کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2192956 1098007 2013 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Suppression of myocardial mitochondrial respiratory function in acute failing hearts made by a short-term Ca2+ free, high Ca2+ coronary perfusion
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Suppression of myocardial mitochondrial respiratory function in acute failing hearts made by a short-term Ca2+ free, high Ca2+ coronary perfusion
چکیده انگلیسی

We made acute cardiac failure in excised cross-circulated canine hearts by a new coronary perfusion protocol consisting of Ca2+ free Tyrode perfusion for the first 10 min, high Ca2+ (16 mmol/l) Tyrode perfusion for the next 5 min, and normal Tyrode perfusion for the last 5 min interrupting blood cross circulation. After 50 min from the blood recirculation, left ventricular contractility was stably depressed to 60% of control. We studied mechanoenergetics of these acute failing hearts for the next 1–3 h. Then, we prepared mitochondria from these excised failing hearts and the support dogs' normal hearts to examine their mitochondria) respiratory function by the respiratory control index (RCI) and the oxygen consumption rate in state III (State III O2). RCI and State III O2 were significantly smaller in the failing hearts than in the normal hearts. However, sham protocol consisting of normal Tyrode coronary perfusion for 20 min did not affect RCI and State III O2. These results revealed that the mitochondria) respiratory function was moderately impaired in these acute failing hearts made by the new short-term Ca2+ intervention. However, no ultrastructural injuries of mitochondria were detected in these failing hearts.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 27, Issue 9, September 1995, Pages 2009–2013
نویسندگان
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