scholarly journals Hyperosmotic Environment Blunts Effectivity of Ischemic Preconditioning Against Ischemia-Reperfusion Injury and Improves Ischemic Tolerance in Non-Preconditioned Isolated Rat Hearts

2016 ◽  
pp. 1045-1051 ◽  
Author(s):  
M. ZÁLEŠÁK ◽  
P. BLAŽÍČEK ◽  
D. PANCZA ◽  
I. GABLOVSKÝ ◽  
V. ŠTRBÁK ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Coronary Occlusion ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Fatty Acid Binding ◽  
Rat Hearts ◽  
Osmotic Activity ◽  
Isolated Rat

Several studies have shown that diabetes mellitus modulates heart resistance to ischemia and abrogates effectivity of cardioprotective interventions, such as ischemic preconditioning (IP). The aim of this study was to evaluate whether the effect of hyperglycemic conditions on the severity of ischemia-reperfusion (I/R) injury in preconditioned and non-preconditioned hearts (controls, C) is related to changes in osmotic activity of glucose. Experiments were performed in isolated rat hearts perfused according to Langendorff exposed to 30-min coronary occlusion/ 120-min reperfusion. IP was induced by two cycles of 5-min coronary occlusion/5-min reperfusion, prior to the long-term I/R. Hyperosmotic (HO) state induced by an addition of mannitol (11 mmol/l) to a standard Krebs-Henseleit perfusion medium significantly decreased the size of infarction and also suppressed a release of heart fatty acid binding protein (h-FABP – biomarker of cell injury) from the non-IP hearts nearly to 50 %, in comparison with normoosmotic (NO) mannitol-free perfusion. However, IP in HO conditions significantly increased the size of infarction and tended to elevate the release of h-FABP to the effluent from the heart. The results indicate that HO environment plays a cardioprotective role in the ischemic myocardium. On the other hand, increased osmolarity, similar to that in the hyperglycemic conditions, may play a pivotal role in a failure of IP to induce cardioprotection in the diabetic myocardium.

scholarly journals Severity of Lethal Ischemia/Reperfusion Injury in Rat Hearts Subjected to Ischemic Preconditioning Is Increased Under Conditions of Simulated Hyperglycemia

2014 ◽  
pp. 577-585
Author(s):  
M. ZÁLEŠÁK ◽  
P. BLAŽÍČEK ◽  
D. PANCZA ◽  
V. LEDVÉNYIOVÁ ◽  
M. BARTEKOVÁ ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Area At Risk ◽  
Fatty Acid Binding ◽  
Rat Hearts ◽  
Elevated Glucose

The aim of our study was to characterize resistance to ischemia/reperfusion (I/R) injury in Langendorff-perfused rat hearts and effectivity of ischemic preconditioning (PC) under condition of simulated acute hyperglycemia (SAHG) by perfusion of the hearts with Krebs-Henseleit (KH) solution with elevated glucose concentration (22 mmol/l). I/R injury was induced by 30-min coronary occlusion followed by 120-min reperfusion and PC by two cycles of 5-min occlusion/5-min reperfusion, prior to I/R. The severity of I/R injury was characterized by determination of the size of infarction (IS, expressed in % of area at risk size) and the amount of heart-type fatty acid binding protein (h-FABP, a marker of cell injury) released from the hearts to the effluent. Significantly smaller IS (8.8±1 %) and lower total amount of released h-FABP (1808±660 pmol) in PC group compared with IS 17.1±1.2 % (p<0.01) and amount of h-FABP (8803±2415 pmol, p<0.05) in the non-PC control hearts perfused with standard KH solution (glucose 11 mmol/l) confirmed protective effects of PC. In contrast, in SAHG groups, PC enhanced IS (21.4±2.2 vs. 14.3±1.3 %, p<0.05) and increased total amount of h-FABP (5541±229 vs. 3458±283 pmol, p<0.05) compared with respective non-PC controls. Results suggest that PC has negative effect on resistance of the hearts to I/R injury under conditions of elevated glucose in vitro.

Effect of estrogen replacement treatment on ischemic preconditioning in isolated rat hearts

2004 ◽  
Vol 82 (5) ◽  
pp. 339-344 ◽  
Author(s):  
Wei-Jie Peng ◽  
Jing Yu ◽  
Sheng Deng ◽  
Jun-Ling Jiang ◽  
Han-Wu Deng ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Ovariectomized Rats ◽  
Mechanical Function ◽  
Estrogen Replacement ◽  
Isolated Hearts ◽  
Replacement Treatment ◽  
Rat Hearts ◽  
Isolated Rat

In the present study, we tested the effects of long-term estrogen replacement treatment on myocardial ischemia-reperfusion injury and on the cardioprotection of ischemic preconditioning in isolated hearts from ovariectomized rats. Ovariectomized rats were treated with 17β-estradiol (30 µg/kg/d, s.c.) for 12 weeks. Isolated rat hearts were perfused in the Langendorff mode. Heart rate, coronary flow, left ventricular pressure and its first derivative (±LVdp/dtmax) were recorded. Fifteen-min global ischemia and 30-min reperfusion caused a significant decrease of cardiac mechanical function, which were not affected by ovariectomy or estrogen replacement treatment. The isolated hearts in all groups could be preconditioned, and the cardioprotection afforded by preconditioning in the sham-operated rats was greater compared with ovariectomized rats with or without estrogen treatment. These results suggest that long-term estrogen replacement treatment exerts no effect on the inhibition of mechanical function after ischemia-reperfusion, and this study also suggests that estrogen does not affect ischemic preconditioning in isolated hearts of ovariectomized rats.Key words: ERT (estrogen replacement treatment), ischemia-reperfusion, ischemic preconditioning, heart, rat.

