SUMMARY The effect on the human lens of prolonged hyperbaric oxygen therapy is reported. Eye examinations were given to 25 patients before, during, and after a series of 150 or more exposures to hyperbaric oxygen. All patients changed refraction in the direction of myopia during treatment. Fifteen of the patients had clear lens nuclei before treatment. Seven of these developed a nuclear cataract with reduced visual acuity during treatment. Reversible lens myopia has previously been noticed as a side effect of exposure to hyperbaric oxygen, but the cataractogenic effect in man has not been reported by other workers. This report strongly supports the theory of an oxidative damage to the lens proteins as a cause of nuclear cataract.
BARR, P.-0. Percutaneous puncture of the radial artery with a niultipurpose TeJon catheter for indwelling use. Acta physiol. scand. 196 1. 51. 343-347. -A Teflon catheter assembly is described, which was designed for percutaneous insertion and indwelling use in the radial artery, and in other superficial blood vessels with calibers of a similar order of magnitude. The advantages of the instrument, which may also be used for percutaneous puncture of other superficial tissues and organs, are reported and discussed, especially with regard to the preferential choice of the radial artery for arterial punctures.
Changes in arterial gas levels in response to constant‐load, dynamic exercise (400 and 700 kpm/min for 6 min) were studied in 8 healthy male subjects by continuous analyses of arterial pH and O2 saturation. During pre‐exercise rest, spontaneous time‐variations in these variables occurred in all individuals at half‐minute intervals or longer. These cyclic fluctuations, which were quite marked in some individuals, probably in part explain differences reported as to the magnitude and direction of changes occurring in response to exercise. To eliminate most of such influences on the observed deviations following the onset of exercise, the time‐averages over the preceding 3 min were chosen as reference levels. Both pH and O2 saturation, when referred to the blood passing through the left heart, remained essentially constant during the first 20–30 sec following the transitions from rest to exercise and from exercise to rest at both work loads. The arterial [H+] rose to reach a plateau during the 3rd and 4th min (average decrease in pH = 0.022 at 400 kpm/min and 0.036 at 700 kpm/min). Calculated arterial PO2, after a transient drop during early exercise, was increased by about 5 mm Hg during the last 3 min of exercise at both loads. About 30 sec after cessation of work, arterial [H+] fell rapidly towards pre‐exercise level, whereas arterial PO2 rose markedly to reach its maximal deviation after about 1.5 min. The shift towards acidosis during exercise was roughly proportional to the relative intensity of work, whereas no such relationship was observed on the part of the concomitant increment in arterial PO2.
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