These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Using the isolated atrial preparation of the guinea-pig and the canine heart lung preparation (HLP) supported by a donor, the effects of guanfacine on the heart, coronary circulation and myocardial energy metabolism were studied and compared with those of clonidine (author's transl)].
    Author: Katano Y, Nakagawa Y, Shimamoto N, Sakai K, Otorii T, Imai S.
    Journal: Nihon Yakurigaku Zasshi; 1980 Sep; 76(5):281-92. PubMed ID: 7009344.
    Abstract:
    In the isolated left atria of the guinea-pig, guanfacine and clonidine (10(-8)--3 x 10(-5) g/ml) produced positive inotropic effects, which were inhibited by tripelennamine, metiamide and propranolol. Up to the concentration of 10(-6) g/ml of these compounds the effects were also inhibited by phentolamine. In the isolated right atria, guanfacine in concentrations over 3 x 10(-6) g/ml, produced a negative, and clonidine, a positive chronotropic effect. Whereas the effect of clonidine was antagonized by metiamide, the effect of guanfacine was not antagonized by any blocking agents we used. In spontaneously beating right atria, the positive inotropic effects induced by guanfacine (10(-8)--10(-5) g/ml) were inhibited by propranolol or tripelennamine, while those of clonidine (10(-8)--10(-4) g/ml) were antagonized by metiamide. In canine HLP, both drugs produced a decrease in the coronary flow which was associated with a slight rise in the right atrial pressure. These effects were inhibited by phentolamine. Both drugs produced a slight decrease in the myocardial O2 consumption and an improvement of the myocardial redox potential.
    [Abstract] [Full Text] [Related] [New Search]