Oral cicaprost protects from hypercholesterolaemia-induced impairment of coronary vasodilation.
Isolated Langendorff-hearts prepared from cholesterol fed rabbits (1% cholesterol for 3 months) showed a significant impairment in endothelium-dependent relaxation after short-term infusion of bradykinin (0.05 mumol/l) and carbamoylcholine (0.1 mumol/l). Generation of the endothelial mediators nitric oxide and prostacyclin by bradykinin was enhanced in hypercholesterolemia. Cicaprost treatment (5 micrograms/kg x d) largely prevented the hypercholesterolemia-related impairment of coronary vasodilation and nitric oxide release. It is concluded that (i) impairment of endothelium-dependent relaxation in the coronary microcirculation of hypercholesterolemic rabbits is not due to diminished endothelium-dependent mediator release but rather to accelerated inactivation or reduced activity of the released mediators and that (ii) oral cicaprost beneficially influence these alterations.
Woditsch
I
I
Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf, FRG.
Hohlfeld
T
T
Strobach
H
H
Schrör
K
K
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000284:Administration, Oral; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D011464:Epoprostenol / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism / Q000627:therapeutic use; D006937:Hypercholesterolemia / Q000150:complications*; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000378:metabolism; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects*
D009569:Nitric Oxide; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; C043867:cicaprost