Potassium and the Hypothermic Heart

Mavor, G. E.; Harder, René; McEvoy, Richard K.; McCoord, Augusta B.; Mahoney, Earle B.

doi:10.1152/ajplegacy.1956.185.3.515

Cited by 14 publications

(3 citation statements)

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“…The low plasma levels of potassium ob¬ served during hypothermia in the control animals are consistent with the observations of Swan 7 and Mavor 8 …”

Section: Commentsupporting

confidence: 89%

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Aminoacetic Acid (Glycine) as an Antifibrillary Agent in Hypothermia

Beavers¹,

Covino²

1957

Arch Surg

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“…The low plasma levels of potassium ob¬ served during hypothermia in the control animals are consistent with the observations of Swan 7 and Mavor 8 …”

Section: Commentsupporting

confidence: 89%

“…8 and Melville and Mazurkiewicz 10 that ventricular fibrillation occurred in the normo¬ thermic isolated rabbit heart perfused with solutions containing subnormal concentra¬ tions of potassium. Thus, the fall in plasma potassium during general body cooling may¬ be one of the factors predisposing to ven¬ tricular fibrillation.…”

Section: And Their Associatesmentioning

confidence: 97%

Aminoacetic Acid (Glycine) as an Antifibrillary Agent in Hypothermia

Beavers¹,

Covino²

1957

Arch Surg

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“…Since changes in the level of blood potassium may be responsible for some of the effects of hypothermia (Elliot & Crismon, 1947;Mavor, Harder, McEvoy, McCoord & Mahoney, 1956) the effects of injecting small amounts of Locke's solution with varying potassium content was investigated in one experiment. The solution was injected through a polythene catheter into the aortic arch during synchronous vagal stimulation.…”

Section: Resultsmentioning

confidence: 99%

The effect of temperature on facilitation in the vagus

Mainwood¹

1959

The Journal of Physiology

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Previous investigations have shown that slowing of the heart in the rat increases suddenly when a critical frequency of vagal stimulation is reached (Mainwood, 1957). Similar frequency-effect curves have been observed in vasomotor responses to sympathetic stimulation. These are attributed to the building up of a steady-state level of transmitter substance at the nerve ending when its rate of liberation from the terminals just exceeds its rate of elimination (Folkow, 1952).If there is a similar effect at the vagal terminals, the critical stimulation frequency should depend upon the rate of elimination of liberated acetylcholine from the pace-maker region. The elimination of acetylcholine may be through either hydrolysis by cholinesterase or simple diffusion (Eccles & Jaeger, 1958). Each of these proceses has a well defined temperature coefficient and so the relation between body temperature and the critical frequency may be calculated in each case. Such predictions can only hold true if the amount of acetylcholine liberated from the terminals is not influenced by body temperature.In the case of preganglionic sympathetic terminals it has been shown that there is a fall in acetylcholine output as the temperature is lowered (Brown, 1954) though this appears to be very small over the temperature range considered here at low stimulation frequencies (Kostial & Vouk, 1956). Thus one may expect that the influence of temperature on the critical frequency, as calculated from the change in rate of acetylcholine elimination, would be a little greater than the observed effect.Contrary to expectation the observed effect of body temperature on vagal slowing was found to be much greater than was predicted (Mainwood, 1957). One possible explanation was that each vagal impulse leaves a secondary effect on the pace-maker itself which decays at a slower rate than the acetylcholine. Other observations seemed to support this possibility. 14 PHYSIO. CxLVI

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