[Beta adrenergic blockade and subtotal thyroidectomy in thyrotoxic patients. A prospective study in 30 patients treated with propranolol].
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Biomedical subjects
Publications and source records attributed to B Lind.
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Cadmium concentrations in liver biopsies, blood, and bile were measured by atomic absorption spectrophotometry in 23 patients in connection with routine gallstone operations. On a group basis cadmium in blood was a good indicator of cadmium in liver, and the estimated linear relationship agreed well with calculations from a formerly proposed metabolic model. Cadmium in bile was also analyzed, and an average of about 2.5 ng of Cd/g wet weight was found. This is about 10 times more than would have been expected form the metabolic model and suggests that bile might be an important excretion route for cadmium. Definite conclusions cannot be drawn, however, since the results could not be cross-checked with neutron activation analysis, due to insufficient sensitivity of the latter method.
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The infrated detection apparatus used in breast thermography is relatively costly and therefore is not widely available to less populated areas in the country. The use of liquid cholesterol crystals, applied to the breast (applied over a water-base black dye) has already been described in the literature as an effective substitute for infrared instrument thermography. This method, however, has been hampered by the time and troublesome effort necessary for removal of the substances upon completion of the study. The object of this study was to devise a feasible method of cutaneous breast thermography using liquid cholesterol esters, as in prior studies, but by applying them to an easily removable black base. As a result the length of the examination has been shortened, and patients have found the examination to be aesthetically more acceptable. With this improved method, liquid crystal thermography of the breast (and other areas) should become more widely applicable.
Local reactions during and after i.v. injection of two different formulations of diazepam were studied. Two-thirds of the patients felt pain during the injection. Verfied or probable thrombophlebitis occurred with increasing frequency following operation, indicating a late onset. One month after discharge, 29% of those who had received diazepam in glycoferol-alcohol-benzoic acid complained of tender injection sites, compared with only 10% of the patients who received diazepam in cremophor EL. The difference is significant, indicating an influence of the solvent system.
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Dog models of total brain ischaemia for the study of pathophysiological mechanisms and post-resuscitative therapy used since 1970 are reviewed. Attempts to produce isolated total cerebral ischaemia in dogs either failed to stop cerebral circulation completely because of the abundance of collateral vessels or involved complex operations with blood loss. Complete airway obstruction resulted in various periods of asphyxia preceding asystole. Total circulatory arrest by ventricular fibrillation for 12 min or longer, resulting in gross neurological deficit, required cardiopulmonary resuscitation of variable duration and often required thoracotomy to restart spontaneous circulation. An acceptable model for short-term studies was obtained by clamping the ascending aorta for 15 min. This resulted in control of perfusion pressure with precise timing of onset and termination of cerebral ischaemia, and an isoelectric electroencephalogram within a mean time of 37 (26-44) s; it retained its ability to restore spontaneous circulation promptly with special supportive therapy, and a severe neurological deficit was evident for 20 h after ischaemia. Reliable total brain ischaemia suitable for long-term survival studies could not be developed in the dog without major surgical procedures, as it has been in the rhesus monkey. Sixteen minutes of high-pressure neck occlusion with a tourniquet and special intensive care resulted in major neurological deficit with survival for at least 7 days, and proved suitable for simultaneous study of neurological, physiological and histological changes.
Cross-clamping of the ascending aorta in dogs for 15 min produced severe neurological deficit, observed for up to 20 h. Immediately after restoration of the circulation, the intracranial pressure in the cisterna magna increased transiently to a mean peak of 22.8 Torr (SD +/- 1.7) because of a compensatory increase in systemic arterial pressure, without a fall in cerebral perfusion pressure. The intracranial pressure returned to control values 15-30 min after ischaemia and showed no secondary rise during the 8 h of observation. The electroencephalogram became isoelectric 34 +/- 6.5 s (mean +/-SD) after circulatory occlusion, and was abnormal when it reappeared 5 h 36 min (SD +/- 2 h 4 min) after the circulation was restored. The electrical impedance of the brain increased immediately after ischaemia and returned rapidly towards pre-ischaemic values during re-perfusion. The cerebral water had not increased measurably 4 h after ischaemia. After ischaemia, the lactate concentration in the cerebrospinal fluid increased to 4.7 mequiv./1(SEM +/-0.1) and the pH decreased to 7.17 (SEM +/-0.02); both returned to control values after 3.5 h. The cerebral glucose uptake was decreased 35 min after ischaemia, cerebral oxygen uptake remained unchanged but cerebral blood flow decreased (P less than 0.05 at 90 min). Immediately after cardiac arrest, recovery was impaired more by the presence of focal abnormal brain perfusion than by intracranial hypertension.
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