抄録
Background: Hypertrophied RV (HRV) due to PH results in RV heart failure. We hypothesized that mechanical stress of HRV impairs coronary microcirculation with increased superoxide. Methods: Male SD rats (8 weeks old) were divided into two groups (Normal: n=40 and HRV: n=49). In HRV group, Monocrotaline (MCT) was administered at 5-week age to induce PH. RV coronary arterioles (<100μm) were visualized in vivo with our intravital videomicroscope. After cyclooxigenase blockade, vascular responses to ACh were examined under 4 conditions, Control, L-NAME, L-NAME + tetraethylammonium (TEA) and SOD. Difference of%dilation between Control and L-NAME was used as index for NO-contribution, and that between L-NAME and L-NAME + TEA as EDHF. Superoxide in RV was measured by lucigenin chemiluminescence. Results: RV systolic pressure was greatly increased in HRV (75±12 vs 33±3 mmHg, p<.05). In HRV, ACh-induced vasodilation was significantly reduced (by 51%, p<.05). NO-mediated vasodilation in HRV was greatly decreased (by 74%). EDHF-mediated vasodilation in HRV was robust, but decreased (by 43%). Eventually, relative vasodilatory contribution of EDHF increased (59 vs 51%). Superoxide was significantly elevated in HRV (330±31 vs 255±88 cpm/mg, P<.05). Decreased vasodilation in HRV was improved after SOD (by 33%, p<.05). Conclusion: NO-mediated vasodilation of coronary arterioles was impaired in HRV, while vasodilatory ability of EDHF was relatively robust. Increased superoxide in HRV may be involved crucially in NO dysfunction. [Jpn J Physiol 55 Suppl:S103 (2005)]
