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To determine the degree of damage occurring during preparation and storage of platelet concentrates, the percent release of B-thromboglobulin (BTG) and percent leakage of the cytosolic protein lactic dehydrogenase was determined sequentially from phlebotomy to the end of storage for 72 h at 20-24 degrees C. The effect of storage temperature, pH, and radiation was also evaluated. The results showed that during preparation of platelet concentrate a large degree of release was found after resuspension of the platelet button formed after the high-speed centrifugation. During storage the percent BTG release increased from 18.1 to 40.2% (p less than 0.05). The percent release seen during storage at 4 degrees C (72 h) was 19.2%, while that seen for platelets subjected to temperature cycling at 4-37 degrees C was 24.9%. Both of these values were significantly less (p less than 0.05) than that seen for concentrates stored at room temperature. A negative correlation between pH and BTG release was found (r = -0.64). Irradiation to 10,000 rad did not induce the release reaction or lactic dehydrogenase leakage. We conclude that the degree of in vitro platelet release is dependent on the preparative manipulations, and gentler protocols for preparation and storage of platelets should be investigated.

A 40-year-old man with jejunoileal bypass developed a syndrome of bizarre behavior, slurred speech, ataxic gait, and inappropriate affect, associated with a metabolic acidosis characterized by an increase in the anion gap. Serum L-lactate level was normal, but high-resolution proton nuclear magnetic resonance spectrums of the patient's serum showed a high concentration of lactate. A diagnosis of D-lactic acidosis was confirmed by a specific enzymatic assay for D-lactate. The D-lactic acidosis was cleared using antibiotic therapy, suggesting that D-lactate is produced from fermentation of ingested carbohydrate by colonic bacteria. Nuclear magnetic resonance spectroscopy is a rapid screening test for identifying organic acids in patients with unexplained acidosis. Neuropsychiatric symptoms in patients with short bowel syndrome may be associated with D-lactic acidosis.

We have recently seen two cases of propranolol poisoning. In both instances, plasma propranolol levels were elevated. Both patients experienced generalized seizures and had a transient intraventricular conduction defect on electrocardiogram. The literature on intoxication of propranolol and other beta-adrenoceptor blocking drugs suggests that the effects of massive propranolol intoxication observed in our patients can be explained on the basis of the pharmacologic properties of propranolol. Therapy consisted of gastric lavage and agents to antagonize the beta-adrenoceptor blockade effect. Both patients recovered.