ISSN:
1573-4919
Schlagwort(e):
coronary circulation
;
heart
;
hydrogen peroxide
;
nitric oxide
;
oxidative stress
;
vasodilation
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Biologie
,
Chemie und Pharmazie
,
Medizin
Notizen:
Abstract Oxidative stress mediated by hydrogen peroxide (H2O2) increases coronary flow (CF) in Langendorff-perfused rat hearts. We investigated the possible role of nitric oxide (NO) in H2O2-induced vasolidation. A dose-response study was conducted to find a concentration of H2O2 which increased CF without influencing left ventricular developed (LVDP) or end-diastolic (LVEDP) pressures. 80 (n = 10),100 (n = 7), 120 (n = 7),140 (n = 7),160 (n = 7), and 180 (n = 10) μM H2O2 was infused for 10 min, followed by recovery for 50 min. 80 μM H2O2 increased CF to a maximum of 143 ± 4 (mean ± S.E.M) percent of initial value after 15 min observation (p 〈 0.001 compared to buffer only), with no effect on LVDP or LVEDP. Another series of hearts were perfused with N-nitro-L-Arginine methylester (L-NAME, 1 μM), methylene blue (MB, 50 μM), or haemoglobin (Hb, 10 μM), without (n = 7 in each) or with (n = 10 in each) 80 μM H2O2 for 10 min. L-NAME, MB, and Hb alone increased CF, but attenuated the H2O2-induced increase of CF. LVDP was depressed when L-NAME, MB, or Hb were given in conjunction with 80 μM H2O2. In summary, H2O2 concentration-dependently increased LVEDP and depressed LVDP. The H2O2-induced increase of CF was independent of concentration. Inhibition of NO synthesis, action, or soluble guanylate cyclase attenuated the H2O2-induced increase of CF, and depressed LVDP when given together with H2O2. H2O2 induces a NO-dependent vasodilation, and inhibition of NO is detrimental to left ventricular function after H2O2-mediated oxidative stress.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF00226057
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