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Biomedical subjects

J S Kooner

Publications and source records attributed to J S Kooner.

43 records · Page 3Linked to original sources
PubMed1988

Haemodynamic, hormonal and urinary responses to postural change in tetraplegic and paraplegic man.

We have studied the haemodynamic, hormonal and urinary effects of postural change in 6 tetraplegic patients, 6 paraplegic patients and 6 normal subjects. Measurements of blood pressure and heart rate, plasma renin activity, plasma aldosterone, urine volume and electrolyte excretion were made for 60 minutes while sitting and 60 minutes while recumbent. In tetraplegics the blood pressure was lower when sitting and rose during recumbency, unlike paraplegics and normal subjects. Plasma renin activity and aldosterone were higher in tetraplegics when sitting compared to normal subjects and did not fall during recumbency. Urine output increased significantly after recumbency in tetraplegics, but not in paraplegics or normal subjects. Both urinary sodium and potassium excretion were lower in tetraplegics and higher in paraplegics compared to normal subjects when sitting. In paraplegics the fall in both sodium and potassium excretion did not appear to be related to change in posture. Our observations indicate that recumbency induces a diuresis in tetraplegics but not in paraplegics or in normal subjects. The diuresis in tetraplegics may be related to the accompanying haemodynamic and hormonal changes induced by recumbency.

Aldosterone↗
PubMed1988

Cardiovascular and neurohormonal changes following central sympathetic blockade with clonidine in human unilateral renal artery stenosis.

The role of central pressor mechanisms in the maintenance of blood pressure in six hypertensive patients with angiographically proven unilateral renal artery stenosis was investigated by studying the haemodynamic and hormonal responses before and after central sympathetic blockade with clonidine. To assess the dependency of blood pressure on the direct effects of angiotensin II, the same patients were studied on a separate occasion after administration of the angiotensin converting enzyme (ACE) inhibitor, captopril. There was a substantial fall in blood pressure after administration of clonidine with a smaller fall after captopril. Clonidine-induced hypotension was accompanied by a fall in cardiac output, through a reduction in the stroke volume and heart rate. Forearm vascular resistance was unchanged. There was a selective decrease in digital skin vascular resistance and plasma noradrenaline, indicating reduced sympathetic activity. Plasma renin activity and aldosterone levels did not fall. After administration of captopril, there was a fall in cardiac output due to a fall in the stroke volume but not in the heart rate. Forearm vascular resistance, digital skin vascular resistance and plasma noradrenaline were unchanged. Plasma renin activity rose and plasma aldosterone fell. We conclude that in our hypertensive patients with renal artery stenosis, clonidine lowered blood pressure by a reduction in central sympathetic activity independently of renin suppression. In these patients captopril had minimal hypotensive effects, indicating a smaller role for the direct vascular effects of angiotensin II.

Adult↗
PubMed1988

Vascular effects of clonidine in patients with tetraplegia and unilateral brachial plexus injury.

Evidence from studies in both animals and in tetraplegics with complete cervical spinal cord transection and preganglionic lesion, indicates that clonidine lowers blood pressure predominantly by a centrally mediated action. We have investigated the haemodynamic basis of this action and performed additional studies in patients with unilateral brachial plexus injury and postganglionic lesions, to further determine the site and mechanism of its action. Blood pressure fell after clonidine in normal subjects but not in tetraplegics. In normal subjects, the fall in blood pressure was associated with a fall in cardiac output, due to a fall in both heart rate and stroke volume. Digital skin vasodilatation occurred after clonidine in normal subjects and only in the innervated limb in patients with unilateral brachial plexus injury. In tetraplegics and in the denervated limb in unilateral brachial plexus injury, there was no vasodilatation; instead a vasoconstrictor response occurred, due to the peripheral adrenoceptor action of clonidine. We conclude that the fall in blood pressure and cardiac output in normal subjects after clonidine were due to its central sympatholytic action. Digital skin vasodilatation after clonidine in normal subjects and the innervated limb in unilateral brachial plexus injury was due to the withdrawal of vasoconstrictor tone and requires intact descending sympathetic pathways.

Adult↗
PubMed1987

Intravenous dihydroergotamine to relieve pelvic congestion with pain in young women.

The selective venoconstrictor dihydroergotamine (DHE) was given intravenously to 12 women with evidence of pelvic congestion. In 6 the effect of the drug on pelvic veins was observed by pelvic venography. After DHE there was a mean reduction of 35% in the diameter of the pelvic veins measured and the contrast medium cleared rapidly, with a visible reduction in pelvic congestion. In the other 6 women DHE was given during an acute attack of pelvic pain. The effect of the drug on pain relief was assessed by a single-blind crossover trial with intravenous saline as the placebo and by a visual analogue scale to assess the intensity of pain. Pain was significantly lower post-DHE 4 and 8 h and 2 and 4 days after treatment than after placebo. The results confirm a close association between demonstrable pelvic congestion and pelvic pain.

Acute Disease↗
PubMed1987

Neurogenic components of hypertension in human renal artery stenosis.

In renal artery stenosis activation of the renin-angiotensin system elevates blood pressure by direct peripheral effects and probably through stimulation of sympathetic activity, which can be induced by angiotensin-II either centrally or peripherally. In animals specific brain lesions and afferent renal denervation can either attenuate or prevent renovascular hypertension. We investigated the neurogenic mechanisms responsible for hypertension in 21 patients with unilateral renal artery stenosis off drug therapy, by studying the cardiovascular and hormonal effects of Clonidine. The responses to Captopril served as an indicator of the peripheral effects of angiotensin-II. Both oral and intravenous Clonidine lowered blood pressure substantially and for a prolonged period even in patients who had been refractory to multiple antihypertensive drug therapy. Levels of plasma renin activity were unchanged after Clonidine. Plasma noradrenaline levels fell. Pressor responses to infused angiotensin-II were not reduced. These data suggest that Clonidine lowers blood pressure independently of hormonal and peripheral vascular interactions and is consistent with its predominantly central sympatholytic effects. Oral Captopril, unlike Clonidine, had variable hypotensive effects directly related to the basal level of plasma renin activity. The largest reductions were observed in those with the highest level of renin. Our studies indicate that neurogenic mechanisms, probably centrally mediated, have an important and often major role in maintaining hypertension in human renal artery stenosis. These may result from the central effects of angiotensin-II, and/or from increased afferent renal nerve activity, as demonstrated experimentally. The neurogenic components maintaining hypertension in renal artery stenosis are largely dependent on renal ischaemia as revascularisation (by surgery or angioplasty) or nephrectomy, either ameliorates or cures the hypertension in the majority of our patients.

Aortography↗
PubMed1986

The influence of topical anaesthetic agent at bronchoalveolar lavage upon cellular yield and identification and upon macrophage function.

The influence of cocaine and lignocaine as local anaesthetic agent upon the results obtained at bronchoalveolar lavage was investigated. No differences were found. A functional activity of macrophages was assessed when the cells were stored in lavage fluid. A time-dependent decrease occurred which was related to lack of nutrients rather than the anaesthetic concentration.

Bronchi↗