Effects of digoxin in isolated human pulmonary vessels.

Acta Pharmacologica Et Toxicologica
E Mikkelsen


In isoalted human pulmonary arteries and veins the contractile response to noradrenaline (1.8 X 10(-5)M) was 33 +/- 7.4% and 20 +/- 4.5% (Mean +/- S.E.M.) of that induced by potassium (127 mM). A variable degree of spontaneous contractile activity was recorded in the vein preparations. This activity was abolished by nifedipine (2.9 X 10(-6)M). Digoxin (10(-6)M) induced contractions in pulmonary vessels. In the arteries, the digoxin contraction developed slowly and reached a maximum amplitude of 90 +/- 4% (Mean +/- S.E.M.) of the potassium evoked contraction. In the veins, the amplitude of the digoxin contraction was 32 +/- 5% of that induced by potassium. Digoxin (10(-6)M) also increased the maximum response to noradrenaline and potassium in both arteries and veins. In the arteries, the noradrenaline and potassium contractions increased to 211 +/- 6.8% and 145 +/- 8.9 of control, and in the veins to 169 +/- 13.5% and 163 +/- 9.9%, respectively. Nifedipine in concentrations which completely relaxes arterial and venous preparations contracted by potassium, had only a slight relaxing effect on digoxin induced contraction. It is concluded that digoxin increases the tension in pulmonary arteries and veins, and increases the maximum ...Continue Reading


Jul 1, 1979·Acta Pharmacologica Et Toxicologica·E MikkelsenO L Pedersen
Oct 1, 1978·Acta Pharmacologica Et Toxicologica·E MikkelsenO L Pedersen
Jun 1, 1975·The American Journal of Physiology·P D JoinerA L Hyman
Mar 15, 1973·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·C van BreemenR Deth
Sep 1, 1968·American Heart Journal·L M LindeG Sarna
Mar 1, 1972·The Journal of Cell Biology·C E DevineA P Somlyo
Feb 1, 1968·The American Journal of Cardiology·M AkbarianW H Abelmann

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May 1, 1984·Progress in Cardiovascular Diseases·T W SmithJ D Marsh
Mar 1, 1984·Progress in Cardiovascular Diseases·T W SmithJ D Marsh
Jul 1, 1984·Progress in Cardiovascular Diseases·T W SmithJ D Marsh

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