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The purpose of this investigation was to quantitate the rate of uric acid production in patients following acute myocardial infarction. In previous reports (Spring et al. 1960) it was observed that serum uric acid levels could be elevated following acute myocardial infarction. In view of other metabolic changes which have been observed such as the increased excretion of catecholamines and their metabolites and changes of glucose tolerance and lipid metabolism, it seemed adviseable to investigate abnormalities of uric acid metabolism in terms of pool size and turnover rates. 7 male patients who had had uncomplicated myocardial infarctions were admitted to the study following informed consent. The criteria of myocardial infarction were dependent upon clinical, electrocardiographic and biochemical enzyme changes. The patients were selected to exclude those with pre-existing disease and were restricted to those patients whose post-operative course did not require the administration of drugs particularly diuretics. The patients were admitted to an investigative ward from the coronary care unit between the 2nd and 5th day following infarction.

It is presumed that a region of myocardium does not always have the same blood flow. The purpose of this communication is to examine those factors which are determinants for changing regional flow. We have divided the determinants into three types. Those affecting a regional variation in blood flow which has a random distribution and a cyclic character which will be termed spatial and temporal heterogeneity (1). The second group are the determinants of the transmural distribution of coronary blood flow which were described by Griggs et al (2), Buckberg et al (3) and modified by L’Abbate et al (4). Finally, there are those determinants which are present when coronary artery obstruction occurs and collaterals develop which redistribute myocardial blood flow in a geographical sense (5,6).

An 8 year old girl with clinical and laboratory findings compatible with Glycogen Storage Disease Type I was admitted to the Investigative Unit for study of the origin of her hyperuricemia. Outstanding physical signs on this child were her protruberant abdomen with greatly enlarged liver. Her weight was at the 9th percentile for her age and her height at the 3rd percentile. Laboratory findings showed a serum cholesterol of 390mg% and triglycerides of 1630mg%. The total fasting free fatty acids were 1.16μM/ml and the blood lactate on repeated determinations ranged from 5 to 7.6μM/ml. Serum uric acid levels ranged from 6.5 to 7mg% (Uricase method). Hypoglycemia was not an important feature of her disease at this stage. While in the hospital she was maintained on a low purine calorically adequate diet but this was supplemented by various carbonated beverages and candy bars. Her diet was estimated to contain 45gm of protein, 50mg of purine, 70gm of fat and 220gm of carbohydrate. Uric acid-2-C14 was injected and complete urine collections made at 12 hourly intervals for the first 3 days and then subsequently at 24 hourly intervals for the next 4 days.