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Biomedical subjects
Publications and source records attributed to J R Cox.
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Two groups of depressed subjects, one with a history of recurrent depression, the other with a history of persistent apathy, were given lithium carbonate 1,200 mg q.i.d. and supplementart potassium 1,200 mg t.d.s. for 1 week. Measurements were made before and after the lithium treatment of total body water (tritium space), extracellular fluid (sulphate space), total exchangeable sodium (Nae) and total exchangeable potassium (Ke) using sodium-24 and potassium-42 multiple isotope dilution techniques. Prior to treatment when compared with a group of normal subjects, both depressed groups showed changes in body fluid volumes and electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while intracellular sodium was raised. After treatment with lithium the values in the apathetic group showed little change but the group with recurrent depression showed a significant increase in intracellular fluid (p less than 0.025), Ke (p less than 0.001), intracellular potassium (p less than 0.025) and a significant decrease in Nae (p less than 0.05). There was a marked increase in mood in the group with recurrent depression but not in the apathetic group following lithium treatment. These findings suggest that recurrent depression, both in clinical improvement, mood and also correction of water and also correction of water and electrolyte disturbances arise, but not in patients with long-standing apathy.
Red cell anisocytosis as assessed using the Coulter Channelyzer C-1000 showed an increase with progressive anaemia in 25 patients with macrocytosis due to B12 and/or folate deficiency. In deficiency of a single factor, the degree of anisocytosis increased with progressive anaemia. In five cases with B12 and folate deficiency combined, anisocytosis was markedly increased out of proportion to the degree of anaemia present. Iron stores were also reduced in four of these cases. It is suggested that objective measurement of anisocytosis is of early diagnostic value in the assessment of multiple haematinic factor deficiency, for example, in macrocytic anaemia associated with malabsorption states and unexpected multiple deficiency states.
The relation between ventricular dysrhythmia during the first 20 hours after hospitalization for acute myocardial infarction and enzymatically estimated infarct size was studied prospectively. The duration of dyshythmia was measured by the total time during which the average premature ventricular depolarization (PVC) rate was above 25 PVCs/hr. This index was significantly correlated with infarct size index (ISI) and the strength and significance of the correlation increased when patients with previous, remote myocardial infarction were excluded. An initially expected correlation between PVC frequency and average heart rate was not observed. In a subset of patients selected to include the entire range of ISI, median PVC coupling interval did not correlate with ISI or heart rate. Our results confirm the general reduction of PVC frequency with time after hospital admission. An analysis of total lidocaine administered for therapeutc purposes and dysrhythmia evaluated by retrospective computer analysis disclosed a moderately strong and significant correlation. These findings indicate that persistence and severity of ventricular dysrhythmia in the first 20 hours after hospitalization for myocardial infarction are related to enzymatically estimated infarct size.
1. Body weight was measured through forty consecutive illnesses in seventeen patients with oedema in association with chronic bronchitis and hypoxia. All patients were taking diuretic drugs at the time. 2. Body weight increased little as peripheral oedema and a raised jugular venous pressure appeared. The subsequent weight-loss during treatment was usually greater than the pre-treatment weight-gain. Body weight increased slowly in convalescence to equal or exceed hospital admission weight without a deterioration of general health or reappearance of oedema. 3. Total body water, exchangeable sodium and exchangeable potassium were measured in patients after treatment of the acute illness and clearance of oedema and again in six patients of the group 2-3 months later in convalescence. Total exchangeable sodium was normal or slightly reduced after treatment of oedema and in convalescence between recurrent acute illnesses. Even when gross oedema was present exchangeable sodium was substantially increased in only one of three patients studied at this stage. Total exchangeable potassium was invariably severely depressed. 4. Large changes of body tissue weight without comparable change in exchangeable sodium support previous evidence that oedema in hypoxic bronchitis is not simply a further form of congestive cardiac failure. 5. It is suggested that at least some of the tissue loss in acute exacerbations is a direct result of hypoxaemia and similar to that observed at high altitude. Part of the oedema fluid is thought to be derived from intracellular water released during dissolution of tissue matrix.
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In order to determine whether ventricular arrhythmia is quantitatively related to infarct size estimated enzymatically we studied 31 patients with acute myocardial infarction without cargiogenic shock. Infarct size index was estimated from hourly serum creatine kinase (CK) changes during periods of 48 to 72 hours. Ventricular arrhythmia was quantified by automated analysis of continuous electrocardiographic recordings over a period of 20 hours with the use of the Argus/H computer system. Patients were classified into three groups according to infarct size index. Patients in all groups had similar average heart rate, blood pressure, serum potassium, and arterial pH and PCO2 values during the first 10 hours after admission. The total number of ventricular ectopic beats (VEB), frequency of couplets, and ventricular tachycardia, and peak rate of ventricular ectopic beats during the first 10 hours after admission were all related to infarct size index. For example, patients with small, medium, and large estimated infarct size averaged 26, 104, and 405 ventricular ectopic beats, respectively. These results suggest that the severity of ventricular arrhythmia early after myocardial infarction is related to the extent of myocardial injury as estimated enzymatically. Thus the apparent efficacy and therefore the evaluation of antiarrhythmic agents early after myocardial infarction may be influenced by the magnitude of injury sustained by the heart.
In a double-blind comparison between naftidrofuryl and placebo, naftidrofuryl-treated patients improved significantly on scales completed by the nurse, occupational therapist and physician. No improvement was found for placbo-treated patients. When the response to each treatment was compared, naftidrofuryl was found to be significantly better than placebo on both nurse and physician assessment. There was considerable variation between assessors which suggests that they were measuring different aspects of the patients' condition. There was also considerable variation in patient response, some improved on naftidrofuryl and some deteriorated; some improved on placebo and some deteriorated. However, overall it would seem that patients admitted to hospital with confusional states benefit from treatment with naftidrofuryl.
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Sodium appetite was studied in rats with lesions destroying the entire amygdaloid nuclear complex. The rats were totally aphagic and adipsic for several days following lesioning but regained nearly normal levels of food and water intake about 2 to 3 weeks postoperatively. Intake of 3% saline was observed after induction of sodium appetite by treatment with a mineralocorticoid and a natriuretic agent. Rats with amygdaloid lesions generally manifested severe but not total loss of sodium appetite. Regulation of water intake was also moderately to severely impaired. Suggestive evidence was obtained that recovery of sodium appetite in amygdalectomized rats can be enhanced by postoperative experience with sodium appetite and saline reinforcement.