SUMMARY1. Slowly adapting cutaneous mechanoreceptors, in the cat and primates, have been studied by histological and neurophysiological methods.2. Each touch corpuscle is a dome-shaped elevation of the epidermis, whose deepest layer contains up to fifty specialized tactile cells.3. Nerve plates, enclosed by the tactile cell (Merkel cells), are connected to a single myelinated axon in the dense collagenous core of the corpuscle.4. The corpuscle generated > 1000 impulses/sec when excited by vertical surface pressure. The response was highly localized and showed a low mechanical threshold, the frequency being dependent upon' the velocity and amplitude of the displacement. There was a period of rapid adaptation before a sustained response which might continue for > 30 min.5. A quantitative analysis of the responses to excitation by displacements of differing amplitude, velocity and duration is included.6. The discharge of touch corpuscle units evoked by a mechanical stimulus was temperature-sensitive, and was enhanced by a fall in skin temperature.

Mortlock, R. P. (U.S. Army Chemical Corps, Frederick, Md.). Gluconate metabolism of Pasteurella pestis. J. Bacteriol. 84:53-59. 1962.-During a study of gluconate metabolism by a virulent strain of Pasteurella pestis, evidence was obtained for the presence of gluconokinase, 6-phosphogluconate dehydrogenase, transketolase, and 2-keto-3-deoxy-6-phosphogluconate dehydrase in cell-free extracts. A study of the products of 6-phosphogluconate degradation by extracts indicated that 6-phosphogluconate was metabolized by both the 6-phosphogluconate dehydrogenase-transketolase pathway and the Entner-Doudoroff pathway. No evidence could be obtained for the presence of an active glucose-6-phosphate dehydrogenase.

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1 In eight normotensive male volunteers indomethacin decreased both the peak urine flow rate and total sodium excreted within 1 h of an intravenous dose of frusemide.2 Resting effective renal plasma flow and glomerular filtration rate were unchanged by indomethacin, but the increase in both parameters after frusemide was inhibited.3 The early increase in plasma renin activity after frusemide was inhibited by indomethacin. 4 Indomethacin decreased urinary excretion of PGE by 80% and the increase after frusemide was abolished. 5 The urinary excretion of a metabolite of systemic PGI2was unaltered in the 40-60 min period following frusemide.6 The early haemodynamic effects of frusemide are likely to be prostaglandin mediated, but there was no evidence of any change in systemic PGI2 synthesis after frusemide.

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

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