scholarly journals Impact of endothelial dysfunction on the course of acute ST-elevation myocardial infarction and its correction by remote ischemic preconditioning

2020 ◽  
Vol 92 (1) ◽  
pp. 10-14
Author(s):  
V N Manchurov ◽  
A M Lebedeva ◽  
N B Ryazankina ◽  
E Yu Vasilieva ◽  
A V Shpektor
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Ischemic Preconditioning ◽  
Brachial Artery ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Lower Percentage ◽  
Control Group ◽  
Primary Pci

Aim of the study - to assess the effect of remote ischemic preconditioning (RIPC) on the incidence of endothelial dysfunction (ED) and its impact on hospital prognosis in patients with ST segment elevation acute myocardial infarction (STEMI). Materials and methods. We conducted a single - centre, open - label prospective study that included 173 patients with STEMI who underwent primary percutaneous coronary intervention within the first 24 hours of the symptoms onset. Before the PCI, patients were randomized into two groups. In the first group (n=86) during the preparation for PCI, we performed RIPC procedure by inflation of the cuff of the tonometer to 200 mm Hg and its further deflation on patient's shoulder, thus creating short cycles of controlled ischemia/reperfusion in hand (4 cycles of ischemia/reperfusion for 5/5 minutes respectively). In the second, control group (n=87), the standard primary PCI was performed without the previous RIPC. Evaluation of the endothelial function was performed on the 2-7th day after admission using the endothelium - dependent flow - mediated dilatation test (FMD) of the brachial artery. Primary endpoints in this study included the presence of ED, in - hospital mortality, life - threatening arrhythmias (ventricular fibrillation/ventricular tachycardia after first 24 hours upon admission), stent thrombosis, clinical signs of heart failure, and a combined endpoint consisting of all the listed above. Results. The median values for FMD-test did not differ significantly between the study groups upon admission. Assessment of the FMD of the brachial artery on the 2-7th day after PCI showed that among the patients who underwent RIPC there was a significantly lower percentage of patients with ED than in the patients with STEMI who did not undergo RIPC before PCI (43.1% vs. 75.8% respectively, p=0.0001). We found a significant reduction in the incidence of heart failure and of combined endpoint in the group of patients without ED compared with patients with ED: 0% vs. 9.3% (n=7; p=0.023) and 3.8% (n=2) vs. 16% (n=12; p=0.032) respectively. When assessing the effect of RIPC on hospital prognosis, we also found a significant decrease in the incidence of heart failure and a trend towards a decrease in the combined endpoint in the group of patients who underwent RIPC compared to the control group: 1.5% (n=1) vs. 9.7% (n=6; p=0.045) and 6.2% (n=4) vs. 16.1% (n=10; p=0.073) respectively. Conclusion. Performance of RIPC before the primary PCI significantly reduces the incidence of ED in patients with STEMI on the 2-7th day of the disease onset. The presence of ED in patients with STEMI is associated with a significant increase in the incidence of heart failure and of the combined endpoint during in - hospital period. RIPC significantly reduces the incidence of heart failure in patients with STEMI during in - hospital period.

Remote Ischemic Preconditioning Protects Against Endothelial Dysfunction in a Human Model of Systemic Inflammation: A Randomized Clinical Trial

2021 ◽  
Author(s):  
Marco Orlandi ◽  
Stefano Masi ◽  
Devina Bhowruth ◽  
Yago Leira ◽  
Georgios Georgiopoulos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Systemic Inflammation ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Human Model ◽  
Control Group ◽  
Flow Mediated Dilatation ◽  
And Oxidative Stress

Objective: Inflammation, oxidative stress, and endothelial dysfunction are known to contribute to ischemia-reperfusion injury. Remote ischemic preconditioning (RIPC) protects from endothelial dysfunction and the damage induced by ischemia-reperfusion. Using intensive periodontal treatment (IPT), an established human model of acute systemic inflammation, we investigated whether RIPC prevents endothelial dysfunction and modulates systemic levels of inflammation and oxidative stress. Approach and Results: Forty-nine participants with periodontitis were randomly allocated to receive either 3 cycles of ischemia-reperfusion on the upper limb (N=25, RIPC) or a sham procedure (N=24, control) before IPT. Endothelial function assessed by flow-mediated dilatation of the brachial artery, inflammatory cytokines, markers of vascular injury, and oxidative stress were evaluated at baseline, day 1, and day 7 after IPT. Twenty-four hours post-IPT, the RIPC group had lower levels of IL (interleukin)-10 and IL-12 compared with the control group ( P <0.05). RIPC attenuated the IPT-induced increase in IL-1β, E-selectin, sICAM-3 (soluble intercellular adhesion molecule 3), and s-thrombomodulin levels between the baseline and day 1 ( P for interaction <0.1). Conversely, oxidative stress was differentially increased at day1 in the RIPC group compared with the control group ( P for interaction <0.1). This was accompanied by a better flow-mediated dilatation (mean difference 1.75% [95% CI, 0.428–3.07], P =0.011). After 7 days from IPT, most of the inflammatory markers endothelial-dependent and -independent vasodilation were similar between groups. Conclusions: RIPC prevented acute endothelial dysfunction by modulation of inflammation and oxidation processes in patients with periodontitis following exposure to an acute inflammatory stimulus. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03072342.

