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The local effects of systemic digoxin on the cutaneous microcirculation
M Grossmann1, M J Jamieson, W Kirch
1Department of Pharmacology, University of Texas Health Science Center, San Antonio, USA. mgrossma@rcs.urz.tu-dresden.de
European Journal of Clinical Pharmacology
|July 29, 1999
Summary
Digoxin does not affect blood vessel response to vasodilators but enhances vasoconstriction to norepinephrine. This heart medication lowers resting blood pressure and heart rate, impacting cutaneous vascular conductance.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Dermatology
Background:
- Digoxin is a cardiac glycoside used for heart failure and arrhythmias.
- Its effects on peripheral vasculature, particularly cutaneous blood flow, are not fully understood.
- Investigating digoxin's impact on vascular responses is crucial for understanding its systemic effects.
Purpose of the Study:
- To determine if digoxin alters cutaneous vascular responses to acetylcholine (endothelium-dependent vasodilator) and norepinephrine (vasoconstrictor).
- To assess digoxin's effect on baseline cutaneous vascular conductance (CVC) and hemodynamic parameters.
Main Methods:
- A double-blind, cross-over study involving 12 healthy subjects.
- Subjects received digoxin or placebo for 11 days.
- Dose-response curves for acetylcholine and norepinephrine iontophoresis were measured using Laser Doppler Flux (LDF) and Mean Arterial Pressure (MAP) to calculate CVC.
Main Results:
- Digoxin treatment resulted in significantly lower resting blood pressure and heart rate.
- Baseline CVC was significantly higher under digoxin treatment.
- Digoxin augmented the vasoconstrictive effect of norepinephrine but did not alter the response to acetylcholine.
Conclusions:
- Digoxin does not modify the cutaneous vascular response to endothelium-dependent vasodilation.
- Digoxin reduces resting heart rate, blood pressure, and baseline cutaneous blood flow.
- The drug enhances the vasoconstrictive effect of norepinephrine, suggesting a direct vascular action rather than a direct effect on lowering diastolic blood pressure.