Biomedical subjects
Publications and source records attributed to L Benson.
Banding of the pulmonary artery is a difficult procedure that often requires band readjustment. A new technique for placing and adjusting pulmonary artery bands using an adjustable snare is presented, together with cases illustrating its application.
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Infusions with stepwise increasing concentrations of epinephrine (from 2.5 to 10 micrograms/min) and norepinephrine (0.5-2.0 micrograms/min) were given to normal subjects. During infusion of epinephrine there was a clear rise of the serum parathyroid hormone (PTH) levels already at the lowest concentration. Concomitantly there was a fall in the serum concentrations of calcium. The PTH levels returned to baseline promptly after termination of infusion whereas hypocalcaemia persisted up to 30 minutes, indicating a primary response of PTH to epinephrine. When propranolol was given prior to and during the epinephrine infusion no significant changes occurred for either PTH or calcium. During infusion of norepinephrine no consistent significant changes were noted for either PTH or serum calcium. Thus, our data do not support any concept of a basal adrenergic tone which normally modulates the secretion of PTH. However, during conditions of stress the beta-adrenergic stimulation night be of importance.
In-vitro and in-vivo studies have suggested a role for the adrenergic system in the regulation of secretion of parathyroid hormone (PTH). In the present study the effects of insulin induced hypoglycaemia on serum concentrations of PTH, cortisol, calcium and phosphate were evaluated in ten healthy subjects. Maximum hypoglycaemia occurred 25 to 35 min after administration of insulin at a standard dose of 0.15 U/kg body weight. All this time there was a slight and transient increase of the serum calcium concentrations whereas there was a marked drop in the serum phosphate levels with a nadir 15 min after maximum hypoglycaemia. Cortisol levels were below baseline when blood glucose was as lowest but increased to a maximum level of 200% 60 minutes after maximum hypoglycaemia. Serum PTH levels increased significantly and reached a maximum of 130% of baseline values concomitant with maximum hypoglycaemia, whereafter they returned to pre-insulin-injection levels within 15 minutes. These findings indicate that during stress endogenous catecholamines affect the secretion of PTH which could be of physiologic importance. In five patients with primary hyperparathyroidism there was, however, no increase in the PTH levels, although they displayed the same response to hypoglycaemia for cortisol and phosphate. This supports previous suggestions that these patients have an impaired capacity to respond to circulating catecholamines.
The effects of physical exercise on plasma ionized calcium, total serum calcium and parathyroid hormone (PTH) concentrations were evaluated in healthy subjects submitted to work on an ergometer bicycle. When the workload was increased stepwise there was a significant increase (P less than 0.001) in the calcium concentrations (ionized calcium from 1.13 +/- 0.03 (SD) to 1.24 +/- 0.03 mmol 1(-1) and total calcium from 2.35 +/- 0.07 to 2.48 +/- 0.07 mmol 1(-1] when the workload exceeded approximately 65% of the estimated maximum--i.e. a load that caused accumulation in blood of lactic acid. The rise in plasma ionized calcium was, therefore, presumably largely attributed to the acidosis but reduction of plasma volume and influx from extracellular sources might also have contributed. Beta blockade (with oral intake of propranolol) reduced physical capacity, shortened the duration of work and caused less acidosis. These factors were probably responsible for a smaller rise in ionized calcium during beta blockade (7 +/- 4%) than in control studies (21 +/- 5%) without medication in subjects examined during short-term maximal exercise. Long-term (1 h) steady-state work which caused fatigue without producing lactic acidosis did not affect the calcium concentrations. Despite the effects of work on calcium levels there was no discernible suppression of the PTH concentrations. This might have been due to a concomitant stimulation of PTH secretion by work.
Experimental studies have suggested that in primary hyperparathyroidism (HPT) the cells of the hyperfunctioning parathyroid tissue retain some capacity for stimulation and that an increase in secretion of parathyroid hormone (PTH) can occur when the extracellular calcium concentration is lowered within the hypercalcaemic range. We have tested this hypothesis in 23 patients with HPT, 10 patients with hypercalcaemia of other origin (7 of whom had disseminated malignant disease) and 17 normal subjects. In all three groups a single injection of 100 MRC units of salmon calcitonin caused a reduction in serum calcium of approximately 3 to 5%. In the hypercalcaemic patients this reduction was correlated to the basal calcium level (r = -0.57, P less than 0.01). In the patients with HPT, although they all remained hypercalcaemic, the decrease in serum calcium was associated with a mean increase in serum PTH of 10%. Only in 2 patients did such an increase fail to occur despite an adequate decrease in serum calcium. These 2 patients had high basal PTH levels and the lack of response might have been due to a high degree of autonomous parathyroid function. Calcitonin also reduced serum calcium and increased serum PTH in normal subjects. None of the patients with hypercalcaemia of other origin than primary HPT displayed a secretory PTH response to serum calcium reduction. Thus, this test could be of practical clinical value, particularly in patients with borderline PTH values. A calcitonin-induced rise in PTH while serum calcium is lowered within the hypercalcaemic range strongly suggests primary HPT.
