The infarct size-limiting effect of ischemic postconditioning (IPOC) is suppressed in isolated hyperhomocysteinemic (Hhcy) rat hearts: The reasonable role of PKC-δ

2009 ◽  
Vol 63 (10) ◽  
pp. 787-791 ◽  
Author(s):  
Ankur Rohilla ◽  
Pitchai Balakumar
Keyword(s):  
Infarct Size ◽  
Ischemic Postconditioning ◽  
Rat Hearts

Abstract 1568: Loss of Ischemic Postconditioning in the Mouse Hearts Lacking Adenosine A 1 or Bradykinin B 2 Receptors

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Lei Xi ◽  
Anindita Das ◽  
Zhi-Qing Zhao ◽  
Vanessa F Merino ◽  
Michael Bader ◽  
...  
Keyword(s):  
Infarct Size ◽  
G Protein ◽  
Contractile Function ◽  
Gene Knockout ◽  
Myocardial Infarct ◽  
Membrane Receptors ◽  
Ischemic Postconditioning ◽  
Myocardial Infarct Size ◽  
G Protein Coupled

Background: Ischemic postconditioning (PostC) is a recently described cardioprotective modality against reperfusion injury, through a series of brief episodes of reperfusion/ischemia at the very onset of reperfusion. It has been well recognized that PostC can activate cellular signaling cascade, in which the role of G protein-coupled membrane receptors serving as upstream triggers of PostC remains to be established. Hence the goal of this study was to determine a definitive role of adenosine A 1 receptors (A1) and bradykinin B 1 or B 2 receptors (B1 or B2) in PostC, using gene knockout (KO) mice. Methods & Results: The hearts isolated from adult male C57BL/6J wild-type mice (C57-WT) or A1, B1, or B2 KO mice (n=7–9 per group) were subjected to 20 min of zero-flow global ischemia and 30 min of reperfusion with or without PostC in a Langendorff isolated, buffer-perfused heart model. PostC, consisted of 6 cycles of 10 sec of reperfusion and 10 sec of ischemia, significantly reduced myocardial infarct size (22.8±3.1%, Mean±SEM) as compared with C57-WT controls (35.1±2.8%, P<0.05). As shown in Figure below, the infarct-limiting protection of PostC was absent in A1-KO (34.9±2.7%) or B2-KO (33.3±1.7%) and was partially attenuated in B1-KO (25.6±2.9%) mice, as compared with the corresponding non-PostC controls under same genetic background (P>0.05). However, cardiac contractile function and coronary flow at the end of reperfusion were not significantly altered by PostC. Conclusion: PostC-induced infarct size reduction in globally ischemic mouse hearts is triggered by activation of multiple G protein-coupled membrane receptors, which include A1, B2, and, to a lesser extent, B1 receptors.

scholarly journals The role of protein kinase C and PI3-kinase in the mechanism of the cardioprotective effect of remote ischemic postconditioning

2022 ◽  
Vol 20 (4) ◽  
pp. 6-10
Author(s):  
A. V. Mukhomedzyanov ◽  
N. V. Naryzhnaya ◽  
L. N. Maslov
Keyword(s):  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Coronary Blood Flow ◽  
Pi3 Kinase ◽  
Ischemic Postconditioning ◽  
Kinase C ◽  
Remote Ischemic Postconditioning

Background. Acute myocardial infarction (AMI) with ST segment elevation is associated with high incidence of complications. Mortality from AMI is about 5%, which has not decreased in recent years. Revascularization provides recovery of coronary blood flow, but also contributes to the occurrence of reperfusion injury to the heart. Remote ischemic postconditioning (RIPostC) is a promising, non-invasive method that can effectively and safely reduce the infarct size.The aim of the study was to investigate the role of protein kinase C and PI3-kinase in the development of the infarct-limiting effect of remote ischemic postconditioning.Materials and methods. The study was performed on Wistar rats. Coronary artery occlusion (45 min) and reperfusion (2 h) were performed. The infarct size (IS) and the size of area at risk (AAR) were assessed. RIPostC was modeled by applying tourniquets to the hind limbs in the hip joint immediately after the restoration of coronary blood flow. All inhibitors were administered intravenously 10 min before reperfusion.Results. In the control group, the IS / AAR ratio was 44%. RIPostC reduced the IS / AAR ratio by about 50%. Preliminary administration of the protein kinase C inhibitor chelerythrine and the PI3-kinase inhibitor wortmannin eliminated the cardioprotective effect of RIPostC.Conclusion. The mechanism of the infarct-limiting effect of RIPostC is implemented through activation of protein kinase C and PI3-kinase. 

