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Biomedical subjects

M D Esler

Publications and source records attributed to M D Esler.

138 records · Page 8Linked to original sources
PubMed1975

Altered cardiac responsiveness and regulation in the normal cardiac output type of borderline hypertension.

Of 145 patients with borderline hypertension, 30% had increased resting cardiac index (QI), whereas the remainder had normal values. The specific aim of this study was to investigate cardiac regulation in patients who had normal resting QI. Eighty-five control subjects were used for comparison. At rest, patients with normal QI showed evidence of decreased parasympathetic inhibition; the QI after injection of atropine increased less than in control subjects. After complete cardiac autonomic blockade with propranolol and atropine, QI and stroke volume were significantly lower in patients than in control subjects. The mechanism of this low QI was further analyzed. Central blood volume, which strongly correlates with stroke volume, was used as an estimate of the cardiac venous filling. After blockade, stroke volume was decreased in patients, but central blood volume was normal. Patients also showed a decreased heart rate and QI response to infusion of isoproterenol. It is therefore postulated that two components may be responsible for the low QI in the "denervated" heart: patients exhibit a decreased responsiveness to sympathetic stimulation, and they may also be less responsive to venous filling. Behind the facade of cardiac normality in these borderline hypertensive patients with normal cardiac output, there is evidence of altered autonomic control of the heart (decreased vagal inhibition) and of changed cardiac response to sympathetic stimulation and possibly to venous filling.

Adult↗
PubMedDate not supplied

Influence of variation in dietary sodium intake on biochemical indices of sympathetic activity in normal man.

The effects of variation in dietary sodium intake on biochemical indices of sympathetic activity were investigated in normal subjects. Sodium restriction for 7 days (mean urinary sodium excretion 21 mmol/day, s.e.m. = 4) increased supine plasma noradrenaline concentration significantly (1.78 nmol/l, s.e.m. = 0.23) compared to levels during medium sodium intake (1.31 nmol/l, s.e.m. = 0.14) and high sodium intake (1.35 nmol/l, s.e.m. = 0.25), when urinary sodium excretion averaged 186 (s.e.m. = 24) and 310 (s.e.m. = 43) mmol/l respectively. Plasma adrenaline concentrations did not vary significantly. During sodium restriction, the apparent release rate of noradrenaline increased significantly; noradrenaline clearance remained unchanged. No changes were observed in the heart rate response after beta-adrenoceptor stimulation with isoprenaline, suggesting that increased sympathetic activity during sodium restriction did not necessarily alter cardiac beta-receptor sensitivity. The responses to cardiac autonomic blockade with propranolol and atropine did not vary with sodium intake. These observations suggest that the sympathetic response to sodium restriction may not be generalized, excluding, in particular, the sympathetic nerves to the heart.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Role of cardiac and vascular amplifiers in the maintenance of hypertension and the effect of reversal of cardiovascular hypertrophy.

Changes in amplifying capacities of the hypertrophied heart and resistance vessels account for the characteristic evolution of haemodynamic patterns in the course of essential hypertension. Reversal of hypertrophy in established essential hypertension requires prolonged control of blood pressure. Redevelopment of hypertension on stopping drug therapy is slowest if there has been reversal of both vascular and cardiac hypertrophy. It may be possible to subsequently maintain normal blood pressure in a proportion of patients by non-pharmacological means following the initial period of drug therapy. Preliminary findings suggest that in a majority of patients the sympathetic nervous system may be overactive, whilst a smaller subset may have dysfunction of volume regulation.

Animals↗
PubMedDate not supplied

Central nervous system noradrenergic control of sympathetic outflow in normotensive and hypertensive humans.

We applied transmitter washout methodology, sampling internal jugular venous plasma via a percutaneously placed catheter, to study CNS norepinephrine release in humans and its relation to peripheral sympathetic activity. Norepinephrine overflows into the venous drainage of the brain, as do its precursor, DOPA, and metabolites DHPG and MHPG, indicating that the blood-brain barrier provides an incomplete impediment to their outward flux from the brain. Pharmacological testing with two drugs which altered CNS norepinephrine turnover, the tricyclic antidepressant desipramine and the ganglionic blocker, trimethaphan, demonstrated a direct relation existed between CNS norepinephrine release and sympathetic nerve firing rates. In essential hypertension, the sympathetic activation commonly present was associated with, and possibly caused by increased CNS release of norepinephrine, manifested in elevated overflow of norepinephrine, MHPG and DHPG from the brain. Bilateral jugular sampling, coupled with a cerebral venous sinus scan to delineate the drainage pattern, demonstrated that this increased norepinephrine release was confined to subcortical forebrain regions.

Blood Pressure↗