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首页> 美国卫生研究院文献>American Journal of Physiology - Heart and Circulatory Physiology >Adenosine A2A receptor activation reduces infarct size in the isolated perfused mouse heart by inhibiting resident cardiac mast cell degranulation
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Adenosine A2A receptor activation reduces infarct size in the isolated perfused mouse heart by inhibiting resident cardiac mast cell degranulation

机译：腺苷A2A受体激活通过抑制驻地心脏肥大细胞脱颗粒而减少了离体灌注小鼠心脏的梗死面积

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Mast cells are found in the heart and contribute to reperfusion injury following myocardial ischemia. Since the activation of A2A adenosine receptors (A2AARs) inhibits reperfusion injury, we hypothesized that ATL146e (a selective A2AAR agonist) might protect hearts in part by reducing cardiac mast cell degranulation. Hearts were isolated from five groups of congenic mice: A2AAR+/+ mice, A2AAR−/− mice, mast cell-deficient (KitW-sh/W-sh) mice, and chimeric mice prepared by transplanting bone marrow from A2AAR−/− or A2AAR+/+ mice to radiation-ablated A2AAR+/+ mice. Six weeks after bone marrow transplantation, cardiac mast cells were repopulated with >90% donor cells. In isolated, perfused hearts subjected to ischemia-reperfusion injury, ATL146e or CGS-21680 (100 nmol/l) decreased infarct size (IS; percent area at risk) from 38 ± 2% to 24 ± 2% and 22 ± 2% in ATL146e- and CGS-21680-treated hearts, respectively (P < 0.05) and significantly reduced mast cell degranulation, measured as tryptase release into reperfusion buffer. These changes were absent in A2AAR−/− hearts and in hearts from chimeric mice with A2AAR−/− bone marrow. Vehicle-treated KitW-sh/W-sh mice had lower IS (11 ± 3%) than WT mice, and ATL146e had no significant protective effect (16 ± 3%). These data suggest that in ex vivo, buffer-perfused hearts, mast cell degranulation contributes to ischemia-reperfusion injury. In addition, our data suggest that A2AAR activation is cardioprotective in the isolated heart, at least in part by attenuating resident mast cell degranulation.
机译：在心脏中发现肥大细胞，并在心肌缺血后导致再灌注损伤。由于A2A腺苷受体（A2AARs）的激活抑制了再灌注损伤，我们假设ATL146e（一种选择性的A2AAR激动剂）可能通过减少心脏肥大细胞脱颗粒而部分保护心脏。从五组同基因小鼠中分离出心脏：A2AAR + / + 小鼠，A2AAR -// 小鼠，肥大细胞缺陷（Kit W-sh / W -sh ）小鼠和通过将A2AAR -// 或A2AAR + / + 小鼠的骨髓移植到放射消融的A2AAR + / + 小鼠。骨髓移植六周后，心脏肥大细胞中的供体细胞> 90％。在受到缺血再灌注损伤的离体灌注心脏中，ATL146e或CGS-21680（100 nmol / l）将梗死面积（IS；危险区域百分比）从38±2％降低至24±2％和22±2％。分别用ATL146e和CGS-21680处理的心脏（P <0.05），肥大细胞脱颗粒的程度明显降低，以类胰蛋白酶释放到再灌注缓冲液中的量度。这些变化在A2AAR -/-心脏以及具有A2AAR -/-骨髓的嵌合小鼠的心脏中均不存在。媒介物处理过的Kit W-sh / W-sh 小鼠的IS（11±3％）比WT小鼠低，而ATL146e没有明显的保护作用（16±3％）。这些数据表明，在离体的，缓冲液灌注的心脏中，肥大细胞脱粒有助于缺血-再灌注损伤。此外，我们的数据表明A2AAR激活在离体心脏中具有心脏保护作用，至少部分是通过减弱常驻肥大细胞脱颗粒而实现的。

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