FHSA medical advisers: friends or foes?
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Biomedical subjects
Publications and source records attributed to J Bligh.
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The principal cause of the immediate transient elevation in ventilation (VE, L.min-1) and oxygen uptake (VO2, L.min-1), when a human subject is immersed in cold water is considered to be the stimulation of cutaneous cold receptors. The present study demonstrates that the initial VE and VO2 responses are comprised of a thermogenic and a hydrostatic component. The peak values in VE reached (mean +/- SD) 66.8 +/- 22.3, 53.9 +/- 38.1, 32.2 +/- 15.4, 22.5 +/- 3.6, 19.5 +/- 4.6 L.min-1 during the first minute of immersion in 10 degrees, 15 degrees, 20 degrees, 28 degrees and 40 degrees C water, respectively. Similarly, peaks (mean +/- SD) in VO2 of 1.22 +/- 0.25, 1.01 +/- 0.32, 0.98 +/- 0.39, 0.81 +/- 0.09, and 0.78 +/- 0.26 L.O2.min-1, were reached when subjects were immersed in 10 degrees, 15 degrees, 20 degrees, 28 degrees, and 40 degrees C water. It is concluded that the observed increases in VO2 during the first minute of immersion are partly due to the increased hydrostatic pressure causing a shift of venous blood towards the thoracic region, and a transient increase in the uptake of oxygen into the blood.
To detect shifts in the threshold core temperature (Tc) for sweating caused by particular nonthermal stresses, it is necessary to stabilize or standardize all other environmental and physiological variables which cause such shifts. It is, however, difficult to cause progressive changes in Tc without also causing changes in skin temperature (Tsk). This study compares the technique of body warming by immersion in water at 40 degrees C, and subsequent body cooling in water at 28 degrees C, to determine the core threshold for sweating, with one by which Tc was raised by cycling exercise in air at 20 degrees C, and then lowered by immersion in water at 28 degrees C. The first of these procedures involved considerable shifts in Tsk upon immersion in water at 40 degrees C, and again upon transfer to water at 28 degrees C; the second procedure caused only small changes in Tsk. The onset of sweating at a lower esophageal temperature (Tes) during immersion in water at 40 degrees C (36.9 +/- 0.1 degrees C) than during exercise (37.4 +/- 0.3 degree C) is attributed to the high Tsk since Tes was then unchanged. Likewise, the rapid decline in the sweat rate during immersion at 28 degrees C had the same time course to extinction after the pretreatments. This related more to the Tsk, which was common, than to the levels or rates of change of Tes, which both differed between techniques. Tes fell most rapidly, and thus sweating was extinguished at a lower Tes, following 40 degrees C immersion than following exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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Of the amino acids that affect the activity of central neurons, aspartate and glutamate (which exert generally excitatory influences) and glycine, taurine, and gamma-aminobutyric acid (GABA) (which generally exert inhibitory influences) are the strongest neurotransmitter candidates. As with other putative transmitter substances, their effects on body temperature when injected into the cerebral ventricles or the preoptic hypothalamus tend to vary within and between species. These effects are uninterpretable without accompanying information regarding effector activity changes and the influences of dose and ambient temperature. Observations necessary for analysis of apparent action have been made in studies of the effects of intracerebroventricular injections of these amino acids into sheep. Aspartate and glutamate have similar excitatory effects on the neural pathways that activate both heat production and heat loss effectors. Glycine appears to be without effect.
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1. Changes in cardiovascular and renal functions following injection of noradrenaline, 5-hydroxytryptamine and carbachol into one lateral cerebral ventricle were investigated in conscious sheep at ambient air temperatures of 0 and 40 degrees C. The dose rates used were known to produce predictable changes in thermoregulation in sheep. 2. The changes in body temperature, respiratory frequency and shivering caused by the intracerebroventricular (I.C.V.) injections of noradrenaline, 5-hydroxytryptamine and carbachol were as reported previously. 3. The cardiovascular and renal responses of the sheep at both high and low ambient temperatures were consistent for each transmitter indicating that these activities had no major dependence on the type of thermoregulatory response. 4. I.C.V. injection of noradrenaline increased heart rate and decreased pulse pressure but caused no change in mean arterial blood pressure (B.P.). Urine flow rate, sodium clearance, potassium clearance and osmolal clearance were decreased whereas solute-free water reabsorption was unaltered. 5. I.C.V. injection of 5-hydroxytryptamine caused no significant alterations in either cardiovascular or renal function. 6. I.C.V. injection of carbachol increased systolic and diastolic B.P., heart rate and haematocrit. Sodium, potassium and osmolal clearances were increased after administration of carbachol. 7. The changes in renal function after noradrenaline and carbachol injection could be explained by the concurrent changes in cardiovascular function.
Local hyperthermia is relatively safe, while whole-body hyperthermia is potentially dangerous because the therapeutically effective elevation of body temperature is close to the tolerable limit to hyperthermia beyond which permanent damage may be caused. Here consideration is given to the most reliable index of body temperature during hyperthermia and the techniques for raising body temperature. The possibility of effecting local brain cooling and thereby increasing the margin of safety during whole-body hyperthermia is also considered.
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L-Aspartic acid was injected into a lateral cerebral ventricle of the sheep at ambient temperatures between 0 degrees and 40 degrees C. Doses of 100 or 500 nmoles-kg-1 caused a rise in heat production and/or a decrease in heat loss; rectal temperature rose. Atropine sulphate attenuated or prevented these effects.
L-glutamic acid injected in doses of 200--1000 n moles . kg-1 into the cerebral ventricles of sheep had dose-dependent thermoregulatory effects: an increase in heat production and/or a decrease in respiratory frequency, and a rise in rectal temperature. A dose of 800 nmoles . kg-1 had effects comparable with those of a similar injection of 3 nmoles . kg-1 carbamylcholine.
The thermoregulatory effects of dopamine (DA), given by intracerebroventricular (i.c.v.) injection to sheep, have been examined and compared with those of i.c.v. noradrenaline (NA). At ambient temperatures (Ta) of 20 degrees and 30 degrees C both DA (200 nmol . kg-1) and NA (100 nmol . kg-1) induced constriction of the ear vessels, a decrease in respiratory frequency and an increase in rectal temperature (Tr). At Ta of 10 degrees and 0 degrees C both substances caused a decrease in heat production and a fall in Tr. The DA receptor blocker spiroperone (30 nmol . kg-1, i.c.v.), which itself had a vasodilatatory effect at 20 degrees C Ta, blocked the peripheral vasoconstriction and slightly attenuated the rise in Tr normally caused by i.c.v. DA or NA at this Ta, but did not eliminate the suppression of respiratory frequency. During i.c.v. infusion, at 20 degrees C Ta, with the DA-beta-hydroxylase inhibitor FLA-63, the effect of i.c.v. DA on Tr was attenuated, while that of NA was enhanced. These results suggest that in sheep central thermoregulatory system there are DA receptors which stimulate the pathway that controls peripheral vasomotor tone. The inhibitory effect of NA and DA on heat production and evaporative heat loss is probably mediated by noradrenergic receptors, which can also be activated by DA both directly and after its conversion to NA.
The morphology and lipid content of adipose tissue from sheep subjected to cold acclimatisation were examined. In two sheep the perirenal adipose tissue contained virtually no triglyceride (less than 2 mg/100 mg wet tissue) and the appearance on electron microscopy was typical of that of a depleted white fat cell. The morphological, chemical and physiological evidence indicates that, in the sheep, white adipose tissue does not revert to brown adipose tissue during depletion resulting from cold acclimatisation.
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