scholarly journals Role of nitric oxide synthases in the infarct size-reducing effect conferred by heat stress in isolated rat hearts

2001 ◽  
Vol 132 (8) ◽  
pp. 1845-1851 ◽  
Author(s):  
Claire Arnaud ◽  
Aline Laubriet ◽  
Marie Joyeux ◽  
Diane Godin-Ribuot ◽  
Luc Rochette ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Infarct Size ◽  
Nitric Oxide Synthases ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Endothelin-B Receptors and Left Ventricular Dysfunction after Regional versus Global Ischaemia-Reperfusion in Rat Hearts

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Sofia-Iris Bibli ◽  
Eleni V. Toli ◽  
Agapi D. Vilaeti ◽  
Varnavas C. Varnavas ◽  
Giannis G. Baltogiannis ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Infarct Size ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Wild Type ◽  
Global Ischaemia ◽  
Ischaemia Reperfusion ◽  
Rat Hearts

Background. Endothelin-1 (ET-1) is implicated in left ventricular dysfunction after ischaemia-reperfusion. ETA and ETB receptors mediate diverse actions, but it is unknown whether these actions depend on ischaemia type and duration. We investigated the role of ETB receptors after four ischaemia-reperfusion protocols in isolated rat hearts.Methods. Left ventricular haemodynamic variables were measured in the Langendorff-perfused model after 40- and 20-minute regional or global ischaemia, followed by 30-minute reperfusion. Wild-type (n=39) and ETB-deficient (n=41) rats were compared. Infarct size was measured using fluorescent microspheres after regional ischaemia-reperfusion.Results. Left ventricular dysfunction was more prominent in ETB-deficient rats, particularly after regional ischaemia. Infarct size was smaller (P=0.006) in wild-type (31.5±4.4%) than ETB-deficient (45.0±7.3%) rats after 40 minutes of regional ischaemia-reperfusion. Although the recovery of left ventricular function was poorer after 40-minute ischaemia-reperfusion, end-diastolic pressure in ETB-deficient rats was higher after 20 than after 40 minutes of regional ischaemia-reperfusion.Conclusion. ETB receptors exert cytoprotective effects in the rat heart, mainly after regional ischaemia-reperfusion. Longer periods of ischaemia suppress the recovery of left ventricular function after reperfusion, but the role of ETB receptors may be more important during the early phases.

scholarly journals Importance of timing of magnesium administration in the isolated ischemic-reperfused rat heart: role of K-ATP channels

2008 ◽  
pp. 839-846
Author(s):  
M Bazargan ◽  
M Faghihi ◽  
M Chitsaz
Keyword(s):  
Cardiac Function ◽  
Infarct Size ◽  
Rat Heart ◽  
Katp Channels ◽  
Left Ventricular ◽  
Cardiovascular Disorders ◽  
Protective Effects ◽  
Triphenyltetrazolium Chloride ◽  
Rat Hearts

