Effect Of Remote Ischemic Postconditioning Research Articles

Anti-Inflammatory and Antipruritic Effects of Remote Ischaemic Postconditioning in a Mouse Model of Experimental Allergic Contact Dermatitis.

Background and Objectives: Allergic contact dermatitis is a common type IV hypersensitivity reaction characterised by redness, itching, oedema and thickening of the skin. It occurs in about 7% of the population and its incidence is increasing. It has been observed that the preconditioning of tissues by exposing them to transient ischemia increases resistance to subsequent permanent ischemia, and this phenomenon is called ischemic preconditioning. It has been shown that conditioning in one organ can also protect other organs. The protective effect of remote ischemic preconditioning is thought to be based on the induction of anti-inflammatory responses. The aim of this project was to investigate the anti-inflammatory and antipruritic effects of remote ischemic postconditioning in a mouse model of experimental allergic contact dermatitis. Methods: Experimental allergic contact dermatitis was induced with 1-fluoro-2,4-dinitrobenzene. Remote ischemic postconditioning was performed at 3 and 25 h after the challenge. Ear thickness and number of scratches 24 and 48 h after challenge, as well as cytokine levels and the infiltration of mast cells, neutrophils, CD4+ and CD8+ T lymphocytes in serum and ear tissue at 48 h were measured to determine the effect of RIPsC. Results: Remote ischemic postconditioning decreased ear thickness, one of the symptoms of allergic contact dermatitis (p < 0.0001). It had no significant effect on the number of scratches. It reduced serum IL-17 levels (p < 0.01). It alleviated local inflammation by suppressing CD8+ T lymphocyte and neutrophil infiltration. Conclusions: It was concluded that remote ischemic postconditioning may alleviate the symptoms of allergic contact dermatitis by suppressing CD8+ T lymphocyte and neutrophil infiltration and reducing IL-17 secretion.

Autonomic function may mediate the neuroprotection of remote ischemic postconditioning in stroke: A randomized controlled trial

ObjectivesTo evaluate the effect of remote ischemic postconditioning (RIPostC) on the prognosis of acute ischemic stroke(AIS) patients and investigate the mediating role of autonomic function in the neuroprotection of RIPostC. Materials and Methods132 AIS patients were randomized into two groups. Patients received four cycles of 5-min inflation to a pressure of 200 mmHg(i.e., RIPostC) or patients’ diastolic BP(i.e., shame), followed by 5 min of deflation on healthy upper limbs once a day for 30 days. The main outcome was neurological outcome including the National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), and Barthel index(BI). The second outcome measure was autonomic function measured by heart rate variability(HRV). ResultsCompared with the baseline, the post-intervention NIHSS score was significantly reduced in both groups (P<0.001). NIHSS score was significantly lower in the control group than intervention group at day 7.[RIPostC:3(1,5) versus shame:2(1,4); P=0.030]. mRS scored lower in the intervention group compared with the control group at day 90 follow-up(RIPostC:0.5±2.0 versus shame:1.0±2.0;P=0.016). The goodness-of-fit test revealed a significant difference between the generalized estimating equation model of mRS and BI scores of uncontrolled-HRV and controlled-HRV(P<0.05, both). The results of bootstrap revealed a complete mediation effect of HRV between group on mRS[indirect effect: −0.267 (LLCI = −0.549, ULCI = −0.048), the direct effect: −0.443 (LLCI = −0.831, ULCI = 0.118)]. ConclusionThis is the first human-based study providing evidence for a mediation role of autonomic function between RIpostC and prognosis in AIS patients. It indicated that RIPostC could improve the neurological outcome of AIS patients. Autonomic function may play a mediating role in this association. Trial registrationThe clinical trials registration number for this study is NCT02777099 (ClinicalTrials.gov Identifier)

Retracted: Cardiac Magnetic Resonance Assessment of the Protective Effect of Remote Ischemic Postconditioning on Coronary Microcirculation after Reperfusion Therapy for Acute ST-Segment Elevation Myocardial Infarction.

[This retracts the article DOI: 10.1155/2022/5629763.].

