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Biomedical subjects

D Robertshaw

Publications and source records attributed to D Robertshaw.

At least 37 records · Page 2Linked to original sources

Cardiopulmonary response to acute altitude exposure: water loading and denitrogenation.

In order to determine if a positive water balance would impair cardiovascular and ventilatory adjustments during acute altitude exposure, six healthy male subjects were exposed to 4570 m for 2 h with and without water loading. No significant differences in any of the measured variables were observed between normal and overhydrated subjects. In order to determine if rapid ascent to altitude involves the formation of nitrogen bubbles which could impair gas exchange, 11 subjects were exposed to 4570 m with and without denitrogenation (by breathing 100% O2 prior to ascent) and 6 subjects were exposed to normobaric hypoxia (14% O2). Prior O2 breathing reduced the hyperventilatory and alkalotic responses to altitude, tachycardia did not develop, and systemic blood pressure fell, despite the fact that arterial desaturation was similar to that during the untreated altitude exposure. Reduced urine flow and increased urine osmolality were observed in two subjects at 4570 m, but these changes were not observed in the same subjects after O2 breathing. Breathing 14% O2 also produced the same degree of arterial desaturation but the hyperventilatory response was significantly greater than in the prior altitude exposures. Heart rate, blood pressure, and urine flow and osmolality were not altered and symptoms of altitude illness were minimal. Thus, neither of our hypotheses proved to be correct; however, we did observe a prolonged effect of O2 breathing on the hypoxic ventilatory response, and a potential effect of hypobaria on ventilation.

Acclimatization↗

A comparison of the Phadebas and Phadezym IgE paper immunosorbent test kits.

The Phadebas (isotype label) and Phadezym (enzyme label) paper immunosorbent test kits have been compared. Precision and ease of operation are shown to be comparable for both kits, and the advantages and disadvantages of each are similar. The enzymatic labelled kit seems to provide a suitable alternative for laboratories wishing to measure IgE but who do not have isotope-counting facilities available.

Humans↗

Plasma prolactin responses to acute changes in central blood volume in man.

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Acute effects of hypoxia on renal and endocrine function in normal humans.

The effects of hypoxia upon renal and endocrine function are unclear. Normal water-loaded subjects were exposed to hypoxia for 1 h (inspired PO2 = 74 Torr) in a decompression chamber (5,100 m, n = 8) or by breathing 10.5% oxygen at ambient pressure (n = 4). In four of eight subjects exposed to hypobaric hypoxia: urine flows (V) decreased (mean = 56%), urine osmolality increased (340%), plasma arginine vasopressin (AVP) increased (2,700%), plasma cortisol increased (256%), and mean blood pressure (BP) decreased (18%). V correlated inversely with AVP (r = 0.71, P less than 0.01) while AVP increases correlated with falls in mean BP (r = 0.72, P less than 0.05). Similar results were observed in the subjects exposed to normobaric hypoxia. Plasma aldosterone fell in the four subjects who maintained V on exposure to hypobaric hypoxia, but plasma renin activity did not change. In both groups prolactin levels were variable and solute and creatinine excretion were unchanged. No changes were observed in controls or in subjects exposed to hypobaria alone. Acute hypoxic exposure may produce significant hypotension with consequent increased AVP secretion resulting in diminished V.

Adolescent↗

Response of plasma prolactin to changes in ambient temperature and humidity in man.

The present study examined the relationship between plasma PRL and ambient temperature and relative humidity (RH) in man. Six normal men sat in an environmental room on four occasions. On each occasion, a thermoneutral control period at 27 C dry bulb (db)/16 C wer bulb (wb; 32% RH) was followed by a 90-min exposure to 27 C db/16 C wb, 13 C db/9 C wb, 45 C db/26 C wb, or 27 C db/26 C wb (92% RH) and a recovery period. Blood was drawn at 30-min intervals. Plasma PRL rose 53% (P < 0.05) in the heat and fell 37% (P < 0.05) in the cold in comparisons with control levels. No changes occurred during increased RH alone. Maximum PRL changes were associated with an increase in mean skin temperature of 3.0 C in the heat and a decrease of 4.3 C in the cold. Corresponding changes in auditory meatal temperature were +1.0 and -0.2 C, respectively. Plasma osmolality and serum Na+ and K+ levels did not change, except in the cold where serum K+ rose 0.6 meq/liter (P < 0.01). These data suggest an association between ambient temperature and plasma PRL in man which is not associated with changes in water and electrolyte status.

Adult↗

Hyperhidrosis and the sympatho-adrenal system.

