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Biomedical subjects

W R Keatinge

Publications and source records attributed to W R Keatinge.

At least 73 records · Page 4Linked to original sources
PubMed1975

Depression of sublingual temperature by cold saliva.

Sublingual and oesophageal temperatures were compared at various air temperatures in 16 subjects. In warm air (25-44 degrees C) sublingual temperatures stabilized within plus or minus 0-45 degrees C of oesophageal temperatures, but in air at room temperature (18-24 degrees C) they were sometimes as much as 1-1 degrees C below and in cold air (5-10 degrees C) as much as 4-4 degrees C below oesophageal readings. The sublingual-oesophageal temperature difference in cold air was greatly reduced by keeping the face warm, but it was not reduced in two patients breathing through tracheostomies and thereby eliminating cold air flow from the nose and pharynx. Parotid saliva temperature was low and saliva flow high during exposure, and cold saliva seemed to be mainly responsible for the erratic depression of sublingual temperature in the cold. These results indicate hazards in the casual use of sublingual temperatures, and indicate that external heat may have to be supplied to enable them to give reliable clinical assessments of body temperature.

Adolescent↗
PubMed1975

Responses of inner and outer muscle of the sheep carotid artery to injury.

1. Direct injury to the smooth muscle of the sheep carotid artery in vivo caused large, persistent and sharply limited annular contraction, even with tetrodotoxin 10(-5)M present to block nerves. 2. Surcose gap records from artery strips showed that mechanical injury caused slow, prolonged depolarization of the smooth muscle that spread for a few millimetres in a circular direction in relation to the intact artery wall with an apparent space constant of 1-26--3.49 mm. In the longitudinal direction, no depolarization was recorded 1 mm from the site of injury. No spikes were recorded more than 1 mm in either direction from the site of injury except when procaine, which facilitates electrical activity in the smooth muscle, was present. 3. When responses of inner and outer muscle were recorded separately, injury caused comparable contraction of both parts. 4. Clotted blood caused large contractions of intact artery strips; it contracted inner much more than outer muscle. 5. The main factors in the intact vessel's response to injury therefore seem to be inner and outer muscles' direct response to injury, reinforced by spread of depolarization round the vessel wall, and inner muscle's response to vasoconstrictor agents released by clotting blood.

Animals↗
PubMed1975

Deep body temperature from aural canal with servo-controlled heating to outer ear.

A portable battery-powered device was used to measure temperature in the external aural canal by a thermistor while keeping the temperature of the outer ear, monitored by a second thermistor at the same level by servo-controlled heating. Aural canal temperature then always stabilized within 0.35 degrees C of esophageal in moving air at between 18 and 45 degrees C. It often did so in colder air, but stabilization was slow even after brief exposure to the cold air. Aural temperature then paralleled esophageal within 0.35 degrees C during rapid changes in deep body temperature while rectal temperature was seriously depressed in cold air. These conclusions were based on 30 experiments on 11 male and 7 female subjects.

Body Temperature↗
PubMed1974

Effects of procaine and lignocaine on electrical and mechanical activity of smooth muscle of sheep carotid arteries.

1 Procaine in concentrations up to 20 mM facilitated or induced electrical and mechanical activity in arterial smooth muscle, even with tetrodotoxin present.2 Procaine (up to 20 mM) caused relaxation when electrical activity was blocked by prior potassium depolarization.3 Procaine (1 mM) reduced mechanical responses to noradrenaline (1 muM) which were not accompanied by action potentials. It generally reduced mechanical responses to noradrenaline (1 mM) while increasing electrical activity induced by this.4 Lignocaine (1 mM) did not facilitate electrical activity significantly; it relaxed arteries in saline or potassium-rich solution and reduced mechanical responses to noradrenaline.5 High concentrations of procaine (at least 80 mM) or lignocaine (at least 20 mM) blocked electrical activity and caused contraction followed by relaxation and complete unresponsiveness.

Animals↗
PubMed1973

Elevation in set point for body temperature regulation after prolonged exercise.

1. In nine healthy men, after prolonged exercise (approximately 37 km walk and 2.5 km ascent and descent in 9 hr) deep body temperature at rest stabilized at a higher level than in the absence of previous exercise.2. The increase, approximately 0.36 degrees C, was recorded at both oral and rectal sites. It persisted while the subjects rested in warm and in cool surroundings, and disappeared about 11 hr after the end of exercise.3. The increase in body temperature after exercise was accompanied by a similar increase in the body temperature at which sweating started during body heating.4. After exercise the subjects' metabolic response to cold air (13.6 degrees C) was normal or increased in spite of the elevation in body temperature.5. Blood glucose concentration was never lower than 3.1 mM during these experiments.6. The temperature changes are most easily explained by mild pyrexia due to the release of endogenous pyrogen associated with minor tissue damage.

Adult↗
PubMed1973

Failure of thermoregulation in the cold during hypoglycaemia induced by exercise and ethanol.

