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J T Barnard

Publications and source records attributed to J T Barnard.

5 recordsLinked to original sources
PubMed1985

Tissue digoxin concentrations and digoxin effect during the quinidine-digoxin interaction.

Quinidine elevates serum digoxin concentration in part by reducing the volume of distribution of digoxin, which implies that quinidine displaces digoxin from tissues. The purposes of this study were to: 1) measure the effect of quinidine on tissue digoxin concentrations, and 2) determine if quinidine alters the relation between myocardial digoxin concentration and digoxin effect on myocardial monovalent cation transport. Eighteen dogs were treated with tritiated digoxin until the steady-state serum digoxin concentration was between 1.0 and 1.5 ng/ml. All dogs continued receiving the same dose of digoxin while nine dogs were given quinidine as well. Quinidine was continued until the serum digoxin concentration had increased by at least 25%. At the end of treatment, the serum digoxin concentration in dogs treated with digoxin was 1.2 +/- 0.1 ng/ml compared with 2.1 +/- 0.5 ng/ml in dogs treated with digoxin and quinidine in combination (p less than 0.001). Digoxin concentration in myocardium, skeletal muscle, liver, kidney, stellate ganglion, vagus nerve, femoral nerve, brain and brainstem medulla was higher in dogs treated with a combination of digoxin and quinidine than in dogs treated with digoxin alone, but remained proportional to the serum digoxin concentration in all tissues except the brainstem medulla. Myocardial monovalent cation transport was measured using rubidium-86. The effect of digoxin on myocardial monovalent cation transport did not increase as the serum and myocardial digoxin concentrations increased after quinidine administration.

Animals↗
PubMed1984

Myocardial monovalent cation transport during the quinidine-digoxin interaction in dogs.

To study the relationship of the serum digoxin concentration to the digoxin effect on monovalent cation transport during the quinidine-digoxin interaction, we used radiolabeled rubidium to measure monovalent cation active transport in myocardial biopsy samples from dogs. In a preliminary study, we showed that quinidine did not affect rubidium uptake by myocardial samples from intact dogs. Then, we studied four groups, each consisting of 13 dogs, which received either saline, low dose digoxin, high dose digoxin, or low dose digoxin plus quinidine treatment. In these groups of dogs, the following steady state serum digoxin concentrations were achieved: saline-treated, 0 ng/ml; low dose digoxin, 1.2 +/- 0.2 ng/ml (mean +/- SD); high dose digoxin, 2.4 +/- 0.4 ng/ml; and low-dose digoxin plus quinidine treated, 2.3 +/- 1.1 ng/ml. Compared to control values, rubidium uptake was decreased by 17% in dogs treated with low dose digoxin (P less than 0.05) and by 38% in dogs treated with high dose digoxin (P less than 0.01 vs. saline-treated, P less than 0.01 vs. low dose digoxin). Although low dose digoxin plus quinidine-treated dogs had the same mean serum digoxin concentration as the high dose digoxin-treated dogs, rubidium uptake in low dose digoxin plus quinidine-treated dogs was decreased by only 17% compared to control (P less than 0.05 vs. saline-treated, (P less than 0.01 vs. high dose digoxin). During the quinidine-digoxin interaction in the intact dog, the reduction in myocardial rubidium uptake is less than expected from the increase in serum digoxin concentration.

Animals↗