There is a growing interest for the beneficial effect of magnesium (Mg) in cardiovascular disorders. A number of cardiovascular disorders including myocardial infarction, arrhythmias and congestive heart failure have been associated with low extracellular or intracellular concentrations of Mg. The efficiency of the preconditioning effect of Mg on cardiac function and infarct size in the globally ischemic-reperfused isolated rat heart was studied together with the role of ATP-sensitive potassium (KATP) channels in protection induced by Mg. Rat hearts were Langendorff perfused, subjected to 30 min of global ischemia and 90 min of reperfusion, including treatment groups which focused on different times of Mg (8 mmol/l) use. Infarct size was measured by triphenyltetrazolium chloride (TTC) method. The left ventricular function was assessed by left ventricular developed pressure (LVDP), heart rate (HR) and coronary flow (CF). The administration of Mg before ischemia had an anti-infarct effect in rat hearts and improved cardiac function. The protective effects of magnesium was abolished by the blocking of KATP channels and suggests that K-ATP channel has an important role in the heart protection effect of Mg as a preconditioning agent.

dl-3-Hydroxybutyrate administration prevents myocardial damage after coronary occlusion in rat hearts

2002 ◽  
Vol 283 (5) ◽  
pp. H1968-H1974 ◽  
Author(s):  
Zhitian Zou ◽  
Shiro Sasaguri ◽  
Katare Gopalrao Rajesh ◽  
Ryoko Suzuki
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Rat Hearts ◽  
High Concentrations ◽  
Myocardial Infarction Size

To investigate the role of high concentrations of dl-3-hydroxybutyrate (DL-3-HB) in preventing heart damage after prolonged fasting, infarct size and the incidence of apoptosis caused by ischemia-reperfusion were determined in four groups of Wistar rats. Fed rats (±DL-3-HB group) and fasted rats (±DL-3-HB group) were subjected to 30 min of left coronary artery occlusion and 120 min of reperfusion. DL-3-HB was administered intravenously 60 min before the coronary artery occlusion. Infarct size, defined by triphenylyetrazolium chloride (TTC) staining, was reduced from 72 ± 3% (fed group), 75 ± 5% (fed + DL-3-HB group), and 70 ± 5% (fasting group), respectively, to 26 ± 4% ( P < 0.01 vs. fasting + DL-3-HB group). Apoptosis, as defined by single-stranded DNA staining, was significantly reduced in the subendocardial region in the fasting + DL-3-HB group (9 ± 2%) compared with the other groups (39 ± 6% in the fed group, 37 ± 5% in the fed + DL-3-HB group, and 34 ± 3% in the fasting group; P < 0.01). In addition, levels of ATP in the fasting + DL-3-HB group were significantly higher compared with other groups after 30 min of ischemia and 120 min of reperfusion ( P < 0.01). In conclusion, the present study demonstrates that high concentrations of DL-3-HB reduces myocardial infarction size and apoptosis induced by ischemia-reperfusion, possibly by providing increased energy substrate to the fasted rat myocardium.

Critical role of age, strain and number of cycles in ischemic postconditioning

2007 ◽  
Vol 42 (6) ◽  
pp. S186-S187 ◽  
Author(s):  
Sarin Somers ◽  
Lydia Lacerda ◽  
Naushaad Suleman ◽  
Lionel Opie ◽  
Sandrine Lecour
Keyword(s):  
Critical Role ◽  
Ischemic Postconditioning ◽  
Number Of Cycles

scholarly journals F006 Critical role of ERK1/2 in erythropoietin-mediated cardioprotection compared with ischemic postconditioning

2009 ◽  
Vol 102 ◽  
pp. S55
Author(s):  
N. Ghaboura ◽  
S. Tamareille ◽  
F. Treguer ◽  
D. Khachman ◽  
D. Henrion ◽  
...  
Keyword(s):  
Critical Role ◽  
Ischemic Postconditioning

Per-unit-living tissue normalization of real-time RT-PCR data in ischemic rat hearts

2012 ◽  
Vol 44 (12) ◽  
pp. 651-656 ◽  
Author(s):  
S. Ellefsen ◽  
M. Bliksøen ◽  
A. Rutkovskiy ◽  
I. B. Johansen ◽  
M.-L. Kaljusto ◽  
...  
Keyword(s):  
Infarct Size ◽  
Real Time ◽  
Reference Genes ◽  
Stable Expression ◽  
Unit Weight ◽  
Living Tissue ◽  
Rt Pcr ◽  
Internal Reference ◽  
Total Rna ◽  
Rat Hearts

