Whole-blood specimens were transported through an installed 485-meter pneumatic-tube system dedicated to blood transport. The system featured constant-speed, low-carrier-velocity travel (3.6 m/sec) with controlled deceleration prior to arrival at its destination. Inserts were designed with ample use of padding to minimize agitation during transport and landing. Serum potassium, hemoglobin, and lactate dehydrogenase activity and whole-blood pH, PCO2, and PO2 were not altered in freshly drawn blood transported in this system. Partial filling or heparinization of the specimen containers did not alter the results. When specimens were allowed to clot prior to pneumatic-tube transport, significantly higher levels of serum lactate dehydrogenase were obtained. This study demonstrates that transport of whole-blood specimens by pneumatic tube without damage to blood components is feasible.

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Phosphodiesterase I (EC 3.1.4.1) activity was detected in normal human blood serum. The enzyme is stable at laboratory temperature for three days, but is inactivated at pH <7. The pH for optimum activity increases with the substrate concentration (under the conditions used, from pH 9.0 to 10.2) and, conversely, the Km increases with pH and buffer concentration. The enzyme is inhibited by ethylenediaminetetraacetate but not by phosphate (0.1 mol/liter). We developed a simple quantitative method for its determination, based on hydrolysis of the p-nitrophenyl ester of thymidine 5'-monophosphate and subsequent measurement of the liberated p-nitrophenol at 400 nm in NaOH (0.1 mol/liter). Normal values (mean ± 2 SD) were determined to be 33 ± 6.4 U/liter. Preliminary studies indicate that phosphodiesterase I activity is greater than normal in serum of patients with necrotic changes in the liver or kidney or in cases of breast cancer, but not in that of patients with myocardial infarction, bone cancer, lung cancer, or chronic liver cirrhosis.

SODIUM NITROPI:tUSSmE was introduced for the elective induction of hypotension during general anaesthesia because of its apparent pharmacological efficacy. 1 Increased experience with this drug has led to the realization that its toxic potential is greater than previously believed. Several recently reported deaths following use of sodium nitroprusside have been attributed to the accumulation of the nitroprusside metabolite, cyanide. 2,s This has resulted in a series of revisions in the recommended dosage of sodium nitroprusside. Based on clinical experience and theoretical considerations, Davies, et al. "~ recommended that 3.5 mg/kg is the maximum dose of sodium nitroprusside that can be administered safely. Posner, et al.,4 in reporting their studies of nitroprusside-induced cyanide poisoning in baboons, further recommended that the sodium nitroprusside infusion rate be limited to 10/zg/kg/min and that the maximum dose not exceed 3 mg/kg. Most recently, Vesey, et al. '~ recommended that the total dose of sodium nitroprusside should not exceed 1.5 mg/kg during short-term infusions.In this paper the extent of cyanide accumulation and toxicity in patients receiving sodium nitroprusside infusions during intracranial surgery is reported. The doses of sodium nitroprusside employed in these studies fall within the range most recently recommended, that is, less than 1.5 mg/kg. PATIENTS AND METHODSEight female and five male patients (aged 13-66) undergoing surgery for repair of an intracranial aneurysm, were studied. Sodium nitroprusside was infused during the operation to produce hypotension as required by the surgeon. The infusion times and doses are listed in Table I. Five patients undergoing craniotomy without elective induction of hypotension were studied as a control group.Morphine and hyoscine were administered as premedication. All patients were operated on in a horizontal position. Anaesthesia was induced by thiopentone with tracheal intubation under pancuronium and was maintained using 65 per cent nitrous oxide in oxygen and morphine with intermittent pancuronium. A halothane