Participation of Leptin and Corticosterone in the Decrease in Infarct-Limiting Efficiency of Remote Postconditioning and in the Development of Arterial Hypertension in Metabolic Syndrome in Rats

We studied the effect of induced metabolic syndrome (MetS) on the effectiveness of the infarct-limiting effect of remote ischemic postconditioning (RP) in Wistar rats. The involvement of leptin and corticosterone in the formation of arterial hypertension (AH) and in reduction of the effectiveness of RP in MetS was also studied. MetS was induced by high-carbohydrate high-fat diet with replacement of drinking water with 20% fructose solution for 90 days. MetS simulation led to obesity, AH, impaired lipid and carbohydrate metabolism, hyperleptinemia, and moderate stress. All animals were subjected to 45-min coronary occlusion and 120-min reperfusion. In the RP groups, tourniquets were applied on the hind limbs in the area of the hip joint immediately after the end of ischemia (3 cycles consisting of 5-min ischemia and 5-min reperfusion). A direct correlation was found between the severity of AH in rats with MetS and the levels of corticosterone and leptin. In rats with MetS, the effectiveness of RP decreased: a direct correlation between the infarct size and serum content of leptin was revealed in rats with MetS+RP. Corticosterone seems to be one of the factors of AH development in rats with MetS.

No Differences in Cerebral Immunohistochemical Markers following Remote Ischemic Postconditioning in Newborn Piglets with Hypoxia-Ischemia.

Despite therapeutic hypothermia, neonates with hypoxic-ischemic encephalopathy still develop neurological disabilities. We have previously investigated neuroprotection by remote ischemic postconditioning (RIPC) in newborn piglets following hypoxia-ischemia (HI). The aim of this study was to further investigate potential effects of RIPC on cerebral immunohistochemical markers related to edema, apoptosis, and angiogenesis. Brain expression of aquaporin 4, caspase-3, B-cell lymphoma 2, and vascular endothelial growth factor was analyzed by immunohistochemistry in 23 piglets, randomly selected from a larger study of RIPC after HI. Twenty animals were subjected to 45 minutes of HI and randomized to treatment with and without RIPC, while three animals were randomized to sham procedures. RIPC was conducted by four conditioning cycles of 5-minute ischemia and reperfusion. Piglets were euthanized 72 hours after the HI insult. Piglets subjected to HI treated with and without RIPC were similar at baseline and following the HI insult. However, piglets randomized to HI alone had longer duration of low blood pressure during the insult. We found no differences in the brain expression of the immunohistochemical markers in any regions of interest or the whole brain between the two HI groups. RIPC did not influence brain expression of markers related to edema, apoptosis, or angiogenesis in newborn piglets at 72 hours after HI. These results support previous findings of limited neuroprotective effect by this RIPC protocol. Our results may have been affected by the time of assessment, use of fentanyl as anesthetic, or limitations related to our immunohistochemical methods.

Cardiac Magnetic Resonance Assessment of the Protective Effect of Remote Ischemic Postconditioning on Coronary Microcirculation after Reperfusion Therapy for Acute ST-Segment Elevation Myocardial Infarction.

This study intends to evaluate the characteristics of coronary microcirculatory function in patients with myocardial infarction undergoing reperfusion and its predictive value in assessing cardiac function, myocardial activity, recovery of ventricular wall motion after infarction, and distant myocardial remodeling by cardiac magnetic resonance technique (CMRI). Materials and Methods. The 293 cases of patients with myocardial infarction treated in our hospital from August 2017 to August 2021 were selected as the subjects of this retrospective study, 13 cases were shed due to transfer and moving, and the rest were divided into 140 cases each in the emergency and elective groups according to emergency percutaneous coronary intervention (PCI) and elective PCI. The patients' myocardial infarct volume ventricular volume, microcirculatory obstruction volume ventricular volume, microcirculatory obstruction volume/myocardial infarct volume, and LVEF, combined with BP and troponin T, were analysed by CMR for comparative analysis, hemodynamic, and cardiac function index differences. Results. The hemodynamics (CO, CI, SV, SI, LVSW1, and LCW) measured at different times were significantly different between the two groups; patients in the emergency group had significantly lower EDV and ESV than the elective group at 7-10 d postoperatively; and EDV, ESV, and LVEF improved in both groups after 3 months, while EDV, ESV, and LVEF improved significantly better in the emergency group than in the elective group, and the difference was statistically significant (P < 0.05). The myocardial infarct quality, VSM score, and ventricular wall motion abnormality score were significantly lower in the emergency group than in the elective group from 7 to 10 d after PCI; myocardial infarct quality, VSM score, and ventricular wall motion abnormality score improved in both groups at 3 months after PCI; and the degree of improvement of myocardial infarct quality and VSM score was significantly better in the emergency group than in the elective group (P < 0.05). Conclusion. Acute myocardial infarction patients with significant effect of emergency PCI treatment can be on their postmyocardial infarction left ventricular function, and in the treatment of coronary heart disease, myocardial infarction diagnosis has a certain reference value.