In studies of gene expression in acute ischemic heart tissue, internal reference genes need to show stable expression per-unit-living tissue to hinder dead cells from biasing real-time RT-PCR data. Until now, this important issue has not been appropriately investigated. We hypothesized that the expression of seven internal reference genes would show stable per-unit-living tissue expression in Langendorff-perfused rat hearts subjected to ischemia-reperfusion. This was found for cyclophilin A, GAPDH, RPL-32, and PolR2A mRNA, with GAPDH showing the highest degree of stability ( R = 0.11), suggesting unchanged rates of mRNA transcription in live cells and complete degradation of mRNA from dead cells. The infarct size-dependent degradation of GAPDH was further supported by a close correlation between changes in GAPDH mRNA and changes in RNA quality measured as RNA integrity number (R = 0.90, P < 0.05). In contrast, β-actin and 18S rRNA showed stable expression per-unit-weight tissue and a positive correlation with infarct size (R = 0.61 and R = 0.77, P < 0.05 for both analyses). The amount of total RNA extracted per-unit-weight tissue did not differ between groups despite wide variation in infarct size (7.1–50.1%). When β-actin expression was assessed using four different normalization strategies, GAPDH and geNorm provided appropriate per-unit-living expression, while 18S and total RNA resulted in marked underestimations. In studies of ischemic tissues, we recommend using geometric averaging of carefully selected reference genes for normalization of real-time RT-PCR data. A marked shift in the mRNA/rRNA ratio renders rRNA as useless for normalization purposes.

Cardioprotection with esmolol-based cardioplegia for non-infarcted and infarcted rat hearts

2021 ◽  
Author(s):  
Alexander B Veitinger ◽  
Audrey Komguem ◽  
Lena Assling-Simon ◽  
Martina Heep ◽  
Julia Schipke ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Lactate Production ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Cardioplegic Arrest ◽  
Blood Cardioplegia ◽  
Rat Hearts

Abstract OBJECTIVES Esmolol-based cardioplegic arrest offers better cardioprotection than crystalloid cardioplegia but has been compared experimentally with blood cardioplegia only once. We investigated the influence of esmolol crystalloid cardioplegia (ECCP), esmolol blood cardioplegia (EBCP) and Calafiore blood cardioplegia (Cala) on cardiac function, metabolism and infarct size in non-infarcted and infarcted isolated rat hearts. METHODS Two studies were performed: (i) the hearts were subjected to a 90-min cardioplegic arrest with ECCP, EBCP or Cala and (ii) a regional myocardial infarction was created 30 min before a 90-min cardioplegic arrest. Left ventricular peak developed pressure (LVpdP), velocity of contractility (dLVP/dtmax), velocity of relaxation over time (dLVP/dtmin), heart rate and coronary flow were recorded. In addition, the metabolic parameters were analysed. The infarct size was determined by planimetry, and the myocardial damage was determined by electron microscopy. RESULTS In non-infarcted hearts, cardiac function was better preserved with ECCP than with EBCP or Cala relative to baseline values (LVpdP: 100 ± 28% vs 86 ± 11% vs 57 ± 7%; P = 0.002). Infarcted hearts showed similar haemodynamic recovery for ECCP, EBCP and Cala (LVpdP: 85 ± 46% vs 89 ± 55% vs 56 ± 26%; P = 0.30). The lactate production with EBCP was lower than with ECCP (0.6 ± 0.7 vs 1.4 ± 0.5 μmol/min; P = 0.017). The myocardial infarct size and (ECCP vs EBCP vs Cala: 16 ± 7% vs 15 ± 9% vs 24 ± 13%; P = 0.21) the ultrastructural preservation was similar in all groups. CONCLUSIONS In non-infarcted rat hearts, esmolol-based cardioplegia, particularly ECCP, offers better myocardial protection than Calafiore. After an acute myocardial infarction, cardioprotection with esmolol-based cardioplegia is similar to that with Calafiore.

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