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Biomedical subjects

D A Powis

Publications and source records attributed to D A Powis.

66 records · Page 4Linked to original sources
PubMed1977

Responses of the cardiovascular system of the rat to noradrenaline infusions and their modification by adrenoceptor blocking agents.

1 The effects of noradrenaline upon the cardiovascular system of the rat, anaesthetized with pentobarbitone, have been investigated.2 Noradrenaline produces a dose-dependent increase in mean arterial blood pressure (MABP) which is due entirely to an increase in cardiac output; total peripheral vascular resistance (TPR) remains unchanged.3 Following beta-adrenoceptor blockade the pressor response to infused noradrenaline is enhanced and is now due mainly to an increase in TPR; the increment in cardiac output is reduced.4 After alpha-adrenoceptor blockade the pressor response is greatly reduced; the residual increase in MABP is due solely to an increase in cardiac output.5 After ganglion blockade resting cardiac output and TPR both fall, resulting in a reduction in MABP. The pressor response to noradrenaline is enhanced and is now due to increases in both TPR and in cardiac output.6 The cardiovascular response of the anaesthetized rat to noradrenaline can be explained in terms of classical alpha- and beta-adrenoceptor stimulation by the amine; the unusual form of the response may be due to an effective predominance of beta-adrenoceptor-mediated effects in this species.7 It is suggested that the failure of exogenous noradrenaline to produce a rise in TPR results from a balance between the alpha-adrenoceptor-mediated increase and beta-adrenoceptor-mediated decrease in this variable. However, this proposed balance is lost if resting vasoconstrictor tone is reduced by ganglion blockade.

Adrenergic alpha-Antagonists↗
PubMed1976

Early and late hind-limb vascular responses to stimulation of receptors in the nose of the rabbit.

1. In rabbits under pentobarbitone anaesthesia stimulation of the nasal mucous membrane with ether vapour causes apnoea, bradycardia and a rise in arterial blood pressure. 2. Simultaneous measurements of femoral arterial blood pressure and of femoral arterial or venous blood flow show that vascular resistance increases in both the intact and skinned hind limb in response to nasal stimulation. Evidence is presented to show that the increase in hind-limb vascular resistance is due to vasoconstriction which is relfex in nature. 3. The change in vascular resistance in the hind limb following nasal stimulation may be divided into two distinct phases. The primary (early) phase is mediated by the efferent sympathetic nerves to the limb whereas the secondary (late) phase is mediated by adrenal gland hormones. 4. The secondary phase of the hind-limb vascular response is invariably less pronounced than the primary phase, and with regard to the time course of the appearance of the two phases of the response it appears that following stimulation of the nose there is no mutual reinforcement of sympathetic neural and humoral influences on the hind-limb blood vessels. 5. The cardiovascular response occur in the absence of changes in pulmonary ventilation.

Afferent Pathways↗
PubMed1975

Adrenal weight and catecholamine content in renal and calciferol-induced hypertension in rabbits.

1. Hypertension was produced in rabbits by unilateral renal encapsulation combined with contralateral nephrectomy or by the administration of calciferol and calcium lactate. 2. Weighed post mortem, the adrenal glands from the two hypertensive groups were significantly heavier than those from normotensive animals of similar weight. There was a direct correlation between the adrenal gland weight and the mean arterial blood pressure measured at the time of the terminal experiment. 3. The catecholamine content of the adrenal glands from the two groups of hypertensive animals was similar to that of the normotensive animals. 4. There was histological evidence of adrenal cortical hypertrophy in the glands of the hypertensive groups of animals.

Adrenal Glands↗
PubMed1974

Comparison of the effects of stimulation of the sympathetic vasomotor nerves and the adrenal medullary catecholamines on the hind limb blood vessels of the rabbit.

1. The responses to sympathetic nerve stimulation and to the adrenal medullary hormones have been studied in the hind limb vascular beds of the anaesthetized rabbit.2. Simultaneous measurements of femoral arterial blood pressure and of femoral venous blood flow indicate that stimulation of the sympathetic nerves decreases the calculated vascular conductance in both the intact and skinned hind limbs. Evidence is presented to show that these changes are due to vasoconstriction.3. The vasoconstriction in both skin and muscle vascular beds reaches a maximum at frequencies of stimulation around 15 Hz. No vasodilatation is obtained at any frequency of stimulation.4. The rabbit adrenal gland secretes only adrenaline during splanchnic nerve stimulation at frequencies between 3 and 60 Hz. The amounts liberated from both glands over this frequency range are 25-500 ng.kg body wt.(-1) min(-1).5. Intravenous infusions of adrenaline in concentrations similar to those liberated by the adrenal glands during splanchnic nerve stimulation, and of noradrenaline, cause only vasoconstrictor responses in skin and muscle.6. Simultaneous stimulation of the sympathetic nerves to the hind limb and infusion of adrenaline in quantities that could be liberated by splanchnic nerve stimulation at equivalent frequencies shows that the vasoconstrictor effects exerted by the individual components are additive, though the effects produced by the direct sympathetic nerve supply overshadow those produced by the catecholamine.7. The results are discussed in the context of the possible vascular role of the adrenal medullary hormones in the rabbit.

Adrenal Medulla↗
PubMed1971

Adrenal catecholamine secretion during stimulation of the nasal mucous membrane in the rabbit.

1. Left adrenal venous blood was collected in anaesthetized rabbits and analysed for catecholamine content by either a fluorimetric technique or a bio-assay method using the blood pressure of the pithed rat.2. Stimulation of the nasal mucous membrane with ether vapour or water caused apnoea, bradycardia, a rise in arterial blood pressure and an increase in adrenal medullary catecholamine secretion.3. During the pre-stimulation control periods adrenaline constituted 66% of the total catecholamine present in adrenal venous blood and noradrenaline 34%. These proportions altered during stimulation of the nasal mucous membrane to 72 and 28% respectively. Electrical stimulation of the left splanchnic nerve produced a secretion composed almost entirely of adrenaline.4. The increased catecholamine output elicited during stimulation of the nose occurred in animals whose pulmonary ventilation was maintained constant by means of a pump. It was abolished, however, by local anaesthesia of the nasal passages or by surgical division of the left splanchnic nerve.5. The increased secretion of catecholamines is therefore reflex in nature, and evidence is presented that it is the result of a primary reflex from the nose.

Adrenal Medulla↗