The loss of potassium from frog nerves in anoxia and other conditions.
20 Jan 1950-The Journal of General Physiology (The Rockefeller University Press)-Vol. 33, Iss: 3, pp 195-203
TL;DR: There was some evidence that nerves tended to regain potassium if they were returned to oxygen after a period of anoxia, and addition of acetylcholine to the solution increases the loss of potassium.
Abstract: 1. Frog nerves immersed in Ringer's solution lose on the average 23 per cent more potassium if the solution is equilibrated with pure nitrogen than if equilibrated with oxygen.
2. Tying off the ends of the nerves during immersion increased rather than diminished the loss of potassium.
3. There was some evidence that nerves tended to regain potassium if they were returned to oxygen after a period of anoxia.
4. Addition of acetylcholine to the solution increases the loss of potassium.
5. Equilibration of the solution and nerves with 20 per cent CO2 in O2 increases the loss of K from nerves in Ringer's solution but decreases it in frog blood.
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01 Jan 1960
Abstract: More than thirty years have passed since the appearance of Hober’s treatise1 on the alkali metal ions in this handbook. Since then the literature on the biological functions and effects of these ions has encreased enormously. The mere bulk of material has forced the authors to abandon the vain attempt to cover all the papers with a bearing on the field. Instead they have tried to choose from the abundance primarily what they feel can be organized into a coherent picture of the biological role of the alkali metal ions.
143 citations
01 Jan 1959
TL;DR: More than thirty years have passed since the appearance of Hober's treatise on the alkali metal ions in this handbook as discussed by the authors, and the literature on the biological functions and effects of these ions has encreased enormously.
Abstract: More than thirty years have passed since the appearance of Hober’s treatise1 on the alkali metal ions in this handbook. Since then the literature on the biological functions and effects of these ions has encreased enormously. The mere bulk of material has forced the authors to abandon the vain attempt to cover all the papers with a bearing on the field. Instead they have tried to choose from the abundance primarily what they feel can be organized into a coherent picture of the biological role of the alkali metal ions.
110 citations
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87 citations
TL;DR: The experiments described in this paper were designed to study the effects of hypoxia on the excitability of isolated peripheral nerve and found that vibration perception, motor nerve conduction velocity, and tactile sensation are relatively unaffected by ischaemia in the diabetic subjects, in contrast to that observed in the normal subjects.
Abstract: Steiness (1959) observed that diabetic subjects whose lower limbs were rendered ischaemic with a pneumatic cuff around the thigh were able to perceive a vibratory stimulus applied to the toes for longer periods than non-diabetics. In some diabetic subjects the threshold remained almost unchanged during a 30 minute period of experimental ischaemia. Steiness (1961a, b) showed that it was not possible to increase the time of perception of the stimulus in normal subjects by inducing hyperglycaemia in them, that the abnormal condition in diabetics was reversible, and that it bore some relationship to the state of control of the diabetes. This resistance of the peripheral nerves of diabetic subjects to ischaemia has been confirmed by Castaigne, Cathala, Dry, and Mastropaolo (1966). Gregersen (1968) studied the effects of limb ischaemia on vibration perception threshold, tactile sensation, pain, heat-induced pain sensation, and motor nerve conduction velocity in healthy and diabetic subjects. His results show that vibration perception, motor nerve conduction velocity, and tactile sensation are relativelyunaffected by ischaemia in the diabetic subjects, in contrast to that observed in the normal subjects. The sensations of heat and heat-induced pain, however, remained unchanged during the ischaemia in the diabetics as well as in the control group. Seneviratne and Peiris (1968b) have shown that the evoked sensory nerve action potential of the median nerve of diabetic subjects is resistant to ischaemia produced by vascular occlusion of the upper limb by pneumatic cuff compression. These evoked potentials, in contrast to those of normal subjects, showed a relative constancy of their amplitudes, durations, and latencies during a 30 minute period of complete vascular occlusion. These changes could be demonstrated in all the diabetic subjects studied irrespective of whether or not they had evidence of a neuropathy. None of their diabetic subjects experienced ischaemic or post-ischaemic paraesthesiae, which were a very constant feature of the early ischaemic and postischaemic phases in the control group. It was postulated that these differences in the behaviour of the nerves of diabetic subjects may have been due to the fact that the metabolites released from the tissues of the diabetic during vascular occlusion were essentially different from those produced by the tissues of normal subjects under similar conditions. Alternatively, there may have been no essential difference between the metabolites produced by the normal and diabetic subjects, the relative resistance of the diabetic nerve being due to its ability to maintain its activity under ischaemic conditions. The experiments described in this paper were designed to study the effects of hypoxia on the excitability of isolated peripheral nerve.
87 citations
TL;DR: Observations concerning the threshold for cerebral venous oxygen tension in man support the notion that anoxic symptoms and signs are due to failure of the mechanism for active sodium transport in brain, which is apparently dependent on cerebral energy metabolism.
Abstract: THE OXYGEN tension (PO,) of brain tissue obeys the law of supply and demand. Supply is influenced by arterial oxygen content, cerebral blood flow, and cerebral blood pH (by the Bohr effect), and demand depends soleIy on the functional state of brain metabolism. If the oxygen tension of the blood is reduced (for example, by anoxic anoxia of nitrogen inhalation), presumably a value will be reached below which capillary PO, is insufficient to maintain oxygen diffusion into brain tissue; functional impairment with signs of cerebral anoxia will result. Such thresholds for oxygen tension have been determined for brain preparations; below these cerebral oxygen consumption became decreased and thresholds for cerebral venous PO,-at which electroencephalographic slowing and decreased cerebral metabolism occurred-have also been estimated in animals by several investigators.1-5 There is as yet no comparable data available in man except a few determinations of the levels of oxygen saturation in the internal jugular vein at which loss of consciousness occurred during nitrogen breathing and postural hypotension.6 It has been reported in animals that when tissue or capillary venous pOz fell below threshold during induced anoxia the extracellular sodium ions of the brain decreased and there was an increase of extracellular potassium. This ionic change was said to correlate with electroencephalographic slowing.5,7rs Such data support the notion that anoxic symptoms and signs are due to failure of the mechanism for active sodium transport in brain, which is apparently dependent on cerebral energy metabolism. The present study reports for the first time in man similar observations concerning the threshold for cerebral venous oxygen tension
83 citations