A young woman presented with widespread bilateral infiltrates on chest X-ray and a high fever. Investigations for bacterial, mycobacterial, and fungal infections were negative. A biopsy of the lung showed granulomas, and corticosteroid medication was given on vital indication because of the rapidly progressive disease. There was a dramatic response, with regression of the chest X-ray changes and the fever and the patient was discharged on her own request with a tentative diagnosis of acute sarcoidosis. One month later she was admitted in an alarming state with almost completely consolidated lung and died a few hours later. Autopsy revealed generalized aspergillosis. Renewed extensive investigation of the earlier lung biopsy revealed hyphae. After her death, the case history of an elder brother was traced and revealed that he had died at early age in a generalized granulomatous disease. Although no definite diagnosis can be made, it seems likely that both siblings suffered from a defect in the immune system, probably chronic granulomatous disease of the autosomal recessive type. This disease is sometimes found in young adults without a clear history of earlier infections.
Pulmonary arteriovenous fistulas developed following a superior vena cava-right pulmonary artery shunt in a patient with cyanotic heart disease. An axillary arteriovenous fistula was created to improve oxygenation, but its effectiveness was compromised by the pulmonary fistulas. Transcatheter coil embolization of the pulmonary fistulas was performed with clinical improvement.
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In normal human monocyte macrophages 125I-labeled beta-migrating very low density lipoproteins (125I-beta-VLDL), isolated from the plasma of cholesterol-fed rabbits, and 125I-human low density lipoprotein (LDL) were degraded at similar rates at protein concentrations up to 50 micrograms/ml. The high affinity degradation of 125I-labeled human LDL saturated at approximately 50 micrograms/ml; however, 125I-labeled rabbit beta-VLDL high affinity degradation saturated at 100-120 micrograms/ml. The activity of the beta-VLDL receptor was 3-fold higher than LDL receptor activity on freshly isolated normal monocyte macrophages, but with time-in-culture both receptor activities decreased and were similar after several days. The degradations of both beta-VLDL and LDL were Ca2+ sensitive, were markedly down regulated by sterols, and were up regulated by preincubation of the cells in a lipoprotein-free medium. The beta-VLDL receptor is genetically distinct from the LDL receptor as indicated by its presence on monocyte macrophages from a familial hypercholesterolemic homozygote. Human thoracic duct lymph chylomicrons as well as lipoproteins of Sf 20-5000 from fat-fed normal subjects inhibited the degradation of 125I-labeled rabbit beta-VLDL as effectively as nonradioactive rabbit beta-VLDL. We conclude: 1) the beta-VLDL receptor is genetically distinct from the LDL receptor, and 2) intestinally derived human lipoproteins are recognized by the beta-VLDL receptor on macrophages.
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Experience with high-resolution, real-time sonography of four infants with differing extrathoracic left-to-right shunts is presented. Intracranial and parahepatic arteriovenous malformations gave rise to congestive heart failure as their primary or sole manifestation. Partial anomalous pulmonary venous return to the inferior vena cava in one patient and to the portal vein in another was associated with other congenital cardiac anomalies. Once an arteriovenous malformation was suspected, sonography was useful as the initial imaging procedure to localize it and to direct attention to the most useful and least hazardous studies for detailed evaluation.
The technical features of positron computed tomography are reviewed, and the positron-emitting tracers of flow and metabolism and their relation to physiologic processes are described. The authors report some of their clinical experience with this new modality and emphasize areas of pediatric disorders of the heart that are likely to benefit from positron computed tomography.
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Serum theophylline levels were compared after the administration of a sustained-release (Theo-Dur, Key Pharmaceuticals, USA) vs. a rapid-release (Glyphyllin, Ikapharm, Israel) theophylline preparation to 24 children suffering from chronic bronchial asthma. They received each of the two drugs for a 5-d period, and serum theophylline levels were determined on the 6th d. Therapeutic serum levels were achieved in 66.6 and 75% of the patients receiving sustained-release and rapid-release theophylline preparations, respectively. The peak-trough difference for the rapid-release drug was higher than that of the sustained-release preparations (5.5 +/- 2.6 micrograms/ml vs. 2.6 +/- 2.3 micrograms/ml). Both drugs caused nearly the same low percentage of side effects (15 and 16.6%). A noncompliance rate of 16.6% was found with the rapid-release drug, and all the parents preferred the sustained-release drug is preferable for chronic treatment of children with bronchial asthma, as it maintains more stable serum theophylline levels and has a higher compliance rate.
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The peak ratio of left ventricular systolic pressure/systolic volume (PV) has been shown to be a close approximation to Emax, an index of contractility independent of both preload and afterload. We studied 17 children with left-sided cardiac disease during catheterization by a combined high-fidelity catheter and m-mode echocardiographic technique. Emax, indexed for body surface area, was calculated at rest and during supine exercise at 25% and 50% of maximal upright workload. In addition, we studied 15 control subjects with a noninvasive approximation of peak P/V, the peak systolic LV pressure/smallest systolic LV volume. Patients with left ventricular pressure overload showed an increased Emax value at rest and a further increase with exercise. Patients with left ventricular volume overload or cardiomyopathy had a normal value of Emax at rest and had only small increases with exercise. Patients with both volume and pressure overload had a resting Emax value that was increased, but no further increase occurred with exercise. Emax in children seems to be a sensitive index of contractility during physiologic stress and can be used to assess left ventricular functional reserve capacity both pre- and post-operatively.