Uncoupling Protein Inhibitor Genipin Reduces Protective Effect of Ischemic Preconditioning

2012 ◽  
Vol 3 (3) ◽  
pp. 217-226
Author(s):  
Yulia V. Goshovska ◽  
Tetyana V Shimanskaya ◽  
Vadim F. Sagach
Keyword(s):  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Uncoupling Protein ◽  
Protein Inhibitor

scholarly journals Genipin--uncoupling protein inhibitor--reduces the protective effect of ischemic preconditioning

2012 ◽  
Vol 57 (6) ◽  
pp. 38-45
Author(s):  
IuV Hoshovs'ka ◽  
◽  
TV Shymans'ka ◽  
VF Sahach ◽  
◽  
...  
Keyword(s):  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Uncoupling Protein ◽  
Protein Inhibitor

scholarly journals Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

2002 ◽  
Vol 33 (9) ◽  
pp. 1200-1208 ◽  
Author(s):  
Juan C. Cutrn ◽  
Maria-Giulia Perrelli ◽  
Barbara Cavalieri ◽  
Carmen Peralta ◽  
Joan Rosell Catafau ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Microvascular Dysfunction

scholarly journals Is there a protective effect with remote ischemic preconditioning on contrast-induced acute renal injury after coronary angiography in low-risk patients?

2018 ◽  
Vol 8 (4) ◽  
pp. 38-38
Author(s):  
Sanaz Soleymani ◽  
Hamid Reza Samimagham ◽  
Mohammad Tamaddondar ◽  
Hossein Farshidi ◽  
Mahmood Khayatian ◽  
...  
Keyword(s):  
Coronary Angiography ◽  
Serum Creatinine ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Low Risk ◽  
Remote Ischemic Preconditioning ◽  
Control Group ◽  
Renal Biomarkers ◽  
Significant Difference ◽  
Risk Patients

Introduction: Contrast-induced acute kidney injury (CIN-AKI) is a serious complication of coronary angiography. Given the weaknesses in the common protective methods used to prevent CIN-AKI, a safe and effective strategy is needed. RIPC has been shown to have a nephroprotective effect. Objectives: We aimed to determine the protective effect of RIPC on CIN-AKI after angiography or percutaneous coronary intervention (PCI) in low-risk patients. Patients and Methods: In our study, 140 low-risk patients who needed angiography or PCI, were assigned to either RIPC or control group. In each group, serum creatinine and urinary neutrophil gelatinaseassociated lipocalin (uNGAL) were measured before the procedure. Serum creatinine was measured daily for 2 days and uNGAL was measured 6 and 24 hours after the procedure. Diagnosis of AKI was, according to the Kidney Disease; Improving Global Outcomes (KDIGO) criteria (2012). Results: The mean age in the remote ischemic preconditioning (RIPC) group was 56.8 ± 11.4 years and 56.3 ± 11.8 years in the control group. We observed no significant difference regarding patient’s characteristic and renal biomarkers at baseline. There was no significant difference in the incidence of AKI (P = 0.116). The uNGAL increased by 36.2% 6-hour after the procedure in patients with AKI, while at the same time, this biomarker increased only by 4.3% in patients without AKI. Conclusion: We concluded that RIPC, with 3 cycles of 5-minute ischemia and 5-minute reperfusion, did not decrease CIN-AKI or altering renal biomarkers course in low-risk patients undergoing coronary angiography or PCI. Additionally, uNGAL, seems to be an appropriate biomarker for early diagnosis of CIN-AKI, 6 hours after contrast media exposure.

scholarly journals Down-regulation of Connexin43 in Early Myocardial Ischemia and Protective Effect by Ischemic Preconditioning in Rat Hearts In Vivo

2004 ◽  
Vol 45 (6) ◽  
pp. 1007-1019 ◽  
Author(s):  
Kazuhito Hatanaka ◽  
Hiroyuki Kawata ◽  
Toshihiko Toyofuku ◽  
Ken-ichi Yoshida
Keyword(s):  
Myocardial Ischemia ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Down Regulation ◽  
Rat Hearts

Effect of adenosine receptor blockade: preventing protective preconditioning depends on time of initiation

1993 ◽  
Vol 265 (2) ◽  
pp. H504-H508 ◽  
Author(s):  
J. D. Thornton ◽  
C. S. Thornton ◽  
J. M. Downey
Keyword(s):  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Adenosine Receptor ◽  
Adenosine Receptors ◽  
Receptor Blockade ◽  
Risk Zone ◽  
Time Points ◽  
Adenosine Receptor Antagonist ◽  
Rabbit Myocardium ◽  
Ischemic Period

Ischemic preconditioning protects the rabbit myocardium from infarction from a subsequent ischemia, and adenosine receptors appear to be involved in this protection. The present study attempts to determine when adenosine receptors must be occupied to achieve protection by infusing the adenosine receptor antagonist PD-115,199 at various time points during the study. Open-chest rabbits were subjected to 30 min of regional ischemia followed by 3 h of reperfusion and had 38 +/- 4% infarction of the risk zone. When hearts were preconditioned by 5 min of ischemia and 10 min reperfusion before the 30-min period of ischemia, only 9 +/- 2% infarction occurred. PD-115,199 given 5 min before the ischemic preconditioning episode blocked the protective effect of preconditioning (39 +/- 5% infarction). PD-115,199 also blocked the protection when given between the ischemic preconditioning episode and the 30-min period of ischemia (30 +/- 4% infarction). PD-115,199 given at the end of 30 min of ischemia did not block protection in preconditioned (PC) hearts (17 +/- 5% infarction) and had no effect on non-PC hearts (44 +/- 6% infarction). In prior studies we found that exogenous adenosine could substitute for ischemia to precondition the heart, indicating that adenosine is an initiator of preconditioning. These results, however, indicate that adenosine receptors must also be occupied during the long ischemic period for preconditioning to be protective and suggest that adenosine is a mediator of preconditioning as well.

