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Biomedical subjects

J W Prather

Publications and source records attributed to J W Prather.

10 recordsLinked to original sources

Metabolic consequences of glucose-insulin-potassium infusion in treatment of acute myocardial infarction.

Eighteen patients treated with glucose-insulin-potassium infusion for anaerobic support of acutely ischemic myocardial tissue were studied to ascertain the metabolic consequences of this therapy, for acute myocardial infarction. Twelve patients with acute myocardial infarction were treated in a conventional manner and served as control subjects. The glucose-insulin-potassium solution was composed of 300 g of glucose, 50 units of regular insulin and 80 mEq of potassium ion per liter, and was infused at a rate of 1.5 ml/kg per hour through the right atrial port of an indwelling Swan-Ganz thermodilution catheter. Serial measurements of serum electrolytes, cardiac and hepatic enzymes, glucose and osmolality were obtained every 4 to 6 hours for 4 days. Twenty-four urinary volume and potassium levels were measured daily. Pulmonary arterial end-diastolic pressure was measured hourly and the cardiac index daily for the duration of the study. Serum potassium increased to 5 mEq/liter during the infusion and to more than 6 mEq/liter after infusion in 28 percent of patients. No recognizable complications or arrhythmias accompanied this transient hyperkalemia. Potassium balance studies revealed a net total body potassium ion gain of 120 MEq during the study. The second most frequent finding was an elevation of serum glucose (mean 175 mg/100 ml); in all instances this was controlled with supplemental administration of insulin. The serum osmolality and fluid balance remained normal in all patients during the study. Serum glutamic oxaloacetic transaminase (SGOT) and fraction 5 of lactic dehydrogenase (LDH) were increased in 34 percent of the patients during the last 12 to 18 hours of the glucose-insulin-potassium infusion. Characterization of these enzymes suggested a hepatic origin for these changes. This study suggests that glucose-insulin-potassium infusion is a relatively safe procedure in which postinfusion hyperkalemia is the most serious potential complication.

Aspartate Aminotransferases↗

Reduction of hospital mortality rate of acute myocardial infarction with glucose-insulin-potassium infusion.

Free fatty acids (FFA), the predominant myocardial energy substrate, are present in increased quantities immediately following acute myocardial infarction (AMI) and may cause deleterious alterations in cardiac rhythm, oxygen consumption, and mechanical performance. In an attempt to suppress FFA and simultaneously increase the availability of carbohydrate as a myocardial substrate, 70 patients with unequivocal AMI were administered a right atrial infusion of glucose-insulin-potassium (GIK) (300 gm. of glucose, 50 U. of regular insulin, and 80 mEq. of KC1 per liter of H2O) at a constant rate of 0.5 to 2.0 ml. per kilogram per hour for 48 hours. A dramatic fall in FFA (944 +/- 57 to 289 +/- 16 muEq per liter, p less than 0.0005) occurred during GIK infusion, and FFA rebounded to 420 +/- 39 muEq per liter (p less than 0.005) when GIK was discontinued. The hospital mortality rate in the 70 GIK recipients was compared to that of 64 untreated patients (controls) from the same coronary-care unit during the previous year. GIK and control groups had similar severity of infarction as assessed by prognostic scales of Killip, Peel, and Norris, respectively. The hospital mortality rate was reduced in the GIK recipients compared to the control group (11/70 vs. 19/64, p less than 0.05). In patients without history of prior myocardial infarction, the mortality rate was reduced four-fold in GIK recipients compared to controls (6 vs. 24 per cent, p less than 0.05). Complications of GIK infusion were infrequent and included chiefly hyperglycemia and hyperkalemia, both of which dictated meticulous monitoring of serum chemistries. The data suggest that suppression of plasma FFA with GIK infusion may be associated with a significant reduction in the hospital mortality rate of acute myocardial infarction.

Acute Disease↗

Micromanipulation of pressure in terminal lymphatics in the mesentery.

The terminal lymphatics are a network of highly previous vessels that are distributed in a loose association with the blood capillary bed, in particular along with the collecting venules. The base-line pressure in these lymphatics is close to atmospheric, but after they converge to form valved collecting channels PL is increased with a pressure differential of 1-2 cmH20 built up across each valve. This increment in lymphatic pressure is clearly related to the presence of one-way valves, the contractile activity of the collecting channels, and the comparative impermeability of these channels. The pressure differential required to draw fluid from the interstitium into the lymphatics would appear to reside in the vasomotor activity of the collecting channels, although the data do not rule out changes in Pt coincident with net capillary filtration or absorption.

Animals↗