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We have described a technique whereby the time necessary to reach an equilibrium enrichment of expired CO2 during a primed-constant infusion of [U-13C]glucose was shortened from 7 to 8 h to 1 hour or less. We applied the theory of the primed-constant infusion technique to the bicarbonate pool, with the "constant infusion" of labeled carbon dioxide originating from oxidation of the infused [13C]glucose rather than from a labeled infusion of bicarbonate.

The rate of appearance of unlabelled glucose was calculated from changes in plasma glucose specific radioactivity after a single intravenous injection of labelled glucose and compared with the actual constant infusion rate of unlabelled glucose into an anaesthetized dog with all sources of endogenous glucose production surgically removed. The mean steady-state rate of appearance of unlabelled glucose calculated from the area under the specific radioactivity versus time curve was 7% higher than the actual infusion rate (n = 4), but the difference was not statistically significant. The variability in the rate calculated in this manner was, however, greater than the variability we have reported with rates determined from a primed constant infusion of tracer. Using 15- to 60- or 60- to 120-min specific radioactivity data the mean rate of appearance of glucose, calculated on the assumption of a one-pool model for glucose turnover in vivo, was approximately 60% higher than the actual infusion rate. The results also indicate that it is possible to construct multi-pool models, but it is difficult to equate specific physiological events with the individual terms of the multi-experimental equation which describes the changes in plasma glucose specific radioactivity.

The rate of appearance of unlabelled glucose was calculated from tracer data and compared with the actual rate of infusion of unlabelled glucose into a anaesthetized dog with all sources of endogenous glucose production surgically removed. The mean steady-state rate of appearance of unlabelled glucose calculated from the equilibrium specific radioactivity was insignificantly higher (0.3%) than the actual rate of infusion of unlabelled glucose (n = 6). During non-steady states, a time-variable volume of distribution of glucose (V) was necessary to predict the rate of appearance of unlabelled glucose correctly from the pool-dependent equation described by Steele [(1959) Ann. N.Y. Acad. Sci. 82, 420--430]. Rapid fluctuations in the rate of appearance of glucose could be predicted reasonably well by using a fixed value of V for 40ml/kg, but by using larger fixed values for V (100--160ml/kg) the rates were inaccurate. The pool-dependent two-radiactive-isotope technique described by Issekutz, Issekutz & Elahi [(1974) Can. J. Physiol. Pharmacol. 52, 215--224] predicted single-step increases in the rate of infusion of glucose reasonably accurately, but the Steele (1959) equation was better at predicting sequential changes in the rate of infusion of unlabelled glucose.

A case is presented of a 55‐year old woman with longstanding rheumatoid arthritis who presented with a lump in her right breast and a markedly enlarged right axillary lymph node. Carcinoma of the breast with lymphadenopathy was diagnosed clinically, but excisional biopsy revealed an amyloid tumour of the breast and amyloid lymphadenopathy. Aniyloid tutnour of the breast is an infrequently reported lesion and the association of axillary lymphadenopathy has not been reported before. The literature is reviewed and the need for a tissue diagnosis prior to embarkation on specific therapy is emphasized.

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TABLE II-Mean (± SE of mean) plasma urate concentrations (mmol/l) in patients who suffered AMI according to whether they were given diuretics Day: 1 4 7 14 Diuretics given (n = 38) 0-354 ± 0-015 0 409 ±0-021 * 0-392 +0-018 0-382 ±0-016 Diuretics not given (n = 32) 0 340 ±0-012 0-327 0-015* 0-368 ±0-018 0-368 0-018 *P<0-01. ate concentrations, may play a part in altering the renal handling of urate. These organic acids are thought to share a common secretory mechanism with urate and produce hyperuricaemia by competing with urate for this secretory site.11 12 Possibly also a more rapid turnover of preformed purines or increased de novo synthesis may have produced hyperuricaemia in the AMI group. Further study is in progress to elucidate the mechanism. We thank the physicians of Addenbrooke's Hospital, Cambridge, for allowing us to study patients under their care and Professor H Lehmann for the laboratory facilities. P G was the holder of the Grimshaw-Parkinson Research Studentship at the University of Cambridge and is at present receiving a grant from the Wellcome Trust. Requests for reprints should be addressed to P G