Desmecht D J, Linden A S, Lekeux P M
Department of Pathology, Faculty of Veterinary Medicine, University of Liege, Sart Tilman, Belgium.
Vet Res Commun. 1996;20(1):47-60. doi: 10.1007/BF00346577.
A study was undertaken to provide further information on the ruminal, cardiorespiratory and hypothalamo-pituitary-adrenocortical (HPAC) physiological sequelae of hypocalcaemia in dairy calves. The functional picture observed in standing calves experiencing Na2EDTA-induced progressive hypocalcaemia showed a biphasic pattern. During the first phase (Ca2+ varying between 1.20 +/- 0.09 and 0.64 +/- 0.15 mmol/L, mean +/- SD), the animals became dull and lethargic, shifting their weight from one hind limb to the other, with cool extremities and hypersalivation. Their ventilation was slightly increased but their heart rate, thoracoabdominal pressure, pulmonary mechanics, haemoglobin and temperature remained constant. Conversely, their systemic arterial pressure (SAP) and the amplitude of their ruminal contractions (RCA) were severely decreased. During the second phase (Ca2+ < 0.64 +/- 0.15 mmol/L), there was restlessness, tachycardia, hypertension, polycythaemia and, finally, inability to stay upright. It is suggested that the diminished Ca2+ availability caused smooth-muscle and myocardial dysfunctions which could explain the RCA and SAP changes recorded during the first phase, whereas neural and/or humoral sympathetic discharge probably accounted for the reversal in SAP and heart rate when Ca2+ was decreased further. Serum cortisol increased regularly and remained significantly correlated with Ca2+ in each animal. Moreover, regression of delta cortisol/delta Ca2+ on delta Ca2+/delta Na2EDTA was significant (p < or = 0.001). It was concluded that mild asymptomatic hypocalcaemia severely impairs ruminal function, which will progressively worsen the Ca2+ deficit; that the inability to maintain posture in hypocalcaemia is not due to hypotension; and that the higher the HPAC response to hypocalcaemia, the higher the resistance to its effects. An asymptomatic periparturient cow with barely detectable ruminal activity may merit preventive calcium borogluconate therapy. Also, the physiological role of hypotension in explaining the clinical picture may be less important than other processes, such as neuromuscular failure. Finally, the present results imply a possible HPAC exhaustion in cows with periparturient paretic hypocalcaemia.
开展了一项研究，以获取更多关于奶牛犊低钙血症的瘤胃、心肺和下丘脑 - 垂体 - 肾上腺皮质（HPAC）生理后遗症的信息。在经历Na2EDTA诱导的渐进性低钙血症的站立犊牛中观察到的功能情况呈现双相模式。在第一阶段（Ca2 +在1.20±0.09至0.64±0.15 mmol/L之间变化，平均值±标准差），动物变得迟钝和嗜睡，将体重从一条后肢转移到另一条后肢，四肢发凉且流涎过多。它们的通气量略有增加，但心率、胸腹压力、肺力学、血红蛋白和体温保持恒定。相反，它们的体循环动脉压（SAP）和瘤胃收缩幅度（RCA）严重降低。在第二阶段（Ca2 + <0.64±0.15 mmol/L），出现躁动、心动过速、高血压、红细胞增多症，最终无法保持直立。提示Ca2 +可用性降低导致平滑肌和心肌功能障碍，这可以解释第一阶段记录的RCA和SAP变化，而当Ca2 +进一步降低时，神经和/或体液交感神经放电可能是SAP和心率逆转的原因。血清皮质醇定期升高，并且在每只动物中与Ca2 +保持显著相关。此外，δ皮质醇/δCa2 +对δCa2 + /δNa2EDTA的回归是显著的（p≤0.001）。得出的结论是，轻度无症状低钙血症严重损害瘤胃功能，这将逐渐加重Ca2 +缺乏；低钙血症时无法保持姿势不是由于低血压；并且HPAC对低钙血症的反应越高，对其影响的抵抗力越高。一头围产期无症状且瘤胃活动几乎检测不到的奶牛可能值得预防性使用葡萄糖酸钙硼治疗。此外，低血压在解释临床症状方面的生理作用可能不如其他过程重要
