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Biomedical subjects

J Conway

Publications and source records attributed to J Conway.

At least 163 records · Page 9Linked to original sources
PubMed1983

Assessment of a small microwave (2450 MHz) diathermy applicator as suitable for hyperthermia.

Temperature profiles and depth data have been measured in three different tissue-type phantoms to assess the induced thermal patterns from a modified diathermy applicator with no allowance made for blood flow. Results indicate that tumours up to 50 mm in diameter and 30 mm deep may be therapeutically heated. Increasing the fat thickness has been shown, by these phantom studies, to indicate the need for careful regulation of the surface temperature to reduce large thermal gradients at depth. Field mapping outside the treatment area showed no significant exposure to patient or operator. The applicator is presently being used for a clinical hyperthermia treatment study.

Diathermy↗
PubMed1983

Hypotensive mechanisms of beta blockers.

A review of the available evidence suggests that the antihypertensive action of beta blockers depends partly upon a reduction in plasma renin activity. Since there are abnormalities of cardiac function in hypertension the reduction in cardiac output and heart rate may also contribute to the fall in blood pressure.

Adrenergic beta-Antagonists↗
PubMed1982

Functional interaction between angiotensin and sympathetic reflexes in cats.

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At -50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9-3.2 ng h-1 ml-1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8] ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

Angiotensin II↗
PubMed1982

The relative effect of mental and physical activity on blood-pressure and heart rate during the waking-up process.

1. The morning rise in blood pressure and heart rate was studied in 18 patients with mild blood pressure elevation. Passing from sleep to the drowsy state raised blood pressure and heart rate very little while the awake state (reading a newspaper sitting in bed) increased the mean blood pressure by 13.2 mm Hg and the heart rate by 5.7 beats per minute. 2. Subsequent application of mental stress (arithmetic) in one third of the patients or physical activity in the upright position in another third showed a different pattern of response. Mental stress mainly raised the blood pressure while physical activity in the upright position mainly raised the heart rate.

Activity Cycles↗
PubMed1980

The effects of the antagonists of the renin-angiotensin system on cardiovascular response to lower-body subatmospheric pressure in the anaesthetized cat.

1. Lower-body subatmospheric (negative) pressure led to a prompt reduction in central venous pressure and arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. These reflex responses have been used to investigate the role angiotensin plays in blood pressure control. 2. The initial plasma renin activity (2.9 ng of angiotensin I h-1 ml-1) did not change during the brief lowering of pressure. Before pressure was lowered neither the angiotensin-converting enzyme inhibitor nor a competitive antagonist, [Sar1, Ala8]-angiotensin II, lowered arterial pressure. 3. Nevertheless, after inhibition of the renin-angiotensin system by these agents, the reduction in blood pressure induced by lower-body negative pressure became greater and the blood pressure recovery was impaired. 4. The findings suggest that angiotensin, at a blood concentration which has no direct effect on blood pressure, interacts with the sympathetic nervous system to maintain arterial blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

Angiotensin activates sympathetic reflexes in the anaesthetized cat.

1. Lower-body subatmospheric pressure has been used to stimulate sympathetic reflexes in anaesthetized cats and the effects of an angiotensin converting enzyme inhibitor and [Sar1, Ala8]angiotensin II have been investigated on this reflex. 2. At the prevailing level of renin activity (2.9-3.2 ng of angiotensin I h-1 ml-1) the converting enzyme inhibitor had no effect on blood pressure yet it potentiated the initial fall in blood pressure caused by the reduced pressure and it impaired its recovery. After 10 min, therefore, blood pressure was still reduced after converting enzyme inhibitor treatment whereas in control experiments full recovery occurred within 30 s. 3. When converting enzyme inhibitor was given 75 s after the start of a 10 min period of reduced pressure, at a time when plasma renin activity had not been increased, it caused a greater and more sustained fall in pressure than it caused when administered alone. The angiotensin II antagonist, [Sar1,Ala8]angiotensin II, produced similar effects. 4. These findings suggest that the renin-angiotensin system interacts with the sympathetic nervous system to maintain systemic arterial pressure.

Angiotensin II↗
PubMed1980

The antihypertensive action of beta-adrenoceptor blocking agents.

The fall in blood pressure after the induction of beta-blockade occurs approximately 3 hours after the fall in cardiac output, heart rate and plasma renin activity has occurred. None of the known pharmacological actions of these agents can directly account for the fall in pressure. Further work is required to determine whether the fall in cardiac output is essential or whether these agents affect renal handling of sodium. Studies are also needed of baroceptor function as blood pressure falls.

Adrenergic beta-Antagonists↗
PubMed1978

Aging and the cardiovascular system.

With advancing age blood pressure rises in most populations with the exception of some isolated tribes. In western countries 30 to 40% of the people above the age of 60 years have casual blood pressure levels greater than or equal to 160/95 mm Hg. Advancing age per se produces a number of physiological changes related to blood pressure, such as a decrease in cardiac output, an increase in peripheral vascular resistance and a decrease in plasma renin-angiotensin-aldosterone levels. The mechanism causing the elevation in pressure with age are unknown though increased rigidity of the great vessels contributes to the rise in systolic pressure. There is a decline in the sensitivity of the baroreceptor reflex, but the contribution of this to the elevation of pressure has not be elucidated. Elderly patients with uncomplicated essential hypertension have a low cardiac output and high peripheral vascular resistance. The rise in blood pressure is associated with an increased cardiovascular morbidity and mortality even in the elderly hypertensives. The available data on the efficacy of hypotensive treatment in the elderly is scanty. There are no data proving that hypotensive therapy prolongs life. Controlled studies on the prevention of organ damage especially cerebrovascular accidents are inconclusive, showing either a significant decrease or no effect. Isolated reports illustrate, however, that drastic blood pressure reduction can provoke serious side effects, thus decreasing the quality of life. Hypotensive treatment is indicated in elderly hypertensive patients with hypertensive retinopathy grade III or IV, congestive heart failure or cerebral haemorrhage, in elderly patients with a markedly elevated diastolic blood pressure (greater than or equal to 120 mm Hg) and a trial of hypotensive therapy should be offered in milder forms of hypertension when it is accompanied by certain specific symptoms such as angina, headache and dyspnoe. The management of elderly hypertensive patients is more difficult than in the young. General measures are often not well accepted. The dose adjustment of the hypotensive agent is more critical and volume depletion or orthostatic hypotension are more likely to occur.

Aged↗