Lipoxygenase metabolism of arachidonic acid in ischemic preconditioning and PKC-induced protection in heart

1999 ◽  
Vol 276 (6) ◽  
pp. H2094-H2101 ◽  
Author(s):  
Weina Chen ◽  
Wayne Glasgow ◽  
Elizabeth Murphy ◽  
Charles Steenbergen
Keyword(s):  
Arachidonic Acid ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Arachidonic Acid Metabolism ◽  
Developed Pressure ◽  
12 Lipoxygenase ◽  
Hydroperoxyeicosatetraenoic Acid ◽  
Pkc Activation

We tested the hypothesis that activation of the 12-lipoxygenase (12-LO) pathway of arachidonic acid metabolism contributes to the protective effect of protein kinase C (PKC) activation and ischemic preconditioning (PC), and we report, in perfused rat heart, that both PC and the PKC activator 1,2-dioctanoyl- sn-glycerol (DOG) confer a similar protective effect and stimulate a comparable accumulation of 12-LO metabolites. The 12-LO product, 12( S)-hydroxyeicosatetraenoic acid [12( S)-HETE], was increased in DOG-treated (22.8 ± 4.4 ng/g wet wt) and PC hearts (26.8 ± 5.5 ng/g wet wt) compared with control (13.8 ± 2.1 ng/g wet wt, P < 0.05), and this increase was blocked by 12-LO or PKC inhibitors. Both DOG pretreatment and PC improved recovery of left ventricular developed pressure (LVDP) nearly twofold after 20 min of ischemia; this improvement was blocked by 12-LO inhibitors and was mimicked by infusion of 12-hydroperoxyeicosatetraenoic acid [12( S)-HpETE; 67 ± 6% recovery of LVDP vs. 35 ± 3% for untreated hearts]. Also, the protection afforded by 12( S)-HpETE, as well as by PC, was attenuated by the K+-channel blocker 5-hydroxydecanoate, suggesting that the downstream mechanisms of 12( S)-HpETE-mediated protection are similar to PC. Furthermore, PC stimulates 12-LO metabolism in perfused rabbit heart, and 12-LO inhibition blocks PC-induced cardioprotection. Thus the data suggest that 12-LO metabolism plays an important role in cardioprotection.

scholarly journals The Protective Effect of Ischemic Preconditioning and HMGB1 in Steatotic Liver Grafts from Brain-Dead Donors Submitted to Transplant

2018 ◽  
Vol 102 ◽  
pp. S698
Author(s):  
Elsa Negrete Sánchez ◽  
Cindy G. Avalos de León ◽  
Mónica B. Jiménez Castro ◽  
Araní Casillas-Ramírez ◽  
José Gulfo ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Steatotic Liver ◽  
Brain Dead

Delayed ischemic preconditioning is mediated by opening of ATP-sensitive potassium channels in the rabbit heart

1999 ◽  
Vol 276 (4) ◽  
pp. H1323-H1330 ◽  
Author(s):  
Nelson L. Bernardo ◽  
Michael D’Angelo ◽  
Shinji Okubo ◽  
Archi Joy ◽  
Rakesh C. Kukreja
Keyword(s):  
Protective Effect ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Action Potential Duration ◽  
Rabbit Heart ◽  
Monophasic Action Potential ◽  
Initial Stimulus ◽  
Selective Blocker ◽  
Second Window Of Protection

Cardioprotection from preconditioning reappears 24 h after the initial stimulus. This phenomenon is called the second window of protection (SWOP). We hypothesized that opening of the ATP-sensitive potassium (KATP) channel mediates the protective effect of SWOP. Rabbits were preconditioned (PC) with four cycles of 5-min regional ischemia each followed by 10 min of reperfusion. Twenty-four hours later, the animals were subjected to sustained ischemia for 30 min followed by 180 min of reperfusion (I/R). Glibenclamide (Glib, 0.3 mg/kg ip) or 5-hydroxydecanoate (5-HD, 5 mg/kg iv) was used to block the KATP channel function. Infarct size was reduced from 41.2 ± 2.6% in sham-operated rabbits to 11.6 ± 1.0% in PC rabbits, a 71% reduction ( n = 11, P < 0.01). Treatment with Glib or 5-HD before I/R increased the infarct size to 43.4 ± 2.6 and 37.8 ± 1.9%, respectively ( P < 0.01 vs. PC group, n = 12/group). Sham animals treated with either Glib or 5-HD had an infarct size of 39.0 ± 3.4 and 37.8 ± 1.5%, respectively, which was not different from control (40.0 ± 3.8%) or sham (41.2 ± 2.6%) I/R hearts. Monophasic action potential duration (APD) at 50% repolarization significantly shortened by 28.7, 26.6, and 23.3% in sham animals during 10, 20, and 30 min of ischemia. However, no further augmentation in the shortening of APD was observed in PC hearts. Glib and 5-HD significantly suppressed ischemia-induced epicardial APD shortening, suggesting that 5-HD may not be a selective blocker of the mitochondrial KATP channel in vivo. We conclude that SWOP is mediated by a KATP channel-sensitive mechanism that may have occurred because of the opening of the sarcolemmal KATP channel in vivo.

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