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Medical Research Society 3. MYOCARDIAL NECROSIS INDUCED BY ANGIOTENSIN II D. KREMER, J. J. BROWN, A. F. LEVER, G. LINDOP, J. J. MORTON and J. I. S. ROBERTSON M.R.C. Blood Pressure Unit, and Department of Pathology, Western Infirmary, Glasgow GIl 6NT In a previous study (Gavras et al., 1971, Lancet, ii, 19) it was shown that the administration of angiotensin II can cause focal myocardial necroses in the rabbit. These experiments have been extended by infusing angiotensin II intravenously into rabbits for periods up to 24 h at graded doses, arterial plasma angiotensin II concentration being estimated before, and at intervals during, each infusion. Control animals were infused with saline. Post-mortem, the extent of the cardiac lesions was assessed histologically by a system of scoring. The severity of the induced lesions was shown to be related to the plasma angiotensin II levels attained during infusion. Myocardial necroses in some animals occurred at plasma angiotensin II concentrations known to occur clinically in man. 4. CONTROL OF FOLLICLE STIMULATING HORMONE (FSH) SECRETION IN THE MALE: SITE OF ACTION OF INHIBIN F. J. BRAMBLE, L. E. HOUGHTON, SHEILA S. ECCLES, M. A. F. MURRAY and H. S. JACOBS Leeds General and Bradford Royal Infirmary and St Mary's Hospital Medical School, London, W.2 Previous studies have indicated that the secretion of FSH in the male is controlled partly by androgens and partly by some non androgenic testicular hormone(s)-generally termed inhibin-which is related specifically to spermatogenesis. The chemical nature of this compound is as yet unknown. In an attempt to understand how this compound modulates FSH secretion we have measured sperm count (SC), serum testosterone (T), luteinizing hormone (LH) and FSH and the response to exogenous gonadotrophin releasing hormone (GnRH) in twentyfour adults who had surgical correction of bilateral cryptorchidism in childhood. In those with normal SC, T, LH and FSH, the response to GnRH was normal; in those with aspermia, low T and elevated basal LH and FSH, the response to GnRH was exaggerated. By contrast inpatients with oligospermia or aspermia, raised FSH but normal LH and T, in whom a specificdeficiencyof inhibin may be presumed, the response to GnRH of, FSH but not of LH was exaggerated. We conclude that inhibin modulates the secretion of FSH by an interaction with the pituitary response to GnRH rather than by an action on the hypothalamus. G 3p 5. AUTOMATED RADIOIMMUNOASSAY OF PLASMA OESTRIOL: UNEXPECTED PROBLEMS M. G. R. HULL and P. P. MONRO Department of Obstetrics and Gynaecology, St Mary's Hospital, London, W.2 (Introduced by H. S. JACOBS) A method of suitable speed and throughput (120 samples daily) has been developed to assay pregnancy, plasma unconjugated oestriol (E 3) concentration, employing a specific antiserum (rabbit anti-Ej-fcarboxymethyl-oxime-BSA, 1/60000) supplied by Professor R. Scholler, and 3H.E 3 (53·1 Ci/mM) as label. The useful range is 20-200 pg, equivalent to 2-20 ngjml plasma. The precision of the assay at 3 ng/ml is ±4%. Preliminary mean values obtained in normal pregnancy at 25 and 40 weeks' gestation are 3·5 and 12·8 ng/ml. Ether extracts of 0·1 ml plasma are assayed employing automatic dispensers. High precision associated with the automated method revealed systematic errors otherwise undetectable because of the random errors associated with manual techniques. The major problem observed was a temperature-dependent instability of the ammonium sulphate precipitate, which resulted in an apparent increase of free labelled hormone, possibly due to dissociation of the antigenantibody complex. One consequence of this effect was a spurious increase of plasma E 3 values of up to 50%. Attempts to reduce scintillation fluid volume were unsuccessful. Presumably due to the polarity of E 3 a large excess (30: 1) of a toluene-based mixture was required. Moreover ammonium sulphate caused instability of more expensive one-phase systems. 6. THYROID FUNCTION AFTER MEDICAL AND SURGICAL TREATMENT OF THYROTOXICOSIS AND NON-TOXIC NODULAR GOITRE N. W. OAKLEY, R. D. SIMPSON, F. M. BROOKE, D. BURNETT, T. F. WOODS, N. J. GRIFFITHS, R. GULIN and R. S. MURLEY The Alexander Simpson Laboratory for Metabolic Research, St Mary's Hospital, London, W.2, and St Albans City Hospital, Normandy Road, St Albans, Herts. A high proportion of patients treated for thyrotoxicosis by thyroidectomy or radioactive iodine developed elevated TSH levels while clinically euthyroid and in the presence of normal thyroid function judged by other test criteria. The significance of this finding: is uncertain and it is not clear whether it represents a state of compensated hypothyroidism or early thyroid deficiency,requiringreplacement therapy. Plasma TSH has been measured in 136 patients treated for thyroid disease between 1956 and 1972, subdivided into patients treated surgically for (a)