Bohman V R, Horn F P, Littledike E T, Hurst J G, Griffin D
J Anim Sci. 1983 Dec;57(6):1364-73. doi: 10.2527/jas1983.5761364x.
Thirty-two aged Hereford and Angus cows (avg 10.2 yr old) grazed mixed cereal (wheat and rye) pastures from December 6, 1979 to April 23, 1980 (138 d). On d 104 (March 19), five cows developed tetany. On the day of tetany, the mean plasma Ca of the cows with tetany was 4.1 mg/dl. Cows with tetany had plasma Mg concentrations of 1.7 mg/dl on the day of tetany, but 15 d before tetany and 6 d post-tetany, levels were lower (1.2 mg/dl). Cows with tetany had large increases in plasma parathyroid hormone (PHT) as well as vitamin 1, 25 dihydroxy D3 [1,25(OH)2D], plasma glucose, lactic acid and beta-hydroxybutyric acid. Plasma K of these cows followed a similar trend as plant K, except it was not as pronounced. Plasma inorganic P of these same cows was exceedingly low, less than 3 mg/dl several times, although the forage P did not indicate a P deficiency. Levels of plasma hydroxyproline in these cows indicated that bone resorption may have been low during most of the grazing season, even though levels of plasma hydroxyproline were initially high and high subsequent to tetany. High levels of plasma glucose and lactic acid were associated with the time of tetany. Apparently, cows developed inappetence around the time of tetany, as suggested by the high levels of plasma beta-hydroxybutyric acid. Cows with wheat pasture poisoning appeared to respond to the severe hypocalcemia with large increases in plasma 1,25(OH)2D. Plasma 1,25(OH)2D changes were similar to plasma hydroxyproline changes (and possible bone resorption rates) and seemed inversely proportional to plasma Ca and directly proportional to plasma PTH concentrations. Generally, cerebrospinal fluid (CSF) composition was not affected as much as plasma composition, except for the low levels of CSF Ca. These data indicate that a metabolic deficiency of Ca (hypocalcemia) was the cause of tetany.
1979年12月6日至1980年4月23日(共138天),32头赫里福德和安格斯老龄母牛(平均年龄10.2岁)在混播谷物(小麦和黑麦)的牧场上放牧。在第104天(3月19日),5头母牛出现了搐搦症。发生搐搦症当天,患搐搦症母牛的血浆钙平均为4.1毫克/分升。患搐搦症的母牛在搐搦症当天血浆镁浓度为1.7毫克/分升,但在搐搦症前15天和搐搦症后6天,血浆镁水平较低(1.2毫克/分升)。患搐搦症的母牛血浆甲状旁腺激素(PHT)以及维生素1,25 - 二羟维生素D3 [1,25(OH)2D]大幅增加,同时血浆葡萄糖、乳酸和β - 羟丁酸也增加。这些母牛的血浆钾与植物钾的变化趋势相似,只是不那么明显。这些母牛的血浆无机磷极低,有几次低于3毫克/分升,尽管牧草中的磷含量并未显示出磷缺乏。这些母牛血浆羟脯氨酸水平表明,在大部分放牧季节,骨吸收可能较低,尽管血浆羟脯氨酸水平最初较高且在搐搦症后也较高。血浆葡萄糖和乳酸水平升高与搐搦症发生时间相关。显然,从血浆β - 羟丁酸水平较高可以看出,母牛在搐搦症发生前后出现了食欲不振。患小麦牧场中毒的母牛似乎对严重低钙血症的反应是血浆1,25(OH)2D大幅增加。血浆1,25(OH)2D的变化与血浆羟脯氨酸的变化(以及可能的骨吸收率)相似,似乎与血浆钙呈反比,与血浆PTH浓度成正比。一般来说,脑脊液(CSF)成分受影响程度不如血浆成分,但脑脊液钙水平较低。这些数据表明,钙的代谢缺乏(低钙血症)是搐搦症的病因。