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- W2018808225 abstract "We previously showed that abnormalities of mitochondria (M IT) exist in the failing heart and include hyperplasia, reduced organelle size and structural injury. In the present study, we examined MIT respiration in LV tissue obtained from 11 normal (NL) dogs and 8 dogs with heart failure (HF) produced by intracoronary microembolizations (LV ejection fraction 23 ± 3%). Tissue specimen (30 mg) were obtained from the subendocardial (ENDO) and subepicardial (EPI) halves of the LV wall. Basal (V o ) and state 3 (maximal) respiration (V ADP , after addition of 1 mM ADP) were measured with an oxygraph and Clark electrode using saponin skinned fiber bundles (0.2–0.3 mm). Respiratory rate was calculated in ngatoms of oxygen/min/mg of noncollagen protein. The respiration control ratio (RCR) was calculated as V ADP /V o . V o V ADP V ADP /V o ENDO EPI ENDO EPI ENDO EPI NL 9 ± 2 7 ± 1 46 ± 6 47 ± 1 6 ± 1 7 ± 1 HF 6 ± 1 6 ± 1 20 ± 5 22 ± 5 4 ± 1 4 ± 1 P-value <0.07 <0.5 <0.001 <0.005 <0.04 <0.004 MIT state 3 respiration is significantly reduced in myocardium of dogs with chronic HF. The observed reduction in the RCR confirms the presence of injury to inner MIT membrane. The abnormalities in MIT oxygen utilization support the concept of low energy production in the failing heart." @default.
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- W2018808225 date "1995-02-01" @default.
- W2018808225 modified "2023-09-26" @default.
- W2018808225 title "965-49 Abnormal Mitochondrial Respiration in Myocardium of Dogs with Chronic Heart Failure" @default.
- W2018808225 doi "https://doi.org/10.1016/0735-1097(95)92382-f" @default.
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