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 Na(2)EDT A have been conducted with the prior basic assumption that Na(2)EDTA-s pecific direct or indirect effects on the functions under study were n egligible. The present study aimed at providing unequivocal confirmati on Of such assumption by establishing the pattern of response of blood constituents to intravenous infusions of Na(2)EDTA in calves. Na(2)ED TA infusion in calves allowed effective chelation of blood Ca2+, leadi ng to a progressive hypocalcemia. Magnesium levels remained constant a nd concentrations of other ions Na+, K+, Pi, H+, HCO3-), although sign ificantly altered (P less than or equal to 0.0001), remained within th e normal range. Comparison of enzymes, urea, and creatinine changes pr ecluded renal, hepatic, or muscular parenchymatous damages as being th e cause of dysfunctions in the context of Na(2)EDTA-induced hypocalcem ia. It was not possible, however, to standardize the Na(2)EDTA infusio n characteristics (flow, volume) to obtain previsible Ca2+ decay in di fferent animals. Conversely, monitoring of systemic arterial pressure (SAP) offered a precious tool to estimate the degree of hypocalcemia r eached. Infusion rate must, therefore, be manipulated using careful on -line monitoring of SAP to obtain an experimental range of Ca2+ as lar ge as possible. It was concluded that physiological data collected dur ing Na(2)EDTA perfusions can be reliably discussed in terms of Ca2+ de pendence rather than in terms of either Na(2)EDTA toxicity, electrolyt es maladjustment, acid-base imbalance, impaired blood oxygenation, or hepatic, renal, myocardic, or skeletal muscle damages.