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Biomedical subjects

W R Keatinge

Publications and source records attributed to W R Keatinge.

At least 91 records · Page 5Linked to original sources
PubMed1969

Sudden failure of swimming in cold water.

To investigate the effect of cold water on swimming four men who declared themselves good swimmers were immersed fully clothed on separate days in water at 23.7 degrees and 4.7 degrees C. The time that they were able to swim in the cold water was much shorter than in the warm. The two shortest swims ended after 1.5 and 7.6 minutes, before rectal temperature fell, when the men suddenly floundered after developing respiratory distress with breathing rates of 56-60/min. The other cold swims, by the two fattest men, ended less abruptly with signs of general and peripheral hypothermia.It is concluded that swimming in cold water was stopped partly by respiratory reflexes in the thin men and hypothermia in the fat, and partly by the cold water's high viscosity. The longer swimming times of the fat men are attributed largely to their greater buoyancy enabling them to keep their heads above water during the early hyperventilation.The findings explain some reports of sudden death in cold water. It is clearly highly dangerous to attempt to swim short distances to shore without a life-jacket in water near 0 degrees C.

Adult↗
PubMed1968

Ionic requirements for arterial action potential.

1. Strips of smooth muscle from common carotid arteries of sheep were electrically quiescent in solution containing Na 148 mM and Ca 2.5 mM.2. When Ca was removed they became electrically active. Addition of low concentrations of Ca (0.025-0.075 mM) or Mg (0.025-0.750 mM) stopped their activity while ethylenediamine tetra-acetate (EDTA) (1.25 mM) accelerated it.3. Replacement of Na by Tris or choline stopped the activity in Ca-free solution. After partial replacement of Na electrical activity could be restored by lowering the resting potential but after complete replacement of Na it could not.4. In the presence of Ca (2.5 mM) small spikes could sometimes be induced after 20 min in Na-free Tris solution by lowering the resting potential by an increase in the external K concentration.5. The results indicate that the depolarizing current of action potentials in this smooth muscle was largely carried by Na, although a little may have been carried by Ca in Ca-containing solutions.6. The arteries in general resembled striated muscle rather than intestinal smooth muscle in these respects, but unlike striated muscle their action potentials were not stopped by tetrodotoxin.

Action Potentials↗
PubMed1968

Sodium flux and electrical activity of arterial smooth muscle.

1. The intracellular concentration and transmembrane flux of Na in smooth muscle cells of sheep carotid arteries were measured by identifying a fraction of tissue Na whose efflux was markedly sensitive to removal of external Ca. This allowed intracellular Na to be distinguished from extracellular bound Na exchanging with a similar time constant.2. When the arteries were in solution containing Na 148 mM and Ca 2.5 mM the mean intracellular Na concentration was 7.3 m-mole/kg cell water and the mean transmembrane flux of Na was 0.18 p-mole cm(-2) sec(-1), both values being much lower than reported values for intestinal smooth muscle.3. During electrical activity induced by Ca deprivation the influx of Na increased to 3.2 p-mole cm(-2) sec(-1); a 50% reduction in Na concentration stopped electrical activity and reduced influx by more than 50%, and the excess Na influx per action potential was calculated to be at least 1.0-1.5 p-mole cm(-2).4. Arteries in physiological saline (Ca 2.5 mM) contained 3.48 mumole Ca/g, much of which was bound extracellularly; in Ca-free saline 1.39 mumole Ca/g left the tissue within 3 min, showing that extracellular dissolved Ca diffused freely out of the tissue.5. The results provide further evidence that Na is the principal ion carrying the depolarizing current of action potentials in this smooth muscle.

Action Potentials↗
PubMed1966

Electrical and mechanical response of arteries to stimulation of sympathetic nerves.

1. When common carotid arteries of sheep were studied in vitro by the sucrose-gap method, application of acetylcholine or nicotine caused small irregular spikes of depolarization. The discharge was prevented by hexamethonium, Hydergine, phentolamine, or chronic denervation, indicating that it represented electrical activity of groups of smooth muscle cells induced by the stimulation of sympathetic nerve fibres.2. The size of spikes produced by acetylcholine or nicotine, together with counts of the total number of smooth muscle cells in cross-sections of the arterial strips, indicated that the larger groups of smooth muscle cells activated by one sympathetic nerve fibre contained approximately 1300 cells.3. Sections of arteries treated with hot formaldehyde vapour contained numerous fluorescent fibres which were intensified by previous injection of noradrenaline into the animal and were scanty or absent after chronic sympathetic denervation. They are therefore believed to be post-ganglionic sympathetic nerve fibres.4. Most of these fibres ran circularly in the outer (1/2)-(3/4) of the media. A few ran longitudinally in the adventitia. There were none in the inner (1/4)-(1/2) of the media.5. Electrical stimulation of the cervical sympathetic nerve of anaesthetized sheep caused large contractions of the common carotid artery of the same side, reducing its external diameter by 30-39%.

Acetylcholine↗