Ischemia time impacts on respiratory chain functions and Ca
Animals
Calcium
/ metabolism
Cardiac Surgical Procedures
/ adverse effects
Cations
/ metabolism
Disease Models, Animal
Electron Transport
/ physiology
Heart Arrest, Induced
Intracellular Membranes
/ metabolism
Isolated Heart Preparation
Male
Mitochondria, Heart
/ metabolism
Myocardial Reperfusion Injury
/ metabolism
Myocardium
/ metabolism
Myocytes, Cardiac
/ metabolism
Oxygen Consumption
/ physiology
Rats
Rats, Wistar
Recovery of Function
Sarcolemma
/ metabolism
Time Factors
Warm Ischemia
/ adverse effects
Ischemia reperfusion injury
Ischemia time
Subsarcolemmal mitochondria
Journal
Journal of cardiothoracic surgery
ISSN: 1749-8090
Titre abrégé: J Cardiothorac Surg
Pays: England
ID NLM: 101265113
Informations de publication
Date de publication:
14 May 2019
14 May 2019
Historique:
received:
20
12
2018
accepted:
22
04
2019
entrez:
16
5
2019
pubmed:
16
5
2019
medline:
2
7
2019
Statut:
epublish
Résumé
Mitochondrial impairment can result from myocardial ischemia reperfusion injury (IR). Despite cardioplegic arrest, IR-associated cardiodepression is a major problem in heart surgery. We determined the effect of increasing ischemia time on the respiratory chain (RC) function, the inner membrane polarization and Ca Wistar rat hearts were divided into 4 groups of stop-flow induced warm global IR using a pressure-controlled Langendorff system: 0, 15, 30 and 40 min of ischemia with 30 min of reperfusion, respectively. Myocardial contractility was determined from left ventricular pressure records (dP/dt, dPmax) with an intraventricular balloon. Following reperfusion, SSM were isolated and analyzed regarding electron transport chain (ETC) coupling by polarography (Clark-Type electrode), membrane polarization (JC1 fluorescence) and Ca LV contractility and systolic pressure during reperfusion were impaired by increasing ischemic times. Ischemia reduced ETC oxygen consumption in IR40/30 compared to IR0/30 at complex I-V (8.1 ± 1.2 vs. 18.2 ± 2.0 nmol/min) and II-IV/V (16.4 ± 2.6/14.8 ± 2.3 vs. 2.3 ± 0.6 nmol/min) in state 3 respiration (p < 0.01). Relative membrane potential revealed a distinct hyperpolarization in IR30/30 and IR40/30 (171.5 ± 17.4% and 170.9 ± 13.5%) compared to IR0/30 (p < 0.01), wearing off swiftly after CCCP-induced uncoupling. Excess mitochondrial permeability transition pore (mPTP)-gated Ca Ischemia prolongation in IR injury gradually impaired SSM in terms of respiratory chain function and Ca
Sections du résumé
BACKGROUND
BACKGROUND
Mitochondrial impairment can result from myocardial ischemia reperfusion injury (IR). Despite cardioplegic arrest, IR-associated cardiodepression is a major problem in heart surgery. We determined the effect of increasing ischemia time on the respiratory chain (RC) function, the inner membrane polarization and Ca
METHODS
METHODS
Wistar rat hearts were divided into 4 groups of stop-flow induced warm global IR using a pressure-controlled Langendorff system: 0, 15, 30 and 40 min of ischemia with 30 min of reperfusion, respectively. Myocardial contractility was determined from left ventricular pressure records (dP/dt, dPmax) with an intraventricular balloon. Following reperfusion, SSM were isolated and analyzed regarding electron transport chain (ETC) coupling by polarography (Clark-Type electrode), membrane polarization (JC1 fluorescence) and Ca
RESULTS
RESULTS
LV contractility and systolic pressure during reperfusion were impaired by increasing ischemic times. Ischemia reduced ETC oxygen consumption in IR40/30 compared to IR0/30 at complex I-V (8.1 ± 1.2 vs. 18.2 ± 2.0 nmol/min) and II-IV/V (16.4 ± 2.6/14.8 ± 2.3 vs. 2.3 ± 0.6 nmol/min) in state 3 respiration (p < 0.01). Relative membrane potential revealed a distinct hyperpolarization in IR30/30 and IR40/30 (171.5 ± 17.4% and 170.9 ± 13.5%) compared to IR0/30 (p < 0.01), wearing off swiftly after CCCP-induced uncoupling. Excess mitochondrial permeability transition pore (mPTP)-gated Ca
CONCLUSIONS
CONCLUSIONS
Ischemia prolongation in IR injury gradually impaired SSM in terms of respiratory chain function and Ca
Identifiants
pubmed: 31088484
doi: 10.1186/s13019-019-0911-1
pii: 10.1186/s13019-019-0911-1
pmc: PMC6518521
doi:
Substances chimiques
Cations
0
Calcium
SY7Q814VUP
Types de publication
Evaluation Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
92Références
Arch Biochem Biophys. 1999 Dec 15;372(2):399-407
pubmed: 10600182
Am J Physiol Heart Circ Physiol. 2001 Jan;280(1):H280-93
pubmed: 11123243
Cell Mol Life Sci. 2001 Sep;58(10):1528-37
pubmed: 11693531
Biochem J. 1992 Feb 1;281 ( Pt 3):709-15
pubmed: 1346958
Arch Biochem Biophys. 2003 Dec 15;420(2):279-86
pubmed: 14654067
Biochem J. 2005 Sep 1;390(Pt 2):377-94
pubmed: 16108756
Biochem J. 1991 Feb 15;274 ( Pt 1):133-7
pubmed: 1900416
Basic Res Cardiol. 2009 Mar;104(2):141-7
pubmed: 19242638
Neurochem Res. 2009 Aug;34(8):1469-78
pubmed: 19252983
Eur J Cardiothorac Surg. 2012 Sep;42(3):530-9
pubmed: 22345279
PLoS One. 2012;7(9):e44667
pubmed: 22973464
Thorac Cardiovasc Surg. 2018 Jan;66(1):11-19
pubmed: 29258126
Arch Surg. 1985 Mar;120(3):332-8
pubmed: 2982344
Am J Physiol. 1986 May;250(5 Pt 2):H741-8
pubmed: 3706549
Brain Res. 1993 Feb 26;604(1-2):185-91
pubmed: 8457847
Clin Chem. 1997 Mar;43(3):467-75
pubmed: 9068590
J Biol Chem. 1977 Dec 10;252(23):8731-9
pubmed: 925018