scholarly journals Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning

2016 ◽  
Vol 311 (2) ◽  
pp. H364-H370 ◽  
Author(s):  
Elisabeth A. Lambert ◽  
Colleen J. Thomas ◽  
Robyn Hemmes ◽  
Nina Eikelis ◽  
Atul Pathak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Preconditioning ◽  
Sympathetic Nerve ◽  
Ischemia Reperfusion ◽  
Muscle Sympathetic Nerve Activity ◽  
Reactive Hyperemia ◽  
Late Phase ◽  
Remote Ischemic Preconditioning ◽  
Control Group ◽  
Experimental Ir

Sympathetic neural activation may be detrimentally involved in tissue injury caused by ischemia-reperfusion (IR). We examined the effects of experimental IR in the forearm on sympathetic nerve response, finger reactive hyperemia, and oxidative stress, and the protection afforded by applying remote ischemic preconditioning (RIPC). Ischemia was induced in the forearm for 20 min in healthy volunteers. RIPC was induced by applying two cycles, 5 min each, of ischemia and reperfusion to the upper leg immediately before IR. We examined muscle sympathetic nerve activity (MSNA) in the contralateral leg using microneurography, finger reactive hyperemia [ischemic reactive hyperemia index (RHI)], erythrocyte production of reduced gluthathione (GSH), and plasma nitric oxide (NO) concentration. In controls (no RIPC; n = 15), IR increased MSNA in the early and late phase of ischemia (70% at 5 min; 101% at 15 min). In subjects who underwent RIPC ( n = 15), the increase in MSNA was delayed to the late phase of ischemia and increased only by 40%. GSH increased during ischemia in the control group ( P = 0.05), but not in those who underwent RIPC. Nitrate and nitrite concentration, taken as an index of NO availability, decreased during the reperfusion period in control individuals ( P < 0.05), while no change was observed in those who underwent RIPC. Experimental IR did not affect RHI in the control condition, but a significant vasodilatory response occurred in the RIPC group ( P < 0.05). RIPC attenuated ischemia-induced sympathetic activation, prevented the production of an erythrocyte marker of oxidative stress and the reduction of NO availability, and ameliorated RHI.

scholarly journals Hepatic Remote Ischemic Preconditioning (RIPC) Protects Heart Damages Induced by Ischemia Reperfusion Injury in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Yanlong Ren ◽  
Shujin Lin ◽  
Wenxian Liu ◽  
Huiguo Ding
Keyword(s):  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Remote Ischemic Preconditioning ◽  
Mechanical Activity ◽  
Control Group ◽  
Cardioprotective Effects

It has been convincingly demonstrated that remote ischemic preconditioning (RIPC) can make the myocardium resistant to the subsequent ischemia reperfusion injury (IRI), which causes severe damages by mainly generating cell death. However, the cardioprotective effects of the hepatic RIPC, which is the largest metabolic organ against I/R, have not been fully studied. The aim of our research is whether remote liver RIPC may provide cardioprotective effects against the I/R-induced injury. Here, we generated an I/R mice model in four groups to analyze the effect. The control group is the isolated hearts with 140-min perfusion. I/R group added ischemia in 30 min following 90-min reperfusion. The third group (sham) was subjected to the same procedure as the latter group. The animals in the fourth group selected as the treatment group, underwent a hepatic RIPC by three cycles of 5-min occlusion of the portal triad and then followed by induction of I/R in the isolated heart. The level of myocardial infarction and the preventive effects of RIPC were assessed by pathological characteristics, namely, infarct, enzyme releases, pressure, and cardiac mechanical activity. Subjected to I/R, the hepatic RIPC minimized the infarct size (17.7 ± 4.96 vs. 50.06 ± 5, p &lt; 0.001) and improved the left ventricular-developed pressure (from 47.42 ± 6.27 to 91.62 ± 5.22 mmHg) and the mechanical activity. Release of phosphocreatine kinase-myocardial band (73.86 ± 1.95 vs. 25.93 ± 0.66 IUL−1) and lactate dehydrogenase (299.01 ± 10.7 vs. 152.3 ± 16.7 IUL−1) was also decreased in the RIPC-treated group. These results demonstrate the cardioprotective effects of the hepatic remote preconditioning against the injury caused by I/R in the isolated perfused hearts.

