caa a22 4500 477071902 CHVBK 20180405111428.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF00051126 doi (NATIONALLICENCE)springer-10.1007/BF00051126 Coronary vasomotor responses in cyclosporine-treated piglets [Elektronische Daten] [Guy Berkenboom, Dmitri Brékine, Philippe Unger, Béatrice Gulbis, Jeanine Fontaine] Summary: Chronic treatment with cyclosporine A (Cx) seems to produce a decreased ability of the endothelium to secrete nitric oxide. However, its effect on the coronary arterial system remains controversial. Therefore, coronary arteries isolated from piglets treated by intramuscular injections of Cx 10 mg/kg day, IM, for 22 days were studied in organ baths and compared with those isolated from control animals (IM injections of the Cx solvent). Depolarization-induced contractions (KCl 120 mM) were similar in both groups, whereas the acetylcholine-induced contractions (percent of 120 mM KCl) were enhanced: The area under the curve (AUC) was 245±51 in the Cx group versus 110±15 in the control group (p<0.05). Removal of the endothelium did not significantly modify the acetylcholine-induced contractions in both groups and, therefore, did not attenuate the enhanced responsiveness to acetylcholine in the Cx group. On unrubbed rings contracted with prostaglandin F2α, the endothelium-dependent relaxations from serotonin (in the presence of 1 μM ketanserin) were reduced: The AUC was 479±24 in the Cx group versus 385±22 in the control group (p<0.02). Larger AUC values were also found for bradykinin and substance P in the Cx group: 158±18 versus 55±17 (in the control group, p<0.01) and 198±8 versus 145±12 (p<0.01), respectively. Nevertheless, no alteration in calcium ionophore-induced relaxations was observed: The AUC was 217±10 in the Cx group and 224±18 in the control group (NS). Indomethacin incubation (10 μM) did not prevent the impairment in endothelium-dependent relaxations and did not attenuate the cyclosporine-induced augmentation of acetylcholine-induced contractions. Thus, chronic administration of cyclosporine to piglets impairs the coronary endothelial function and produces functional changes in smooth muscle cells. These alterations may play a role in the occurrence of cardiac graft vasculopathy. Kluwer Academic Publishers, 1996 cyclosporine nationallicence EDRF nationallicence coronary artery nationallicence piglet nationallicence Berkenboom Guy Department of Cardiology, Erasme Hospital, Brussels, Belgium aut Brékine Dmitri Department of Clinical Chemistry, Erasme Hospital, Brussels, Belgium aut Unger Philippe Department of Cardiology, Erasme Hospital, Brussels, Belgium aut Gulbis Béatrice Department of Clinical Chemistry, Erasme Hospital, Brussels, Belgium aut Fontaine Jeanine Pharmacology Department, Institute of Pharmacy, Université Libre de Bruxelles, Brussels, Belgium aut Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10/1(1996-03-01), 17-22 0920-3206 10:1<17 1996 10 10557 https://doi.org/10.1007/BF00051126 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00051126 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Berkenboom Guy Department of Cardiology, Erasme Hospital, Brussels, Belgium aut NATIONALLICENCE 700 1- Brékine Dmitri Department of Clinical Chemistry, Erasme Hospital, Brussels, Belgium aut NATIONALLICENCE 700 1- Unger Philippe Department of Cardiology, Erasme Hospital, Brussels, Belgium aut NATIONALLICENCE 700 1- Gulbis Béatrice Department of Clinical Chemistry, Erasme Hospital, Brussels, Belgium aut NATIONALLICENCE 700 1- Fontaine Jeanine Pharmacology Department, Institute of Pharmacy, Université Libre de Bruxelles, Brussels, Belgium aut NATIONALLICENCE 773 0- Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10/1(1996-03-01), 17-22 0920-3206 10:1<17 1996 10 10557 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer