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Liang 2021 Biomed Pharmacother

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Revision as of 15:06, 24 September 2021 by Plangger Mario (talk | contribs)
Publications in the MiPMap
Liang L, Zhang G, Cheng C, Li H, Jin T, Su C, Xiao Y, Bradley J, Peberdy MA, Ornato JP, Mangino MJ, Tang W (2021) High-resolution respirometry for evaluation of mitochondrial function on brain and heart homogenates in a rat model of cardiac arrest and cardiopulmonary resuscitation. Biomed Pharmacother [Epub ahead of print].

» PMID: 34467895 Open Access

Liang Lian, Zhang Guozhen, Cheng Cheng, Li Hui, Jin Tao, Su Chenglei, Xiao Yan, Bradley Jennifer, Peberdy Mary A, Ornato Joseph P, Mangino Martin J, Tang Wanchun (2021) Biomed Pharmacother

Abstract: The physiology and physiopathology process of mitochondrial function following cardiac arrest remains poorly understood. We aimed to assess mitochondrial respiratory function on the heart and brain homogenates from cardiac arrest rats. The expression level of SIRT1/PGC-1α pathway was measured by immunoblotting. 30 rats were assigned to the CA group and the sham group. Rats of CA were subjected to 6 min of untreated ventricular fibrillation (VF) followed by 8 min of cardiopulmonary resuscitation (CPR). Mitochondrial respiratory function was compromised following CA and I/R injury, as indicated by CIL (451.46 ± 71.48 vs. 909.91 ± 5.51 pmol/min*mg for the heart and 464.14 ± 8.22 vs. 570.53 ± 56.33 pmol/min*mg for the brain), CI (564.04 ± 64.34 vs. 2729.52 ± 347.39 pmol/min*mg for the heart and 726.07 ± 85.78 vs. 1762.82 ± 262.04 pmol/min*mg for the brain), RCR (1.88 ± 0.46 vs. 3.57 ± 0.38 for the heart and 2.05 ± 0.19 vs. 3.49 ± 0.19, for the brain) and OXPHOS coupling efficiency (0.45 ± 0.11 vs. 0.72 ± 0.03 for the heart and 0.52 ± 0.05 vs. 0.71 ± 0.01 for the brain). However, routine respiration was lower in the heart and comparable in the brain after CA. CIV did not change in the heart but was enhanced in the brain. Furthermore, both SIRT1 and PGC-1α were downregulated concurrently in the heart and brain. The mitochondrial respiratory function was compromised following CA and I/R injury, and the major affected respiratory state is complex I-linked respiration. Furthermore, the heart and the brain respond differently to the global I/R injury after CA in mitochondrial respiratory function. Inhibition of the SIRT1/PGC-1α pathway may be a major contributor to the impaired mitochondrial respiratory function. Keywords: Cardiac arrest, High-resolution respirometry, Ischemia-reperfusion injury, Mitochondrial respiratory function, SIRT1/PGC-1α pathway Bioblast editor: Plangger M


Labels: MiParea: Respiration  Pathology: Cardiovascular  Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Heart, Nervous system  Preparation: Homogenate 


Coupling state: LEAK, ROUTINE, OXPHOS  Pathway: N, S, CIV, ROX  HRR: Oxygraph-2k 

2021-09