Aging attenuates the protective effect of ischemic preconditioning against endothelial ischemia-reperfusion injury in humans

2013 ◽  
Vol 304 (12) ◽  
pp. H1727-H1732 ◽  
Author(s):  
Inge van den Munckhof ◽  
Niels Riksen ◽  
Joost P. H. Seeger ◽  
Tim H. Schreuder ◽  
George F. Borm ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Ischemic Preconditioning ◽  
Brachial Artery ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
The Elderly ◽  
Upper Arm ◽  
Before And After ◽  
The Impact

Reperfusion is mandatory after ischemia but also triggers ischemia-reperfusion (I/R) injury. Ischemic preconditioning (IPC) can limit endothelial I/R injury. Nonetheless, translation of IPC to the clinical arena is often disappointing. Since application of IPC typically relates to older patients, efficacy of IPC may be attenuated with aging. Our objective was to examine the impact of advanced age on the ability of IPC to protect against endothelial dysfunction due to I/R injury. We included 15 healthy young (20–25 yr) and 15 older (68–77 yr) men. We examined brachial artery endothelial function using flow-mediated dilation (FMD) before and after arm I/R (induced by inflation of an upper-arm blood pressure cuff for 20 min and 15 min of reperfusion). In a randomized order, I/R was preceded by IPC or a control intervention consisting of three cycles of 5 min upper-arm cuff inflation to 220 or 20 mmHg, respectively. As a result, in young men, FMD decreased significantly after I/R (6.4 ± 2.7 to 4.4 ± 2.5%). This decrease was not present when I/R was preceded by IPC (5.9 ± 2.3 to 5.6 ± 2.5%). IPC-induced protection appeared to be significantly reduced in the elderly patients ( P = 0.04). Although FMD decreased after I/R in older men (3.5 ± 1.7 to 2.5 ± 1.0%), IPC could not prevent this (3.7 ± 2.1 to 2.2 ± 1.1%). In conclusion, this study is the first to observe in humans in vivo that older age is associated with an abolished effect of IPC to protect against endothelial dysfunction after I/R in the brachial artery. This provides a possible explanation for the problematic translation of strategies that reduce I/R injury from preclinical work to the clinical arena.

scholarly journals Differential Role of Pim-1 Kinase in Anesthetic-induced and Ischemic Preconditioning against Myocardial Infarction

2009 ◽  
Vol 111 (6) ◽  
pp. 1257-1264 ◽  
Author(s):  
Jan Stumpner ◽  
Andreas Redel ◽  
Anna Kellermann ◽  
Christopher A. Lotz ◽  
Christoph A. Blomeyer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Protein Kinase ◽  
Cytochrome C ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Kinase Inhibitor ◽  
Protein Kinase B ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Area At Risk

Background Ischemic preconditioning (IPC) and anesthetic-induced preconditioning against myocardial infarction are mediated via protein kinase B. Pim-1 kinase acts downstream of protein kinase B and was recently shown to regulate cardiomyocyte survival. The authors tested the hypothesis that IPC and anesthetic-induced preconditioning are mediated by Pim-1 kinase. Methods Pentobarbital-anesthetized male C57Black/6 mice were subjected to 45 min of coronary artery occlusion and 3 h of reperfusion. Animals received no intervention, Pim-1 kinase inhibitor II (10 microg/g intraperitoneally), its vehicle dimethyl sulfoxide (10 microl/g intraperitoneally), or 1.0 minimum alveolar concentration desflurane alone or in combination with Pim-1 kinase inhibitor II (10 microg/g intraperitoneally). IPC was induced by three cycles of 5 min ischemia-reperfusion each, and animals received IPC either alone or in combination with Pim-1 kinase inhibitor II (10 microg/g intraperitoneally). Infarct size was determined with triphenyltetrazolium chloride, and area at risk was determined with Evans blue (Sigma-Aldrich, Taufkirchen, Germany). Protein expression of Pim-1 kinase, Bad, phospho-Bad, and cytosolic content of cytochrome c were measured using Western immunoblotting. Results Infarct size in the control group was 47 + or - 2%. Pim-1 kinase inhibitor II (44 + or - 2%) had no effect on infarct size. Desflurane (17 + or - 3%) and IPC (19 + or - 2%) significantly reduced infarct size compared with control (both P &lt; 0.05 vs. control). Blockade of Pim-1 kinase completely abrogated desflurane-induced preconditioning (43 + or - 3%), whereas IPC (35 + or - 3%) was blocked partially. Desflurane tended to reduce cytosolic content of cytochrome c, which was abrogated by Pim-1 kinase inhibitor II. Conclusion These data suggest that Pim-1 kinase mediates at least in part desflurane-induced preconditioning and IPC against myocardial infarction in mice.

Remote Ischemic Preconditioning and Endothelial Function in Patients with Acute Myocardial Infarction and Primary PCI

2014 ◽  
Vol 127 (7) ◽  
pp. 670-673 ◽  
Author(s):  
Vladimir Manchurov ◽  
Nadezda Ryazankina ◽  
Tatyana Khmara ◽  
Dmitry Skrypnik ◽  
Roman Reztsov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Function ◽  
Ischemic Preconditioning ◽  
Remote Ischemic Preconditioning ◽  
Primary Pci

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

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