Protective effect of remote ischemic postconditioning in rat testes after testicular torsion/detorsion.

Testicular torsion/detorsion can lead to severe testicular damage. The organ-protective effect of remote ischemic postconditioning (RLIPost) against ischemia/reperfusion injury has been characterized; however, it remains unknown whether RLIPost has a testicular protective effect. Here, we tested the hypothesis that RLIPost can protect the testes in a rat model of testicular torsion/detorsion in vivo. Male Sprague-Dawley rats were assigned to sham-operated, control, or remote liver and limb ischemic postconditioning-treated groups. Testicular torsion/detorsion was performed by 3h of testicular torsion (720° clockwise unilateral spermatic cord torsion), followed by 3h of detorsion. For liver and limb ischemic postconditioning, four cycles of 5 min of liver or limb ischemia with 5-min intermittent reperfusion stimuli were conducted at the onset of testicular reperfusion. Liver and limb ischemic postconditioning significantly ameliorated ipsilateral and contralateral testicular swelling responses, preserved morphological integrity and spermatogenesis and inhibited testicular apoptosis. In addition, RLIPost enhanced the phosphorylation of AKT/ERK1/2/GSK-3β/STAT-3 in the ipsilateral testis while suppressing JNK activation in the ipsilateral and contralateral testes. To the best of our knowledge, this study is the first to demonstrate the involvement of RLIPost in an animal model of testicular torsion/detorsion. We showed that RLIPost protects both ipsilateral and contralateral testes against testicular torsion/detorsion in vivo, via at least in part, the RISK and SAFE-mediated signaling pathways.

The efficiency of remote ischemic postconditioning of the myocardium in rats with induced metabolic syndrome depends on the leptin level

Remote postconditioning (RPost) has a great therapeutic potential for protecting the myocardium during ischemiareperfusion in clinical practice. At the same time, an important problem limiting the use of conditioning effects in the clinic is the presence of metabolic disorders in the patient. The aim of this work was to assess the effect of induced metabolic syndrome (iMetS) on the efficacy of the infarct-limiting effect of remote ischemic postconditioning (RPost) in rats and to study the mechanisms of this effect.The study was carried out on Wistar rats. MetS was induced by high-carbohydrate high-fat diet. Criteria of metabolic syndrome were an increase in the weight of animals, abdominal fat volume, the development of arterial hypertension, hypercholesterolemia, an increase in triglycerides in serum, hyperleptinemia, hyperglycemia, the development of a state of insulin resistance by a significant increase in the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index and glucose tolerance. All animals were subjected to 45 min coronary occlusion and 120 min reperfusion.RPost led to a twofold reduction of infarct size in rats with intact metabolism (р &lt; 0.0001), while in rats with iMetS a decrease in infarct size during RPost was 25 % (p = 0.00003), which was significantly lower than in animals without iMetC (р &lt; 0.0001). A direct correlation was found between of infarct size during RPost and the serum leptin level of rats with iMetC.The presented data suggested that a decrease in the efficiency of remote postconditioning in rats with diet-induced metabolic syndrome depends on leptin content in blood.

The role of protein kinase C and PI3-kinase in the mechanism of the cardioprotective effect of 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.

Effects of remote ischemic postconditioning on HIF-1α and other markers in on-pump cardiac surgery.

