Glenda Balderson

The effect of intravenous magnesium sulphate on parathyroid function in primary hyperparathyroidism

Ten patients with primary hyperparathyroidism caused by enlargement of a single parathyroid gland were studied preoperatively. An intravenous bolus of 4 g magnesium sulphate followed by a continuous infusion of 2 g per hour for 3 hours increased serum magnesium from 0.76 to 2.12 mmol/l (median values,p <0.005). Serum C-terminal parathyroid hormone (PTH) decreased from 94 to 78 pmol/l (p <0.005), and serum intact PTH from 7.0 to 4.8 pmol/l (p <0.008). The PTH changes preceded decreases in serum total calcium from 2.79 to 2.55 mmol/1 (p <0.01), and serum ionized calcium from 1.52 to 1.45 mol/1 (p <0.007). Urinary calcium excretion increased and urinary phosphate excretion decreased. Serum phosphorus, pH, albumin, creatinine, alkaline phosphatase, and urinary cyclic AMP showed no significant changes. The study showed that an intravenous magnesium sulphate infusion which at least doubled the normal serum magnesium concentration significantly suppressed PTH secretion in patients with primary hyperparathyroidism and subsequently reduced the serum calcium concentration.RésuméDix patients présentant un hyperparathyroïdisme dû à lhypertrophie dune seule glande parathyroïdienne ont été étudiés avant dêtre opérés. Une injection intraveineuse de sulfate de magnésie, 4 g, en bolus, suivie dune infusion continue de 2 g/h pendant 3 heures a augmenté la concentration sérique en magnésie de 0.76 à 2.12 mmol/l (valeurs médianes,p < 0.005). La concentration en parathormone sérique (PTH), dosée par la méthode immunologique C-terminale a baissé de 94 à 78 pmol/l (p < 0.005) alors que celle de la PTH intacte a baissé de 7.0 à 4.8 pmol/l (p < 0.008). Ces changements en concentration de PTH ont précédé des diminutions en calcium total de 2.79 à 2.55 mmol/l (p < 0.01), et de calcium ionisé de 1.52 à 1.45 mmol/l (p < 0.007). Le taux dexcrétion urinaire de calcium a augmenté alors que lexcrétion en phosphates a diminué. Il ny avait pas de modifications significatives dans les valeurs de la phosphorémie, le pH, lalbuminémie, la créatinine ou les phosphatases alcalines dans le sérum; de même, le taux dAMP cyclique urinaire na pas changé. Cette étude montre quune perfusion intraveineuse de sulfate de magnésie, augmentant la concentration sérique en magnésie dau moins le double, déprime de façon significative la sécrétion en PTH chez les patients présentant un hyperparathyroîdisme primitif et par conséquent a réduit lhypercalcémie.ResumenDiez pacientes con hiperparatiroidismo primario causado por una glándula única aumentada de tamaño fueron estudiados preoperatoriamente. Un bolo intravenoso de 4 g de sulfato de magnesio seguido de una infusión continua a razon de 2 g por hora por 3 horas, produjo un aumento en el magnesio sérico de 0.76 a 2.12 mmol/l (valores promedio,p < 0.005). El nivel sérico de la fracíon C-terminal de la hormona paratiroidea (PTH) descendió de 94 a 78 pmol/l (p < 0.005), y el nivel de la PTH intacta de 7.0 a 4.8 pmol/l (p < 0.008). Los cambios en la PTH precedieron a la disminución en la concentracíon del calcio sérico de 2.79 a 2.55 mmol/l (p < 0.01), y del calcio ionizado sérico de 1.52 a 1.45 mmol/l (p < 0.007). La excreción de calcio urinario aumentó y la excreción de fosfato urinario disminuyó. El fósforo sérico, pH, albúmina, creatinina, fosfatasa alcalina, y AMP cíclica urinaria no mostraron cambios significativos. El estudio demostró que una infusión intravenosa de sulfato de magnesio que logre por lo menos doblar la concentracíon normal de magnesio sérico suprime en forma significativa la secrecíon de PTH en pacientes con hiperparatiroidismo primario y consecuentemente reduce la concentracíon sérica de calcio.Ten patients with primary hyperparathyroidism caused by enlargement of a single parathyroid gland were studied preoperatively. An intravenous bolus of 4 g magnesium sulphate followed by a continuous infusion of 2 g per hour for 3 hours increased serum magnesium from 0.76 to 2.12 mmol/l (median values,p <0.005). Serum C-terminal parathyroid hormone (PTH) decreased from 94 to 78 pmol/l (p <0.005), and serum intact PTH from 7.0 to 4.8 pmol/l (p <0.008). The PTH changes preceded decreases in serum total calcium from 2.79 to 2.55 mmol/1 (p <0.01), and serum ionized calcium from 1.52 to 1.45 mol/1 (p <0.007). Urinary calcium excretion increased and urinary phosphate excretion decreased. Serum phosphorus, pH, albumin, creatinine, alkaline phosphatase, and urinary cyclic AMP showed no significant changes. The study showed that an intravenous magnesium sulphate infusion which at least doubled the normal serum magnesium concentration significantly suppressed PTH secretion in patients with primary hyperparathyroidism and subsequently reduced the serum calcium concentration. Dix patients présentant un hyperparathyroïdisme dû à lhypertrophie dune seule glande parathyroïdienne ont été étudiés avant dêtre opérés. Une injection intraveineuse de sulfate de magnésie, 4 g, en bolus, suivie dune infusion continue de 2 g/h pendant 3 heures a augmenté la concentration sérique en magnésie de 0.76 à 2.12 mmol/l (valeurs médianes,p < 0.005). La concentration en parathormone sérique (PTH), dosée par la méthode immunologique C-terminale a baissé de 94 à 78 pmol/l (p < 0.005) alors que celle de la PTH intacte a baissé de 7.0 à 4.8 pmol/l (p < 0.008). Ces changements en concentration de PTH ont précédé des diminutions en calcium total de 2.79 à 2.55 mmol/l (p < 0.01), et de calcium ionisé de 1.52 à 1.45 mmol/l (p < 0.007). Le taux dexcrétion urinaire de calcium a augmenté alors que lexcrétion en phosphates a diminué. Il ny avait pas de modifications significatives dans les valeurs de la phosphorémie, le pH, lalbuminémie, la créatinine ou les phosphatases alcalines dans le sérum; de même, le taux dAMP cyclique urinaire na pas changé. Cette étude montre quune perfusion intraveineuse de sulfate de magnésie, augmentant la concentration sérique en magnésie dau moins le double, déprime de façon significative la sécrétion en PTH chez les patients présentant un hyperparathyroîdisme primitif et par conséquent a réduit lhypercalcémie. Diez pacientes con hiperparatiroidismo primario causado por una glándula única aumentada de tamaño fueron estudiados preoperatoriamente. Un bolo intravenoso de 4 g de sulfato de magnesio seguido de una infusión continua a razon de 2 g por hora por 3 horas, produjo un aumento en el magnesio sérico de 0.76 a 2.12 mmol/l (valores promedio,p < 0.005). El nivel sérico de la fracíon C-terminal de la hormona paratiroidea (PTH) descendió de 94 a 78 pmol/l (p < 0.005), y el nivel de la PTH intacta de 7.0 a 4.8 pmol/l (p < 0.008). Los cambios en la PTH precedieron a la disminución en la concentracíon del calcio sérico de 2.79 a 2.55 mmol/l (p < 0.01), y del calcio ionizado sérico de 1.52 a 1.45 mmol/l (p < 0.007). La excreción de calcio urinario aumentó y la excreción de fosfato urinario disminuyó. El fósforo sérico, pH, albúmina, creatinina, fosfatasa alcalina, y AMP cíclica urinaria no mostraron cambios significativos. El estudio demostró que una infusión intravenosa de sulfato de magnesio que logre por lo menos doblar la concentracíon normal de magnesio sérico suprime en forma significativa la secrecíon de PTH en pacientes con hiperparatiroidismo primario y consecuentemente reduce la concentracíon sérica de calcio.