Some disorders in which excessive sweating, hyperhidrosis, is a symptom are also characterized by increased sympatho-adrenal activity. Such disorders are hypotension, hypoglycemia, pheochromocytoma and hyperthyroidism. Sweat glands are controlled by a cholinergic innervation but can also be stimulated by adrenergic agents whose effects can be blocked by both alpha- and beta-receptor blocking drugs. An adrenergic innervation has also been demonstrated. There is evidence that the adrenergic component of sweating particularly secretion of the adrenal medulla, is responsible for the enhancement of sweating during exercise but not for the hyperhidrosis present in these disorders since sweating in these circumstances can be effectively blocked by cholinergic blocking compounds. Cutaneous vasoconstriction due to elevated plasma catecholamines reduces the rate of evaporation of sweat and allows sweat to accumulate on the skin. It is suggested that in the case of hypotension and insulin hypoglycemia sweating results from general sympathetic stimulation and that adrenal medullary hormones are not an essential component of the response. Hyperhidrosis in pheochromocytoma may be due to central activation of heat loss mechanisms resulting from the passage of plasma catecholamines across the blood-brain barrier combined with increased thermogenesis and cutaneous vasoconstriction. The hyperhidrosis of hyperthyroidism is probably due to increased thermogenesis.

Adrenal Gland Neoplasms↗

Influence of diet on leg uptake of glucose during heavy exercise.

Four young men each performed three treadmill walks to exhaustion at 70% of their respective O2 uptake maxima. Each walk followed 3 days consumption of either a normal mixed (M), high fat and protein (F-P), or high carbohydrate (CHO) diet. The fractional use of carbohydrates for energy during the initial 1/2-hr of work was significantly reduced following the F-P diet as compared with the M or CHO diets (P less than 0.005), averaging 38.2% (F-P), 69.9% (M), and 71.9 (CHO). Carbohydrates energy production was negatively correlated with blood levels of both free fatty acids ( r = -0.62, P less than 0.05) and beta-OH-butyrate (r = - 0.79, P less than 0.005). Work time to exhaustion was closely correlated with the fractional usage of carbohydrates for energy (r = 0.86, P less than 0.001). The femoral arteriovenous blood glucose difference was directly related to the pre-work dietary carbohydrate fraction, with the 30-min work means 0.25 mM (F-P), 0.34 mM (M), and 0.52 mM (CHO). Estimation of leg arteriovenous O2 difference indicated that leg uptake of blood-borne glucose provided approximately 23 +/- 10% (F-P), 30 +/- 8% (M), and 46 +/- 13% (CHO) of the legs' aerobic substrate during the first 30 min of work. These results provide further evidence for the shift from noncarbohydrate to carbohydrate energy sources during exercise as the carbohydrate fraction of the diet is elevated.

Adult↗

Effect of lipid solvents on cutaneous moisture loss.

Application of various lipid solvents and dimethyl sulphoxide to the skin of cattle, sheep, eland and African buffalo exposed to an air temperature of 20 degrees C caused an increase in cutaneous moisture loss. The effect did not occur after exposure to an air temperature of 40 degrees C or after adrenaline administration. Blockage of sweating by either bethanidine or phenoxybenzamine did not affect the response. Camel, donkey, dog and man showed no increase in cutaneous moisture loss after lipid solvent application to the skin. It is concluded that lipid solvents directly stimulate the secretory cells of the sweat glands of members of the family Bovidae and that this is not due to the release of transmitter substance nor to stimulation of adrenergic receptors, but is due to direct stimulation of the sweat glands themselves.

Animals↗

Studies on the nature of sweat gland 'fatigue' in the goat.

1. The nature of the ;fatigue' of sweating that occurs in the goat upon exposure to environmental conditions of 40 degrees C/26 degrees C (dry bulb/wet bulb) has been examined.2. Heat exposure activated all the sweat glands and the decrement in sweating which occurred was due to a decline in the amount of sweat produced by each gland.3. The decline in sweating activity was associated with a decrease in sweat gland volume and a thickening of the glandular wall. The restoration of sweat gland function took approximately 5-6 hr after removing the animal from the hot environment but the restoration of sweat gland volume took longer.4. The volume of sweat produced was greater than the decrease in sweat gland volume and it is concluded that ;fatigue' is due to the rate of expulsion exceeding the rate of sweat production.5. Repeated intravenous injections of adrenaline at 40 degrees C resulted in a decline in sweat output and reduced the normal glandular response to heat exposure.

Animals↗

A comparison of sweat gland activity in eight species of East African bovids.

1. The pattern and control of the sweat glands of eight species of wild bovids has been studied.2. Heat exposure resulted in changes in cutaneous moisture loss which showed considerable species variation. Duiker, Grant's gazelle, Thomson's gazelle and oryx all demonstrated periodic discharges of moisture on to the surface of the skin. Defassa waterbuck and eland exhibited discharges which were accompanied by a gradual rise in basal level. Buffalo showed an immediate large increase which was sustained during the period of heat exposure. Three wildebeest displayed small fluctuations whilst a fourth animal showed a step-wise increment in cutaneous moisture loss.3. The intravenous infusion of adrenaline into the buffalo and one wildebeest caused an increase in cutaneous moisture loss, the magnitude of which was directly related to the size of the dose administered. In three other wildebeest, and all other animals tested, a single injection of adrenaline was necessary to cause a discharge of moisture on to the surface of the skin. Noradrenaline was without effect.4. Heat-induced but not adrenaline-induced sweating was inhibited by the intravenous administration of an adrenergic neurone blocking agent, bethanidine.5. It is concluded that the sweat glands of the wild bovids studied are under adrenergic neurone control, in common with the domestic bovids previously studied, and that there is no correlation between the pattern of sweating and the phylogenetic position of the species.

Animals↗