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A prospective study was made of sequential changes in the metabolism of vitamin D and calcium in 19 allograft recipient during the first year after successful renal transplantation. All but one of the patients received cyclosporine A combined with corticosteroids and azathioprine as immunosuppressive therapy. Shortly after transplantation most patients showed transient hypocalcemia and hypophosphatemia. At the time of transplantation 17 of 19 patients had an elevated plasma intact parathyroid hormone (PTH) level, and at the close of follow-up one in four patients. In six other patients intact PTH was within the reference range, but high in relation to simultaneously measured serum ionized calcium. According, one year after transplantation less than half of the patients showed complete resolution of hyperparathyroidism. The change towards normal in the metabolism of vitamin D began within the first post-transplantation week irrespective of the onset of diuresis. One to two weeks after transplantation 1,25(OH)2D3 and 24,25(OH)2D3 reached the lower limit of normal range. In these renal allograft recipients who received cyclosporine A the long-term values of serum 1,25(OH)2D3 did not differ from those of normal subjects.

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The phospholipase A assay of Hoffmann et al based on the enzymatic photometric determination of the fatty acids liberated from soy-bean phospholipids was compared with the fluorometric assay of Thurén et al. where a synthetic pyrene-labelled substrate is used. Sera from patients with suspected pancreatitis or sepsis were studied. High values compared well while the Hoffmann method was not sensitive enough to detect slightly elevated values in sera from patients with suspected pancreatitis. The phospholipase A2 activities from enzymes purified from human duodenal juice, human sera from patients with sepsis and rat liver mitochondria were characterized in regard to activity towards several synthetic pyrene-labelled substrates, activation by Ca2+ and inhibition by Sr2+ and Mg2+. The enzyme from serum was distinctly different from both the pancreatic secretory and the mitochondrial ones, both in its substrate specificity pattern and in being most strongly inhibited by Mg2+.

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A recommendation concerning basic urine examinations and bacteriological cultures was published in 1983 in Finland including three clinical indication groups with different screening strategies. Close cooperation between laboratory experts and clinicians as well as much training in urine sediment cytology were essential before the new principle became widely accepted. Decreased workload in laboratories in clinically less significant cases was shown with the use of the full capacity and qualities of complete urinalysis when needed. Standardized test procedures combined with sediment staining improved the clinical efficiency of urine microscopy.

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In liver transplant patients low plasma protein, acid base abnormalities and high citrate concentrations in the blood affects the binding of ionized calcium. In the present study plasma ionized calcium as well as serum total plasma calcium were measured in ten patients undergoing liver transplantation because of end-stage liver failure. During the operation, ionized calcium fell to as low as 0.46 mmol/l although calcium chloride was administered frequently at doses of 10 mg/kg. Serum total calcium concentration values did not fall but rose well above normal at the end of the operation. The measuring of total serum calcium may thus be dangerously misleading in patients undergoing liver transplantation.

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Because it is difficult to verify the efficacy of hemorrhagic shock treatment, we compared subcutaneous O2 tension (PscO2) with liver oxygenation in efforts to correct shock in piglets with two different colloids, hydroxyethyl starch (HES-120) and dextran-70. Nineteen animals were bled to shock and the shed blood was retransfused in the control group. Liver oxygenation was measured directly by means of a silicone tube used as a tonometer, and indirectly by calculating liver O2 consumption (VO2). PscO2 was monitored with a needle electrode. The two colloid groups were compared by measuring plasma lactate, and the plasma colloid osmotic pressure (COPp). PscO2 followed closely the changes in liver tissue PO2 during the experiment; it seems to be a useful tool in estimating volume filling during the treatment of hemorrhagic shock. A wider variation was noted in calculated liver VO2 compared with hepatic venous PO2 or liver tissue PO2. Despite the fact that COPp increased to a higher level after the administration of dextran, HES proved to be at least as effective as dextran in restoring mean arterial pressure, cardiac output, liver oxygenation, PscO2, arterial pH, arterial plasma lactate, and liver lactate uptake.

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The possible myotoxic effect of bupivacaine in combination with tourniquet ischemia was evaluated in 11 patients who underwent surgery of an arm under intravenous regional anesthesia. Eleven patients with the same kind of surgery and tourniquet who had general anesthesia served as controls. Venous blood bupivacaine concentrations in the anesthetized arm were high at the end of tourniquet time (27.2-202 micrograms/m1) and varied from 2.3 to 12.3 micrograms/ml 10 min after tourniquet release. Changes in blood-gas tensions and plasma potassium and lactate concentrations before and just after tourniquet release correlated with the ischemia time. Changes in creatine phosphokinase, lactate dehydrogenase and aspartate aminotransferase activities, possible indices of loss of integrity of muscle cell membranes, varied considerably and did not correlate with the ischemia time. There were no significant differences between the two groups in any of the parameters. Electron microscopy revealed no evidence of muscle degeneration 24 hr after the use of tourniquet with either bupivacaine intravenous regional (n = 4) or general anesthesia (n = 3).

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