Digoxin distribution in the dog's left ventricle in the presence of coronary artery ligation

Be, Hopkins; Rr, Taylor; Henderson, C. B.; Burrows, P.C.

doi:10.1016/0022-2828(73)90054-0

Cited by 17 publications

(6 citation statements)

References 20 publications

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“…Previous studies in our own and other laboratories (11,19,20) have demonstrated that after coronary arterial occlusion in canine experimental models, marked reduction in in vivo binding of tritiated digoxin occurs in the region of myocardial ischemia. These findings are attributable, at least in part, to alterations in regional blood flow to ischemic or infarcted myocardium (20).…”

Section: Discussionmentioning

confidence: 86%

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Conroy¹,

Smith²

1976

J. Clin. Invest.

100

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Section: Discussionmentioning

confidence: 86%

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Conroy¹,

Smith²

1976

J. Clin. Invest.

100

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“…Little is known of the influence of heart disease or of lesions producing cardiac volume or pressure overload on the myocardial uptake of digitalis. We have recently observed diminished digitalis tolerance in the dog with circulatory volume overload and cardiac hypertrophy produced by an aortocaval fistula, both in the presence and absence of cardiac failure (Cope, Hopkins & Taylor, 1973). This observation prompted the present study of the myocardial uptake of digoxin in dogs with such fistulae.…”

Section: Introductionmentioning

confidence: 87%

“…Samples were also taken from inner and outer halves of left ventricular myocardium. The measurement of digoxin in the samples has been previously described (Hopkins & Taylor, 1973;Hopkins, Lloyd & Taylor, 1974;Lloyd & Taylor, 1975a). The samples were blotted dry, weighed, homogenized in 8.0 ml of 50% ethanol in water, extracted with the addition of a further 80 ml absolute ethanol, containing 2.0 mg of unlabelled carrier digoxin, and centrifuged at 2,100 g for 40 min.…”

Section: E T H O D Smentioning

confidence: 99%

Increase in Myocardial Digoxin Content Associated With Circulatory Volume Overload in the Dog

Lloyd

Hopkins

Taylor

1976

Clin Exp Pharmacol Physiol

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1. Tritiated (12alpha-3H) digoxin (0-05 mg/kg body weight) was administered intravenously to conscious dogs with circulatory volume overload induced by previous creation of aorto-caval fistulae. Dogs were killed after 5 min, 1, or 4 h, and the myocardium sampled. Digoxin was extracted and counted and results compared to those in normal dogs. 2. At each time, myocardial digoxin concentration of all cardiac chambers in test dogs was greater than normal. Plasma digoxin concentration measured 5 min after administration was greater in dogs with fistulae but the subsequent levels were not different. 3. Anaesthetized and open-chest dogs with fistulae studied 5 min after digoxin administration had greater myocardial concentrations than similarly studied normal dogs. Although myocardial concentrations of digoxin were higher in anaesthetized than in conscious dogs the group with fistulae had higher values than did the normal group, as was the case for unanaesthetized dogs. 4. The basis for the effect of fistula is probably multifactorial. Diminised peripheral blood flow and peripheral digoxin delivery and uptake, resulting initially in higher digoxin levels in plasma perfusing the myocardium, may play a role. Increased myocardial mechanical and metabolic activity almost certainly are important. Cardiac hypertrophy, cardiac failure per se and plasma electrolyte changes are probably not. 5. The results are consistent with previously demonstrated reduced digitalis tolerance in the dog with circulatory volume overload.

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“…Such patients have survived with serum concentrations of up to 20ng/ml. Hopkins et al (1973) and Beller et al (1972) have shown that digoxin distribution in the myocardium can be affected by ischaemia or changes in blood flow to various portions of the heart.…”

Section: Changes In Disease Statementioning

confidence: 96%

Interpretation of the Serum Digoxin Concentration

Weintraub

1977

Clinical Pharmacokinetics

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Significant problems exist in the interpretation of serum digoxin concentration data. Failure to distinguish between results that do not require precise clinical correlation (proof of absorption, presence of drug, etc) and those which depend upon clinical correlation for their meaning ('toxicity' or 'effectiveness') can result in interpretive errors. Problems relating to the source of the serum digoxin concentration can also confound interpretation. Such difficulty may be controllable (obtaining the sample at the proper time, haemolysis, etc) or related to the laboratory technique (cross-reactivity with digoxin metabolites or other medications, technical errors, or lack of precision). Variation within the same patient over time or between patients related to disease (alterations in electrolytes, adrenergic or parasympathomimetic tone, or other medications) may prevent the direct attribution of an observed phenomenon to a particular digoxin concentration. Techniques for determining the effect of digoxin do exist and can be used to gather data for clinical correlations. Ways of improving the interpretaion of serum digoxin concentrations also exist and should be used to improve their value in patient management. The serum digoxin concentration seems to have an important future role. However, we need to know how better to interpret and exploit serum digoxin concentration data.

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Digoxin distribution in the dog's left ventricle in the presence of coronary artery ligation

Cited by 17 publications

References 20 publications

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Increase in Myocardial Digoxin Content Associated With Circulatory Volume Overload in the Dog

Interpretation of the Serum Digoxin Concentration

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