1. After young men had exercised for approximately 2 hr at 70% maximum O(2) uptake, and taken 28 ml. ethanol by mouth, their mean blood glucose fell to 2.17 mM. It fell further to 1.77 mM during a 30 min exposure to air at 14.5 degrees C. Plasma lactate, glycerol, beta-hydroxybutyrate and free fatty acid concentrations increased.2. Rectal temperature fell to reach a mean level of 34.49 degrees C by the end of the cold exposure; oesophageal temperature fell to as low as 33.00 degrees C in one case.3. Virtually no increase in metabolic rate and no visible shivering occurred during the cold exposure.4. Administration of glucose (mean 60.4 g) prevented the falls in temperature, and restored metabolic response to the cold to the size found in control experiments without exercise or ethanol.5. Neither exercise without ethanol or ethanol without exercise significantly lowered the blood glucose or impaired the maintenance of body temperature in the cold.6. One obese subject showed almost as great a fall in blood glucose and depression of metabolic response to cold as the thinner men, but no fall in body temperature.

Adult↗
PubMed1972

Differences in sensitivity to vasoconstrictor drugs within the wall of the sheep carotid artery.

1. Controlled heat damage was used to separate the responses of the outer innervated smooth muscle from those of the inner nerve-free smooth muscle of the sheep carotid artery.2. Preparations of smooth muscle from the inner part of the media gave 50% maximal contractions in response to approximately 1/15 the concentration of noradrenaline needed to produce similar responses from outer smooth muscle. The difference in sensitivity was greater in the lower than the upper parts of the dose-response curves.3. Much of the difference in sensitivity was still seen in the presence of Desipramine and after chronic denervation, and so could not be attributed to uptake of noradrenaline by the nerve fibres in the outer smooth muscle; disappearance of the fibres after denervation was confirmed by fluorescence microscopy.4. Similar but generally smaller differences in sensitivity between inner and outer smooth muscle were seen with respect to histamine, angiotensin II and 5-hydroxytryptamine.5. Sympathetic denervation 10-14 days previously increased the sensitivity of outer strips to noradrenaline; it usually also increased their sensitivity to histamine, suggesting that the change largely represented non-specific denervation super-sensitivity.6. The high sensitivity of the inner smooth muscle is likely to be of value in enabling it to respond to the relatively low concentration of noradrenaline reaching it in life.

Angiotensin II↗
PubMed1972

Mechanical response with reversed electrical response to noradrenaline by Ca-deprived arterial smooth muscle.

1. When sheep carotid arteries had become electrically active after 30 min in Ca-free saline, noradrenaline 0.1 mM caused almost as much contraction as it did with Ca 1.25 mM present; it also caused slight electrical depolarization, usually with increased spike frequency, followed by electrical quiescence.2. In Ca-free saline with EDTA the arteries became profoundly depolarized, and their mechanical responses greatly reduced, within a few minutes. The mechanical responses to noradrenaline that remained were accompanied by electrical repolarization or, after longer periods in EDTA, by no electrical change.3. This residual mechanical responsiveness to noradrenaline, always tested at 36 degrees C, declined on average 26 times as rapidly during exposure to EDTA at 36 degrees C as at 5 degrees C and was not reduced by increasing the concentration of EDTA from 1.25 to 12.5 mM. This temperature-sensitivity was significantly too high to be explained by a diffusion-limited process.4. The results suggest that most of the tissue Ca responsible for contractility in simple Ca-free saline was either free in the extracellular space or in cellular stores that were discharged within a few minutes when free extracellular Ca was removed. They also indicate a small resistant Ca store which did not communicate with the exterior by diffusion, and part of which noradrenaline could utilize for contraction by means not dependent on depolarization conducted from the cell membrane.

Action Potentials↗
PubMed1972

Ca concentration and flux in Ca-deprived arteries.

1. Extracellular Ca and EDTA concentrations in arterial smooth muscle in Ca-free solutions with and without EDTA were estimated from (45)Ca and [(14)C]EDTA washout studies. Ca concentrations were calculated from the measured rate of (45)Ca washout at a given moment, combined with separate determinations of the coefficient of diffusion of Ca in the tissue, while EDTA concentrations were calculated by analysing an exponential phase of [(14)C]EDTA washout and checked by separate determinations of coefficient of diffusion of EDTA in the tissue.2. Extracellular Ca concentrations after 30 min in simple Ca-free saline at 36 degrees C was 0.049 mM at the centre of the tissue and averaged 0.033 mM throughout the tissue; these were well above the value of 0.005 mM-Ca that was found to be the threshold external level for contraction after tissue stores of Ca were removed.3. Extracellular EDTA concentration at the centre of the tissue reached 6.25 mM after 1.9 min in EDTA 12.5 mM at 36 degrees C or after 4.9 min at 5 degrees C. It reached 12.45 mM after 30 min at 5 degrees C, enough to keep free extracellular Ca at this point well below threshold even if all of the Ca in the tissue, determined as 0.42 mumole/g, were suddenly released on warming.4. Ca efflux increased greatly on warming after long periods in cold EDTA, and all measurable Ca left the tissue within 30 min in EDTA 12.5 mM at 36 degrees C although tissue Mg did not fall significantly during this time.5. Contractions elicited by noradrenaline in Ca-free saline, with or without EDTA present, were not associated with any increases in the rate of external loss of Ca greater than 0.001 mumole.g(-1).min(-1).6. Electronmicrographs showed numerous microvesicles that communicated with the extracellular space; also smooth endoplasmic reticulum among other structures that might have contained non-communicating Ca stores.7. The results provide evidence that large responses given by the arteries to noradrenaline in simple Ca-free saline were due to persisting extracellular Ca or to labile Ca stores dependent on this, while small responses obtained after long periods in cold EDTA depended on non-communicating Ca stores whose loss was too temperature-dependent to be limited by diffusion.

Animals↗