Experimental production of hypocalcemia by EDTA infusion in calves: a critical appraisal assessed from the profile of blood chemicals and enzymes.

Physiological studies of the effects of Ca2+ withdrawal using Na2EDTA have been conducted with the prior basic assumption that Na2EDTA-specific direct or indirect effects on the functions under study were negligible. The present study aimed at providing unequivocal confirmation of such assumption by establishing the pattern of response of blood constituents to intravenous infusions of Na2EDTA in calves. Na2EDTA infusion in calves allowed effective chelation of blood Ca2+, leading to a progressive hypocalcemia. Magnesium levels remained constant and concentrations of other ions (Na+, K+, Pi, H+, HCO3-), although significantly altered (P < or = 0.0001), remained within the normal range. Comparison of enzymes, urea, and creatinine changes precluded renal, hepatic, or muscular parenchymatous damages as being the cause of dysfunctions in the context of Na2EDTA-induced hypocalcemia. It was not possible, however, to standardize the Na2EDTA infusion characteristics (flow, volume) to obtain previsible Ca2+ decay in different animals. Conversely, monitoring of systemic arterial pressure (SAP) offered a precious tool to estimate the degree of hypocalcemia reached. Infusion rate must, therefore, be manipulated using careful on-line monitoring of SAP to obtain an experimental range of Ca2+ as large as possible. It was concluded that physiological data collected during Na2EDTA perfusions can be reliably discussed in terms of Ca2+ dependence rather than in terms of either Na2EDTA toxicity, electrolytes maladjustment, acid-base imbalance, impaired blood oxygenation, or hepatic, renal, myocardic, or skeletal muscle damages.