There is a lack of data about the effects of remote ischemic postconditioning (RIPostC) on hypoxia-inducible factor-1α (HIF-1α) plasma levels after on-pump cardiac surgery (OPCS). This study aimed to measure the effects of RIPostC on postoperative HIF-1α plasma levels, cardiac markers and arterial oxygenation in patients undergoing OPCS. This single-centre randomized, double blind, controlled trial, enrolled 70 patients (35 control and 35 RIPostC). RIPostC was performed by 3 cycles (5min of ischemia followed by 5min of reperfusion) administered in upper arm immediately after the pump period. The primary outcome was to measure HIF-1α plasma levels: before surgery (T0), and 2h (T1), 8h (T2), 24h (T3), 36h (T4) and 48h (T5) after RIPostC. As secondary endpoint, Troponin T, CK-MB, CPK plasma levels and PaO2/FiO2 ratio were measured. HIF-1α plasma levels were increased at T1-T3 compared to T0 in both groups (P < 0.001). In the RIPostC group HIF-1α increased compared to the control group: differences between means (95% CI) were 0.034 (0.006-0.06) P = 0.019 at T1; 0.041 (0.013-0.069) P = 0.005 at T2; and 0.021 (0.001-0.042) P = 0.045 at T3. PaO2/FiO2 was higher in the RIPostC group than in the control group: at T3, T4 and T5. Moreover, Troponin T, CK-MB and CPK values decreased in the RIPostC group compared to the control group. HIF-1α plasma levels increased in control patients during for at least 36h after OPCS. RIPostC resulted in even higher HIF-1α levels during at least the first 24h and improved arterial oxygenation and cardiac markers.

Safety and efficacy of remote ischemic postconditioning after thrombolysis in patients with stroke.

To determine the effect of remote ischemic postconditioning (RIPC) on patients with acute ischemic stroke (AIS) undergoing IV thrombolysis (IVT). A single-center randomized controlled trial was performed with patients with AIS receiving IVT. Patients in the RIPC group were administered RIPC treatment (after IVT) during hospitalization. The primary endpoint was a score of 0 or 1 on the modified Rankin scale (mRS) at day 90. The safety, tolerability, and neuroprotection biomarkers associated with RIPC were also evaluated. We collected data from both the RIPC group (n = 34) and the control group (n = 34). The average duration of hospitalization was 11.2 days. There was no significant difference between 2 groups at admission for the NIH Stroke Scale score (p = 0.364) or occur-to-treatment time (p = 0.889). Favorable recovery (mRS score 0-1) at 3 months was obtained in 71.9% of patients in the RIPC group vs 50.0% in the control group (adjusted odds ratio 9.85, 95% confidence interval 1.54-63.16; p = 0.016). We further found significantly lower plasma S100-β (p = 0.007) and higher vascular endothelial growth factor (p = 0.003) levels in the RIPC group than in the control group. Repeated RIPC combined with IVT can significantly facilitate recovery of nerve function and improve clinical prognosis of patients with AIS. NCT03218293. This study provides Class IV evidence that RIPC after tissue plasminogen activator treatment of AIS significantly increases the proportion of patients with an MRS score of 0 or 1 at 90 days.

Significance of nitrogen monoxide in the implementation of the infarctlimiting effect of remote ischemic postconditioning in myocardial ischemia-reperfusion in young and old rats

Modern medicine faces the problem of a steady growth of cardiovascular pathology. Given the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods to prevent or mitigate ischemic myocardial damage and mechanisms for their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to determine the significance of nitric monoxide in realizing the infarction-limiting effect of remote ischemic postconditioning (RIPostC) in myocardial ischemia-reperfusion in young and old rats. The study revealed that RIPostC has a heart attack-limiting effect in myocardial ischemia-reperfusion in both young and old rats; however, under the conditions of the systemic action of the NG-nitro-L-arginine methyl ester inhibitor at a dose of 25 mg/kg (intravenous administration 5 min before the start of reperfusion and 15 min before RIPostC), the effect remains, although not completely, in old rats but not in young rats. Apparently, the NO synthase activity and the blood level of nitric monoxide play a more significant role in the mechanisms of the cardioprotective effects of RIPostC in young rats than in old rats.

