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P Wilmshurst

Publications and source records attributed to P Wilmshurst.

At least 19 recordsLinked to original sources
PubMed1991

Cardiovascular effects of growth hormone treatment in growth-hormone-deficient adults: stimulation of the renin-aldosterone system.

1. In adult humans with growth hormone deficiency, treatment with growth hormone has recently been shown to have major anabolic effects and to improve exercise performance. The cardiovascular effects of growth hormone in adults with growth hormone deficiency were examined in 24 patients treated with recombinant human growth hormone (0.07 units/kg at night) in a double-blind, placebo-controlled trial lasting 6 months. 2. Compared with placebo, resting M-mode echocardiography showed increases in left ventricular end-diastolic dimension and stroke volume in the group treated with recombinant human growth hormone. No differences were noted between the groups with respect to left ventricular end-systolic dimension, fractional shortening, wall thicknesses or mean arterial blood pressure. Left ventricular myocardial mass increased in the group given recombinant human growth hormone. 3. The supine plasma renin activity was increased and remained elevated over the 6 months, whereas the plasma aldosterone concentration was unchanged, after treatment with recombinant human growth hormone. Clinical signs of sodium retention were evident during the first 3 months of treatment with recombinant human growth hormone. 4. We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency resulted in small increases in left ventricular pre-load, due to the sodium-retaining action of growth hormone. Activation of the renin-aldosterone system was involved in such changes. Myocardial hypertrophy was observed without changes in mean arterial pressure, reflecting the anabolic action of growth hormone.

Adult↗
PubMed1988

The bends.

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Decompression Sickness↗
PubMed1988

The bends.

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Adult↗
PubMed1988

New positive inotropic substances--true inotropy or peripheral effects?

A large number of chemical substances increase contractility of isolated animal myocardial preparations. Their augmentation is the result of a number of mechanisms which ultimately increase the available calcium for contractile protein coupling. Although there is some research with drugs which activate calcium channels, present clinical research is mainly confined to agents whose major action on contraction is mediated by an increase in myocyte cyclic AMP. Species and age variations in the inotropic effect are common. These agents have additional cardiac effects (e.g. chronotropic, lusitropic) and non-cardiac actions. They are potent vasodilators. In isolated human myocardium obtained from patients without heart failure, they increase contractility at high concentrations. Generally this effect is attenuated in isolated myocardium obtained from patients and animals with chronic cardiac failure. In myocardium from patients with the most severe heart failure, even very high concentrations fail to increase contractility. Part of this attenuation may be due to reduced receptor number (or sensitivity) when the drug's effect is due to receptor-coupled adenylate cyclase activation. However, a reduced ability to produce and/or respond to cyclic AMP itself is suggested by impaired responses to phosphodiesterase inhibitors. In vivo, these agents have frankly harmful effects in patients with near normal cardiac function. Despite increasing contractility indices, they lower blood pressure, raise heart rate and impair myocardial lactate metabolism without increasing cardiac output. In patients with severe heart failure they produce beneficial resting haemodynamic changes; increased cardiac output and reduced filling pressures with only small changes in blood pressure and heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