In:
Pharmacology, S. Karger AG, Vol. 107, No. 3-4 ( 2022), p. 150-159
Kurzfassung:
〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 This study aimed to assess the influence of different doses of tadalafil on coronary flow and oxidative stress in isolated rat hearts. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 The hearts of male Wistar albino rats ( 〈 i 〉 n 〈 /i 〉 = 48) were retrogradely perfused according to the Langendorff technique at gradually increased constant perfusion pressure (CPP) (40–120 mm Hg). Coronary flow and oxidative stress markers: nitrite oxide (NO) outflow and superoxide anion production in coronary effluent were measured. The experiments were performed during control conditions and in the presence of tadalafil (10, 20, 50, and 200 nM) alone or with Nω-nitro-L-arginine monomethyl ester (L-NAME) (30 μM). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Tadalafil administration significantly increased coronary flow at all CPP values at all administered doses. Tadalafil led to an increase in the NO levels, but a statistically significant NO release increase was found only at the highest dose and highest CPP. Tadalafil did not significantly affect the release of O 〈 sup 〉 2− 〈 /sup 〉 . After inhibiting the nitrite oxide synthase system by L-NAME, tadalafil-induced changes in cardiac flow and NO levels were reversed. L-NAME administration had no pronounced effect on the O 〈 sup 〉 2− 〈 /sup 〉 release. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Tadalafil causes changes in the heart vasculature in a dose-dependent manner. It does not lead to a significant increase in the production of superoxide anion radicals.
Materialart:
Online-Ressource
ISSN:
0031-7012
,
1423-0313
Sprache:
Englisch
Verlag:
S. Karger AG
Publikationsdatum:
2022
ZDB Id:
1483550-2
SSG:
15,3
