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Biomedical subjects

P F Binnion

Publications and source records attributed to P F Binnion.

9 recordsLinked to original sources
PubMed1976

Tissue digoxin concentrations at digoxin intoxication in normal, acutely hypokalemic, and acutely hyperglycemic dogs.

Thirty intact dogs were studied to determine digoxin concentration in various tissues after ventricular tachycardia had been induced by digoxin infusion. A control group was infused solely with digoxin. A second group was made acutely hypokalemic by glucose-insulin infusion before the digoxin infusion. A third group was infused with glucose and digoxin to determine the effect of increased blood glucose levels and osmalarity on the induction of ventricular tachycardia. Results were: (1) The amount of digoxin infused to produce ventricular tachycardia did not differ getween the normal and hypokalemic groups. (2) The concentration of digoxin in various parts of the heart, other muscle tissue, renal cortex, and liver did not differ between the normal and acutely hypokalemic dogs although the amount excreted in bile and urine was reduced in hypokalemia. (3) Acute hypokalemia did not sensitize the myocardium to the arrhythmogenic effects of digoxin. (4) Ventricular tachcardia occurred at a similar plasma digoxin level in normal and acutely hypokalemic dogs. (5) In dogs with a lowered plasma potassium level, junctional tachycardia occurred whereas it did not occur in normal dogs or those with only a high blood glucose level. (6) Ventricular tachycardia occurred in the hyperglycemic dogs at a plasma digoxin level of 170 ng/ml, which was significantly greater than in the other experiments (7) Acute hyperglycemia reduced the mean rate of myocaridal uptake of digoxin into atria and right and left ventricular tissue; and the concentration of digoxin in atria, left ventricle, and interventricular septum was lower at the time of ventricular tachycardia than occurred in normal dogs. (8) Lowering the plasma potassium level in the presence of acute hyperglycemia, which occurred with the glucose-insulin infusion, did increase the myocardial uptake of digoxin. Similar effects of hyperglycemia were noted on mean hepatic uptake and excretion of digoxin and also the renal uptake of the glycoside.

Animals↗
PubMed1976

A comparison of the bioavailability of digoxin in capsule, tablet, and solution taken orally with intravenous digoxin.

Six healthy volunteers were given five single-dose treatments of 0.40 mg digoxin either intravenously, in liquid form, in conventional tablet form (dissolution rate 76 per cent in 1-hour), or in new capsule preparations containing 0.05, 0.10, or 0.20 mg digoxin per capsule. Serum levels, area under the concentration-time curve, and daily urinary digoxin excretion were measured for six days. Higher serum digoxin levels were seen after ingestion of the capsules than after the tablets, with peak levels for the former being 2.2-2.8 times higher than after tablet digoxin. Bioavailability was assessed further by comparing the area under a six-hour concentration-time curve, and again the capsules gave a consistently higher value than the tablets. In addition, the absorption of 0.40 mg digoxin from any of the capsule preparations was much greater than 0.50 mg digoxin in commercially available tablets. The six-day cumulative urinary digoxin excretion was also greater for the capsules than for the 0.20-mg tablets. In comparison with intravenous digoxin, tablets provide 75 per cent maximum bioavailability, whereas the capsule preparations of digoxin improve the bioavailability of digoxin and the 0.20-mg digoxin capsule is absorbed better than 0.25-mg digoxin tablet.

Adult↗
PubMed1975

Tritiated digoxin metabolism after prior treatment with propranolol or diphenylhydantoin sodium.

Digitalis-induced arrhythmias can be suppressed by intravenous potassium, diphenylhydantoin sodium and propranolol. As it is known that hyperkalemia can interfere with the myocardial uptake of digoxin, this study was performed to determine whether diphenylhydantoin sodium or propranolol could exert any antiarrhythmic effect by altering the metabolism of 3H-digoxin and, in particular, the accumulation of the glycoside by cardiac muscle. Three groups of anesthetized dogs were given 6 muCi 3H-digoxin per kilogram intravenously, and in two groups 15 mg/kg diphenylhydantoin sodium or 3 mg/kg propranolol were injected intravenously 15 minutes prior to the glycoside. The concentration of labelled digoxin was measured in plasma up to one hour, and then tissues were removed and analyzed for digoxin content. Diphenylhydantoin sodium did not influence myocardial uptake of digoxin. It is considered its suppressant action on digitalis-induced arrhythmias is not due to any effect on the cardiac accumulation of digoxin. Propranolol did reduce the myocardial uptake of digoxin, but this was not considered of sufficient magnitude to be the main factor in suppressing arrhythmias induced by digitalis. These studies provide evidence that both diphenylhydantoin sodium and propranolol do not have a suppressant effect on digitalis-induced arrhythmias by virtue of any significant interference with the uptake of digoxin by myocardial tissue.

Animals↗