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Biomedical subjects

D Robertshaw

Publications and source records attributed to D Robertshaw.

48 records · Page 3Linked to original sources
PubMed1969

Sweat gland function of the donkey (Equus asinus).

1. Donkeys sweat on exposure to heat and in response to intravenous adrenaline infusion.2. Thermal sweating was abolished by the adrenergic-neurone blocking agent bethanidine but not by atropine.3. Sympathetic decentralization (by preganglionic sympathectomy) abolished thermal sweating but adreno-medullary denervation had no effect.4. Exercise resulted in sweating from both sympathetically innervated and decentralized skin and from the innervated skin of animals which had previously undergone adreno-medullary denervation.5. Insulin-induced hypoglycaemia resulted in sweating from sympathetically decentralized skin and from innervated skin in two out of four animals. Adreno-medullary denervation abolished the sweat gland response to insulin administration.6. Cold exposure inhibited the response of innervated sweat glands but not that of decentralized glands to adrenaline infusion.7. It was concluded that heat-induced and exercise-induced sweating of the donkey is controlled by adrenergic nerves; adreno-medullary secretion may contribute to sweating during exercise, and that cutaneous blood flow is important in the response of the glands to humoral stimulation.

Adrenal Medulla↗
PubMed1968

The pattern and control of sweating in the sheep and the goat.

1. The pattern and control of sweating in one breed of goat and six breeds of sheep have been studied.2. Heat exposure of both sheep and goats resulted in periodic discharges of moisture on to the surface of the skin of the shorn mid-side. The frequency of discharge showed considerable variation between individual animals, varying from less than 1/hr to 14/hr. Approximate counts of the number of active sweat glands suggested that the same glands were involved at each discharge.3. The amount of moisture produced at each discharge declined upon continued heat exposure. The rate of decline was independent of the frequency of discharge.4. Adreno-medullary denervation had no effect on the pattern of sweating in either the sheep or the goat.5. Intravenous adrenaline administration (5 mug/kg body wt.) caused the sweat glands to discharge, but noradrenaline had no effect at the same dose.6. Thermal sweating was inhibited by bethanidine and phenoxybenzamine but not by propranolol. Sweating induced by intravenous adrenaline administration was blocked by phenoxybenzamine but not by bethanidine or propranolol.7. It is concluded that sweating on the mid-side of the sheep and goat is controlled by an adrenergic mechanism, that secretion from the adrenal medulla under conditions of mild heat stress does not stimulate the glands and that sweating is mediated by adrenergic alpha-receptors.

Adrenal Medulla↗
PubMed1967

The mechanism of body temperature changes induced by intraventricular injections of adrenaline, noradrenaline and 5-hydroxytryptamine in the ox (Bos taurus).

1. Adrenaline, noradrenaline and 5-hydroxytryptamine (5-HT) were injected into the lateral ventricle of the ox. The effect of these drugs was measured on the respiratory rate, tidal volume, heat production, skin temperature of the ear, evaporative loss from the skin and the rectal temperature at 20 and 10 degrees C ambient temperature.2. Neither adrenaline (3 mg) nor noradrenaline (3 mg) had any effect on the temperature regulating mechanisms of the ox, except to produce vasoconstriction if vasodilatation was already present due to high ambient temperature or previous injection of 5-HT.3. Injection of 5-HT (5 mg) caused a rise in respiratory rate, a fall in tidal volume and heat production, elevation of ear skin temperature and skin evaporative loss and a decrease in rectal temperature. Sedation of the animals occurred.4. In its reaction to these monoamines the ox is similar to the goat, sheep and rabbit, but is unlike the cat and dog.5. It was concluded that neither adrenaline nor noradrenaline has a role in the central control of temperature regulation in the ox, but that 5-HT may be involved in the control of heat dissipation mechanisms.

Animals↗
PubMed1966

The effect of hyperthermia and localized heating of the anterior hypothalamus on the sympatho-adrenal system of the ox (Bos taurus).

1. Arterial plasma catecholamine concentrations, rectal temperatures and respiratory rates were measured in the unanaesthetized ox in a cool environment (15/11.5 degrees C dry bulb/wet bulb (D.B./W.B.) in a hot, dry environment (40/22 degrees C), in a hot, humid environment (40/39.1 degrees C) and during localized heating of the hypothalamus.2. There was no significant difference in the plasma catecholamine levels of animals exposed to a cool environment (15/11.5 degrees C) and to a hot, dry (40/22 degrees C) environment.3. When the animals became hyperthermic in the hot, humid environment, considerable increases in the plasma levels of adrenaline and smaller increases in noradrenaline concentration occurred.4. Bilateral adreno-medullary denervation abolished the changes in plasma catecholamine levels associated with hyperthermia.5. Localized heating of the anterior hypothalamus in either a cool or a warm environment did not result in any change in plasma catecholamine levels.6. It was concluded that the source of the increased levels of plasma catecholamines during hyperthermia was the adrenal medulla and that the stimulus for their release was a nervous one rather than direct chemical or thermal stimulation of the adrenal medulla. The cause of the increased sympatho-adrenal activity was not apparent, but neither thermal stimulation of cutaneous and hypothalamic receptors nor the associated changes in respiratory activity seemed to be implicated in the response.

Adrenal Glands↗
PubMedDate not supplied

Volume of extravascular lung fluid determined by blood ultrasound velocity and electrical impedance dilution.

A hypertonic sodium chloride bolus passing through the lung has a sound velocity transient that is biphasic when it reaches the carotid artery. This transient is compatible with water moving into the hypertonic bolus from the lung parenchyma, thereby leaving the lung parenchyma hypertonic. Subsequently, as the bolus leaves the lung vasculature, water passes from the blood into the tissue to return the lung tonicity to baseline, giving a moment when net movement is zero, an instant of osmotic equilibrium. Concurrent measurements of impedance track the sodium chloride transient. A theoretic basis for the calculation of extravascular lung water is derived from the water transferred to the blood, the amount of sodium chloride moved from blood to the lung, and the increase in blood osmolarity measured at the moment of equilibrium. Examples from measurements on sheep suggest that two intravenous injections of hypertonic and isotonic sodium chloride, with observations of sound velocity and electrical impedance in the systemic arterial circulation (which could also provide the cardiac output), provide a basis for calculation of lung permeability, water and salt movements, and extravascular lung water estimation.

Animals↗