, lactic acid plus sodium bicarbonate, sodium bicarbonate alone, and sodium lactate alone to four different groups of dogs. The findings of (1) no increase in plasma phosphorus concentration with lactic acid plus sodium bicarbonate versus a marked increment with lactic acid alone, and (2) no difference in the plama phosphorus response to sodium lactate versus sodium bicarbonate indicate that acidemia is necessary for the expression of lactate-induced hyperphosphatemia. The apparent greater propensity for marked hyperphosphatemia in lactic acidosis than in other types of metabolic acidosis remains unexplained, but conceivably might relate to differences in intracellular pH and in the rate of glycolysis.

Download Full-text