1 We assessed the relaxant effect of 17f,-oestradiol (10 -, 10-6 and 10-M) on rabbit isolated coronary arteries precontracted with prostaglandin F2,, (3 x 10-6M), high extracellular potassium (30mM) and Bay K 8644 (10-6M) plus high extracellular potassium (15 mM) by measuring isometric tension. 17fl-Oestradiol (10-6 and 10-5M) induced significant relaxation in coronary arteries from male and female rabbits. No differences were seen between arteries with or without endothelium. There were also' no differences between coronary arteries isolated from male and female rabbits. 2 Inhibitors of endothelium-derived relaxing factor and vasodilator prostanoids, namely, reduced haemoglobin, Nw-nitro-L-arginine methyl ester and indomethacin, did not affect the relaxation induced by 17fl-oestradiol in endothelium-intact coronary arteries.3 Methylene blue, an inhibitor of guanylate cyclase, did not affect the coronary artery relaxation induced by 17/1-oestradiol. 4 The' calcium concentration-dependent contraction curve in potassium-depolarization medium was shifted to the right by 17fl-oestradiol (10-6 and 10-5M) in the rabbit coronary artery and rat aorta. The -log EC50 s of calcium in control and after incubation with 17fi-oestradiol (10-6 and 10 -M) were 3.7 + 0.09, 3.1 + 0.10 and 2.8 + 0.08 respectively in rabbit coronary arteries and 3.8 + 0.11, 3.3 + 0.14 and 2.9 + 0.15 in rat aorta. 5 The results indicate that 17fi-oestradiol induces rabbit coronary artery relaxation by an endotheliumindependent mechanism in vitro. A calcium antagonistic property may be involved in the mechanism of rabbit coronary arterial relaxation by 17fi-oestradiol.

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The aim of the study was to compare histological findings in limb and respiratory muscles from control subjects and patients with heart failure of two different aetiologies. Biopsies of the quadriceps femoris, strap, diaphragm and pectoralis major muscles were taken from each group. The control subjects all had normal left ventricular function, and comprised seven undergoing surgical ablation of electrical pathways and 10 undergoing coronary artery surgery. The heart failure group had severely impaired left ventricular function, and were undergoing cardiac transplantation in all except one case. Ten patients with idiopathic dilated cardiomyopathy and seven with heart failure of ischaemic origin were studied. Conventional histochemical techniques and specific anti-myosin immunofluorescent stains were used. There were no consistent differences in fibre type prevalence or diameter between the groups. There were no important histological abnormalities in the two control groups. There were minor/major changes in four of seven patients with ischaemic heart failure but no major abnormality, whilst in the dilated cardiomyopathy group there were five of 10 patients with minor/major changes and three of 10 with major abnormalities (P < 0.001 vs controls). A variety of changes were seen in both groups of heart failure subjects. These were more marked in the dilated cardiomyopathy than ischaemic group, and suggest the presence of fibre type regeneration and/or transformation. Amongst the findings were tubular aggregates, internalization of nuclei, bizzare staining of myosin and staining of neonatal myosin (seven of 14) and the presence of cores (five of 14). Such changes were more prominent in the diaphragm than in the other muscles. In conclusion, histological abnormalities are present in the limb and respiratory muscles from subjects with heart failure. The changes are most marked in subjects with idiopathic dilated cardiomyopathy, suggesting that there may be a generalized cardiac and skeletal myopathy in these subjects. The presence of histological abnormalities in the respiratory muscles may contribute to the pathogenesis of dyspnoea in heart failure.