The substance concentration of ionized calcium (c Ca2+) in blood, plasma or serum preanalytically may be affected by pH changes of the sample, calcium binding by heparin, and dilution by the anticoagulant solution. pH changes in whole blood can be minimized by anaerobic sampling to avoid loss of Co2, by measuring as soon as possible, or by storing the sample in iced water to avoid lactic acid formation. cCa 2+ and pH should be determined simultaneously. Plasma or serum: If centrifuged in a closed tube, and measured immediately, the pH of the sample will be close to the original value. If a delay has occurred between centrifugation and the measurement, causing substantial loss of Co2, equilibration of the sample with a gas mixture corresponding to pCO2= 5.3 kPa prior to the measurement is recommended. Conversion of the measured values to cCa 2+ (7.4) is only valid if the pH is in the range 7.2-7.6. Ca2+ binding by heparin can be minimized by using either of the following: (1) A final concentration of sodium or lithium heparinate of 15 IU/ml blood or less (2) Calcium titrated heparin with a final concentration of less than 50 IU/ml blood. Dilution effect can be avoided by use of dry heparin in capillaries or syringes. When heparin solutions are used, errors due to dilution or calcium binding can be reduced by using syringes with a heparin solution containing free calcium ions corresponding to the mean concentration of ionized calcium in normal plasma. Conditions for blood collection, storage, and transport to avoid preanalytical errors are described in this paper.

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1 In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication. 2 Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology. 3 After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) 1 the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration. 4 The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, β-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the β-glucuronidase activity showed a 10-fold increase. 5 Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6 Repair was almost complete 7 d following exposure.

Reperfusion of isolated rat hearts with Ca2+-containing medium, after a short Ca2+-free perfusion period, results in irreversible cell damage (calcium paradox). In this investigation the effect of hypothermia during (a) the Ca2+-free perfusion period and (b) the phase of reperfusion with Ca2+-containing medium was studied. Failure of the heart to recover mechanical activity, and creatine kinase release were used to define cell damage. Ca2+-free perfusion was performed at 37 degrees, 30 degrees, 25 degrees and 20 degrees C. Hypothermia during the Ca2+-free period was unable to prevent the calcium paradox. At 37 degrees C a Ca2+-free perfusion was perfusion period of 4 min was sufficient to lead to failure of the hearts to recover mechanical activity and to induce massive enzyme release upon reintroduction of Ca2+. At 20 degrees C the Ca2-free perfusion had to be continued for 25 min to induce failure to recover mechanical activity, and for 80 min to induce massive enzyme release upon reperfusion with Ca2+-containing medium. Hypothermia (10 degrees - 15 degrees C) during the reperfusion phase resulted in a moderate release of creatine kinase. Massive enzyme release occurred as soon as the temperature of the perfusate was raised above 25 degrees C.

1 Fluoride intoxication leads to sudden cardiac death which has been assumed to result from the accompanying severe hypocalcaemia. The aim of this study has been to investigate the suggestion that fluorapatite formation rather than CaF2 precipitation is responsible for this low calcium. 2 Measurements of free Ca2+ and F- ion concentrations in HEPES buffered solutions containing F-, Ca2+, and phosphate ions at different concentrations in the absence and presence of hydroxyapatite showed that the presence of hydroxyapatite enhanced the decrease of Ca2+ and F- concentration. 3 The ratio of Ca2+:F- clearance was 5:1 which is consistent with formation of fluorapatite. These results support the hypothesis that hydroxyapatite acts as a nucleation catalyst for fluorapatite formation and this process is responsible for the hypocalcaemia induced by fluoride intoxication. 4 The proposed mechanism explains also the metabolic acidosis which is frequently seen in cases of fluoride intoxication.