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Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.

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العنوان: Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.
المؤلفون: Shimkunas, Rafael, Makwana, Om, Spaulding, Kimberly, Bazargan, Mona, Khazalpour, Michael, Takaba, Kiyoaki, Soleimani, Mehrdad, Myagmar, Bat-Erdene, Lovett, David H., Simpson, Paul C., Ratcliffe, Mark B., Baker, Anthony J.
المصدر: American Journal of Physiology: Heart & Circulatory Physiology; 2014, Vol. 307 Issue 8, pH1150-H1158, 9p
مصطلحات موضوعية: CYTOPLASMIC filaments, CARDIAC contraction, MYOCARDIAL infarction, MYOSIN, PHOSPHORYLATION, DOXYCYCLINE
مستخلص: After myocardial infarction, a poorly contracting nonischemic border zone forms adjacent to the infarct. The cause of border zone dysfunction is unclear. The goal of this study was to determine the myofilament mechanisms involved in postinfarction border zone dysfunction. Two weeks after anteroapical infarction of sheep hearts, we studied in vitro isometric and isotonic contractions of demembranated myocardium from the infarct border zone and a zone remote from the infarct. Maximal force development (Fmax) of the border zone myocardium was reduced by 31 ± 2% versus the remote zone myocardium (n = 6/group, P < 0.0001). Decreased border zone Fmax was not due to a reduced content of contractile material, as assessed histologically, and from myosin content. Furthermore, decreased border zone Fmax did not involve altered cross-bridge kinetics, as assessed by muscle shortening velocity and force development kinetics. Decreased border zone Fmax was associated with decreased cross-bridge formation, as assessed from muscle stiffness in the absence of ATP where crossbridge formation should be maximized (rigor stiffness was reduced 34 ± 6%, n = 5, P = 0.011 vs. the remote zone). Furthermore, the border zone myocardium had significantly reduced phosphorylation of myosin essential light chain (ELC; 41 ± 10%, n = 4, P < 0.05). However, for animals treated with doxycycline, an inhibitor of matrix metalloproteinases, rigor stiffness and ELC phosphorylation were not reduced in the border zone myocardium, suggesting that doxycycline had a protective effect. In conclusion, myofilament dysfunction contributes to postinfarction border zone dysfunction, myofilament dysfunction involves impaired cross-bridge formation and decreased ELC phosphorylation, and matrix metalloproteinase inhibition may be beneficial for limiting postinfarct border zone dysfunction. [ABSTRACT FROM AUTHOR]
Copyright of American Journal of Physiology: Heart & Circulatory Physiology is the property of American Physiological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
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