Braun U, Blatter M, Büchi R, Hässig M
Department of Farm Animals, University of Zurich, Switzerland.
Schweiz Arch Tierheilkd. 2012 Sep;154(9):381-8. doi: 10.1024/0036-7281/a000368.
Fifteen cows with milk fever were treated with 500ml of 40 % calcium borogluconate (group A) administered intravenously. Fifteen other cows with milk fever received the same treatment, supplemented with 500ml of 10 % sodium phosphate administered intravenously, and 80g calcium as calcium lactate and 70g inorganic phosphorus as sodium phosphate administered orally in drinking water. The cows were monitored and blood samples collected for 3 days to measure the concentrations of total and ionized calcium, inorganic phosphorus and magnesium and the activity of creatine kinase. The two groups did not differ significantly with respect to the course of the disease. In each group 14 cows were cured. A rapid and significant increase in serum calcium concentration from the hypo- to the hypercalcaemic range occurred in both groups within 10min of the start of treatment, followed by a slow and steady decrease to the hypocalcaemic range. Calcium lactate did not prevent the calcium concentration from returning to the hypocalcaemic range, and the calcium profiles of the two groups did not differ significantly. As expected, treatment had little effect on the concentration of inorganic phosphorus in group A. In group B, treatment caused a rapid increase in the concentration of inorganic phosphorus to a maximum 20min after the start of treatment. This was followed by a slow decrease in the phosphorus concentration to the normophosphataemic range. Our findings confirmed that combined intravenous and oral administration of sodium phosphate in cows with periparturient paresis attributable to hypocalcaemia and hypophosphataemia results in a rapid and sustained increase in serum phosphorus, but not in serum calcium concentration. This modified therapy did not improve the success rate of milk fever treatment and further studies are needed to improve treatment of periparturient paresis.
对15头患乳热症的奶牛静脉注射500毫升40%的葡萄糖酸钙(A组)进行治疗。另外15头患乳热症的奶牛接受相同治疗,并补充静脉注射500毫升10%的磷酸钠,以及通过饮水口服80克乳酸钙形式的钙和70克磷酸钠形式的无机磷。对这些奶牛进行了3天的监测,并采集血样以测量总钙、离子钙、无机磷和镁的浓度以及肌酸激酶的活性。两组在疾病进程方面无显著差异。每组中有14头奶牛治愈。两组在治疗开始后10分钟内血清钙浓度均迅速且显著地从低钙血症范围升至高钙血症范围,随后缓慢且稳定地降至低钙血症范围。乳酸钙并未阻止钙浓度回到低钙血症范围,且两组的钙变化曲线无显著差异。正如预期的那样,治疗对A组无机磷浓度影响很小。在B组中,治疗导致无机磷浓度在治疗开始后20分钟迅速升至最高值,随后磷浓度缓慢降至正常磷血症范围。我们的研究结果证实,对于因低钙血症和低磷血症导致的围产期轻瘫奶牛,静脉和口服联合给予磷酸钠会使血清磷迅速且持续升高,但不会使血清钙浓度升高。这种改良疗法并未提高乳热症治疗的成功率,需要进一步研究以改进围产期轻瘫的治疗方法。