ABSTRACT
The mechanisms of myocardial injury and necrosis following transthoracic shocks from a direct current cardiac defibrillator were investigated in adult greyhounds. Myocardial lactate extraction became negative maximally at 1 minute, following two (mean -22% +/- SEM23) or five (-193% +/- 135) shocks and returned to baseline in 6-15 minutes. Myocardial necrosis assessed at 4 hours following the shock period was 0.05 g (+/- 0.03) after two shocks, 6.69 g (+/- 1.76) after five shocks and zero in controls. In further experiments, dogs received five or zero (dummy) shocks and mitochondria were isolated from their hearts following excision within 1 minute of receiving the final shock. Maximal oxygen consumption in right ventricular mitochondria was lower than the unshocked controls with both glutamate (66.9 +/- 9.4 nanoatoms of oxygen/mg per minute, n = 9 vs 86.6 +/- 13.6 nanoatoms/mg per minute, n = 7) and succinate (96.2 +/- 8.7 nanoatoms/mg per minute, n = 9 vs 119.5 +/- 14.4 nanoatoms/mg per minute, n = 7) as substrates. Using electron spin resonance spectroscopy, an increase in a peroxyl-free radical with g = 2.031 was detected in myocardial tissue after two internal shocks (50 joules stored energy, 0.5-minute intervals). We conclude that mitochondrial dysfunction and free-radical generation are likely contributors to cellular injury following multiple countershocks.
Subject(s)
Electric Countershock/adverse effects , Mitochondria, Heart/metabolism , Myocardium/pathology , Animals , Dogs , Electron Spin Resonance Spectroscopy , Female , Free Radicals , Lactates/metabolism , Lactic Acid , Male , Myocardium/metabolism , Oxygen ConsumptionABSTRACT
One hundred patients with active tuberculosis were tested for tuberculin reactivity within 24 hours of their admission to the hospital. Commercial intermediate tuberculin, Tween stabilized intermediate tuberculin and the Tine test as well as a mumps antigen were applied simultaneously. False negative reactions were obtained in 28 per cent with Tine testing and in 21 per cent with Tween stabilized as well as plain tuberculin. These nonreactors were clinically identifiable as seriously ill with manifestations primarily attributable to protein depletion as a result of their illness. This is not specifically related to the effects of tuberculosis itself, but can be demonstrated in patients suffering the same sequelae of other debilitating illness. After two weeks of protein supplementation via a high calorie, high protein, hospital diet, skin reactivity was restored in the vast majority of these nonreactors. It is concluded that the lack of tuberculin reactivity on hospital admission probably results from impaired lymphocyte function in patients suffering serious protein depletion as a result of their illness; it is not attributable to deficiencies in the tuberculin test itself.
Subject(s)
Tuberculin Test , Tuberculosis/diagnosis , Adult , Antigens, Viral/administration & dosage , Female , Humans , Male , Middle Aged , Mumps/immunology , Skin Tests , Tuberculosis/immunology , Tuberculosis/therapySubject(s)
Alcoholism/complications , Ambulatory Care , Tuberculosis/drug therapy , Adult , Aged , Drug Resistance, Microbial , Female , Follow-Up Studies , Humans , Male , Middle Aged , New York , Patient Compliance , Physician-Patient RelationsABSTRACT
A computer-assisted simulation of the 'chart method' of teaching has been developed and was used to provide instruction in clinical decision-making in the diagonosis and treatment of pulmonary diseases. The course requires a student to reach and to defend a diagonisis and to provide appropriate treatment for each of 10 simulated cases. Evaluation of performance and immediate feedback and correction of errors of commission and ommission are an integral part of the course. The course provides a model for development of additional programs in other subject areas.