scholarly journals CaMKII/calpain interaction mediates ischemia/reperfusion injury in isolated rat hearts

2020 ◽  
Vol 11 (5) ◽  
Author(s):  
Hong-Ting Lu ◽  
Ren-Qian Feng ◽  
Jia-Kun Tang ◽  
Jing-Jun Zhou ◽  
Feng Gao ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Isolated Rat

Endothelial Cell Injury in Cardiovascular Surgery: The Systemic Inflammatory Response11Recent discoveries in the field of vascular biology have led to an expanded understanding of the pathogenesis of many of the immediate and long-term complications of patients undergoing cardiovascular operations and interventional cardiologic procedures. In particular, the vascular endothelium has emerged as the central focus of many of the biologic events that affect the preoperative, operative, and postoperative course of nearly all heart surgery patients. A recurring theme in the study of endothelial cell biology is the crucial role that endothelial cell injury plays in the difficulties that our patients encounter. The deleterious effects of endothelial cell injury are most evident in the acute syndromes of vasospasm, coagulopathy, ischemia/reperfusion injury, and the systemic inflammatory response to cardiopulmonary bypass. In addition, chronic endothelial cell injury contributes to the development of anastomotic narrowing and the progression of atherosclerosis, both of which limit the long-term success of coronary artery bypass grafting. Because of the increasingly recognized role of the endothelium in cardiovascular function there is a tremendous amount of basic science information detailing the response of the endothelium to injury. This is the fifth in a series of seven reviews intended as an introduction to the major topics of endothelial cell biology that are of importance to the practicing cardiothoracic surgeon. In particular, the authors have focused on the role that the endothelium has on the development of vasomotor dysfunction, bleeding and thrombosis, neutrophil-endothelial cell interaction, and obstructive arteriopathy. The aim of these reviews is to provide a concise reference point for cardiothoracic surgeons as they evaluate the ever-accumulating research findings and new therapies that stem from the study of the endothelium in response to the insults encountered in cardiothoracic surgery.Edward D. Verrier, MD

1997 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Edward M Boyle, MD ◽  
Timothy H Pohlman, MD ◽  
Marion C Johnson, MD ◽  
Edward D Verrier, MD
Keyword(s):  
Endothelial Cell ◽  
Cell Biology ◽  
Heart Surgery ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Cell Interaction ◽  
Endothelial Cell Injury

scholarly journals 9-Phenanthrol, a TRPM4 Inhibitor, Protects Isolated Rat Hearts from Ischemia–Reperfusion Injury

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e70587 ◽  
Author(s):  
Jing Wang ◽  
Ken Takahashi ◽  
Hulin Piao ◽  
Peng Qu ◽  
Keiji Naruse
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Isolated Rat

Ischemic preconditioning protects by activating prosurvival kinases at reperfusion

2005 ◽  
Vol 288 (2) ◽  
pp. H971-H976 ◽  
Author(s):  
Derek J. Hausenloy ◽  
A. Tsang ◽  
Mihaela M. Mocanu ◽  
Derek M. Yellon
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Volume Ratio ◽  
Sprague Dawley ◽  
Phosphatidylinositol 3 Kinase ◽  
S6 Kinase ◽  
Fourfold Increase ◽  
Rat Hearts ◽  
Reperfusion Phase

Pharmacological activation of the prosurvival kinases Akt and ERK-1/2 at reperfusion, after a period of lethal ischemia, protects the heart against ischemia-reperfusion injury. We hypothesized that ischemic preconditioning (IPC) protects the heart by phosphorylating the prosurvival kinases Akt and ERK-1/2 at reperfusion. In isolated perfused Sprague-Dawley rat hearts subjected to 35 min of lethal ischemia, the phosphorylation states of Akt, ERK-1/2, and p70 S6 kinase (p70S6K) were determined after 15 min of reperfusion, and infarct size was measured after 120 min of reperfusion. IPC induced a biphasic response in Akt and ERK-1/2 phosphorylation during the preconditioning and reperfusion phases after the period of lethal ischemia. IPC induced a fourfold increase in Akt, ERK-1/2, and p70S6K phosphorylation at reperfusion and reduced the infarct risk-to-volume ratio (56.9 ± 5.7 and 20.9 ± 3.6% for control and IPC, respectively, P < 0.01). Inhibiting the IPC-induced phosphorylation of Akt, ERK-1/2, and p70S6K at reperfusion with the phosphatidylinositol 3-kinase (PI3K) inhibitor LY-294002 or the MEK-1/2 inhibitor PD-98059 abrogated IPC-induced protection (46.3 ± 5.8, 49.2 ± 4.0, and 20.9 ± 3.6% for IPC + LY-294002, IPC + PD-98059, and IPC, respectively, P < 0.01), demonstrating that the phosphorylation of these kinases at reperfusion is required for IPC-induced protection. In conclusion, we demonstrate that the reperfusion phase following sustained ischemia plays an essential role in mediating IPC-induced protection. Specifically, we demonstrate that IPC protects the heart by phosphorylating the prosurvival kinases Akt and ERK-1/2 at reperfusion.

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