Acute occlusion of the portal vein in the calf

Complete occlusion of the portal vein for 2 hours has been studied, in the calf, in an attempt to produce survival with appropriate resuscitation. Systemic blood pressure fell immediately on occlusion and the portal blood became markedly acidotic with a rise in packed cell volume and plasma potassium. Circulating blood volume decreased by 50 per cent despite major transfusion. When the occlusion was released, blood pressure returned to normal levels for several hours. However a hemorrhagic enteropathy developed in the small intestine. Large quantities of serosanguineous fluid collected in the intestinal wall and lumen and in the peritoneal cavity. Marked hemo-concentration developed and the animal did not respond to further resuscitation. All animals grew E. coli on portal blood culture after occlusion. It is concluded that sequestration of fluid in the portal circulation is the main cause of death following portal occlusion, but that a rise in plasma potassium, coliform bacteremia, and progressive acid-base disturbances may well be contributory factors.

Changes in Left Ventricular Function Produced by Excision of a Myocardial Infarct

Left ventricular function has been measured in calves before and after the production of a myocardial infarct by ligation of the anterior descending coronary artery. In 20 animals function was measured after the area of the acute infarct had been excised and the left ventricle repaired by direct suture. Infarcts equal to 20% of the left ventricle were found to impair left ventricular function, and significant immediate improvement in function was measured in one-third of the animals in which an infarct was resected.

Immunological results of hepatic assistance procedures

Hemodynamic and immunological effects were studied in eight normal calves during and after hepatic assist with a pig liver. Use of an oxygenator in the circuit allowed control of the rate of perfusion of the liver and using this system no hypotension or metabolic acidosis was observed in the recipient. Porcine protein was present in the sera of six surviving calves up to 14 days after perfusion. No antibodies to this protein were demonstrated either by immunodiffusion or by tanned red cell agglutination. Hypersensitivity and anaphylaxis did not occur when the calves were challenged intravenously with poreine protein and pig liver extract 3 weeks after the initial perfusion. No antibodies were demonstrated in the calf either as a primary response to circulating pig antigen or as a secondary response to a challenge with porcine protein or pig liver extract. Possible reasons for these findings and their significance are discussed.