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Biomedical subjects

K Taubert

Publications and source records attributed to K Taubert.

At least 55 records · Page 3Linked to original sources
PubMed1977

Contraction and resting stiffness of isolated cardiac muscle: effects of inotropic agents.

The purpose of this study was to test the hypothesis that either hypoxia and its combined effects with extracellular calcium (Ca), digoxin, and ouabain, or these positive inotropic agents acting alone or in combination, influence contraction and resting stiffness of isolated papillary muscle. Stiffness was measured utilizing the sinusoidal forcing function technique. Neither an increase in extracellular calcium concentration (from 2.5 to 4.0 mM) nor digoxin or ouabain in either Ca concentration altered contraction or resting stiffness in the well-oxygenated environment. Resting stiffness for any given resting tension was increased at the end of hypoxia only in the presence of digoxin, and this occurred in both 2.5 mM Ca (P less than 0.02) and in 4.0 mM Ca (P = 0.05). Contraction stiffness for any given tension was increased in 2.5 mM Ca by hypoxia alone (P less than 0.05) and by hypoxia in the presence of digoxin (P less than 0.005) and ouabain (P less than 0.02), but was not increased in any experiments conducted in 4.0 mM Ca. The conclusions from these data are that certain experimental conditions of the study evoked different directional changes in stiffness and contractility. Further, changes in contraction stiffness are not always paralleled by changes in resting stiffness.

Animals↗
PubMed1976

Effects of digitalis and calcium on papillary muscles in normal and hypoxic states.

The effects of digoxin and ouabain in 2.5 and 4.0 mM extracellular calcium were studied in well-oxygenated and hypoxic isolated, isometrically contracting cat papillary muscles. Muscle digoxin content was measured at the conclusion of the digoxin experiments. In the well-oxygenated environment muscles in the higher Ca bathing media reached peak glycoside inotropic effect sooner and contained 2.7 times more digoxin. During hypoxia and reoxygenation muscles contracting with glycosides performed no differently than those without a glycoside present. Muscle digoxin content was lowered at the end of hypoxia (P less than 0.05) in 2.5 mM Ca; after reoxygenation digoxin content was significantly greater than either before or after hypoxia (P less than 0.001). Hypoxic depression of muscle performance was attenuated in 4.0 mM Ca but muscles in 2.5 mM Ca showed greater improvement during reoxygenation even though the muscles in 4.0 mM Ca had significantly greater digoxin content at the end of reoxygenation (P less than 0.02). It therefore is concluded that, although altered extracellular calcium can alter performance during hypoxia and reoxygenation, muscle performance is not aided by the presence of digitalis and under these conditions performance cannot be correlated with muscle digoxin levels.

Animals↗
PubMed1975

Serum digoxin levels using an 125I-labelled antigen: Validation of method and observations on cardiac patients.

1. Determinations of serum digoxin levels utilizing commercially available kits with an 125I-labelled antigen were precise and not materially different from results obtained with a 3H-labelled antigen. 2. In order to approximate the steady state level, serum digoxin levels should be drawn either before or at least six hours following the administration of an oral tablet. 3. Concomitantly given thiazide diuretics did not interfere with the absorption of a tablet of digoxin. 4. In the digitalized patient, slow alterations in serum levels after oral administration appeared well correlated with, at least, the negative chronotropic effects of the drug. 5. Maximal exercise testing, a maneuver often applied to cardiac patients, does not significantly alter the serum digoxin level.

Administration, Oral↗
PubMed1975

Altered tissue digoxin uptake after a toxic dose.

Tissue distribution and left ventricular (LV) effects of digoxin were studied after intravenous administration of low and high doses to dogs. LV dP/dt was increased by 0.03 mg/kg digoxin in nine, group A, and digoxin-induced arrhythmias or death occurred after 0.14 mg/kg in nine others, group B. Two hours after dosing during the slow excretion phase confirmed by serial serum sampling, the animals were killed. Serum and tissue extract digoxin determinations were performed by radioimmunoassay. Digoxin levels in group A were serum 3.9 ng/ml, kidney 428 ng/gm wet wt, liver 41, pancreas 39, diaphragn 21, apex, freewall, and septum LV 117-122, right ventricle (RV) 105, left atrium (LA) 51, right atrium (RA) 50, and the serum to apex LV ration was 1:32. The tissue contents and distribution were similar to previous [3H]digoxin data. The concentrations were higher in B; for all p less than 0.001. The toxic to therapeutic concentration ratios were serum 10, kidney 2.8, liver 5.5. pancreas 5,4, diaphragm 6.5, LV 4.3, RV 4.0, LA 3.5, RA 3.4. The serum to LV ratio was lower at 1:13, p less than 0.001. Myocardial toxicity was associated with marked but apparently limited increases in tissue digoxin content in this preparation. The disproportionately high serum level suggests paralysis or saturation of kidney and other tissue binding resulting in lower serum to tissue concentration ratios. Whenever serum to tissue ratios vary from expected values, serum digoxin levels may not be linearly related to tissue content or cardiac effects.

Animals↗