The effect of remote ischemic postconditioning on autonomic function in patients with acute ischemic stroke: A Randomized Controlled Trail

ObjectiveThe evidence for the effect of remote ischemic postconditioning(RIpostC) on autonomic function in patients with acute ischemic stroke(AIS) is lacking and the neural mechanism underlying the protection of RIpostC remains speculative. This trial was aimed to evaluated the efficiency of RIpostC on autonomic function in AIS patients. DesignOne hundred and six AIS patients were included in this prospective, randomized, placebo-controlled trial. Patients in intervention group (n = 57) received 4 cycles of alternating inflation (cuff inflation to 200 mmHg) and deflation for 5 min on healthy upper arm once a day for 30 days. The control group underwent a sham inflation and deflation cycles. Autonomic function was evaluated by heart rate variability (HRV). ResultsAll HRV parameters except for the ratio of low frequency to high frequency (P = 0.101) increased significantly with time (P < 0.001) in the two groups. The value of standard deviation of all normal R-R intervals(SDNN) and high frequency at day7 and day30 and the value of the percent of difference between adjacent normal R-R intervals (pNN50) at day 30 in RIpostC group was significantly higher than that of the sham-RIpostC group(P < 0.05). A significant time-by-group interaction was observed in SDNN、pNN50、and high frequency over time between two groups (P < 0.05). Conclusions30-day RIpostC could improve autonomic function in AIS patients through the enhancement of the total autonomic nerve activity and vagus nerve activity. The mechanism of RIpostC mediating autonomic function needs to be further investigated.

Effect of Remote Ischemic Postconditioning on miRNA-145 and Troponin I levels in STEMI patients undergoing primary percutaneous coronary intervention

Background: Primary Percutaneous Coronary Intervention Procedure (PPCI) results in reperfusion injury which will result in more extensive infarction. Remote Ischemic Postconditioning (RIPC) is a protective strategy to reduce the increase in the area of ??infarction. miRNA-145 also plays a role in the protective effect of IPC and RIPC.&#x0D; &#x0D; Research Methods: This study uses a pre and post test approach only with control group design with experimental research designs. Data is taken at the Integrated Heart Services Installation RSUP Dr. M. Djamil Padang from July to November 2019, 40 patients with ST-segment elevation myocardial infarction (STEMI) performed RIPC. Bivariate analysis was performed to determine differences in levels of miRNA-145 and troponin I in STEMI patients underwent PPCI with and without RIPC using the Wilcoxon test and the Mann Whitney test.&#x0D; &#x0D; Results:A total of 40 patients who underwent the PPCI procedure were divided into two groups PPCI + RIPC (n = 20) and PPCI without RIPC (n = 20). There were no significant differences in the basic characteristics between the two groups. There were no significant difference in escalation of median expression of miRNA-145 in PPCI+ RIPC [pre test 36.33 (27.44-52.39), post test 34.83 (27.65-65.26), p = 0.765] compared to PPCI without RIPC [pre test 31.66 (26.31-43.28), post test 33.43 (26.83-64.97), p = 0.765]. There were an increase in median troponin I levels in both groups, PPCI+ RIPC [pretest 4,104.70 (67.30-40,000.00), post test 30,448.50 (120.00-16.3192.20), p = 0.001] and PPCI without RIPC [pretest 826.50 (17.00-48.259.00), post test 42.784.50 (2,119.00-162.897.00), p = &lt;0.001].&#x0D; &#x0D; Conclusion:There were no significant difference in median expression of miRNA-145 in STEMI patients before and after (48 hours) underwent PPCI+RIPC and PPCI without RIPC. There were a significant difference in median levels of troponin I in STEMI patients before and after (48 hours) underwent PPCI+RIPC and PPCI without RIPC.&#x0D; Keywords: Remote Ischemic Postconditioning, miRNA-145, troponin I

On the significance of hyperlactatemia in the implementation of the infarct-limiting effect of remote ischemic postconditioning in myocardial ischemia-reperfusion in the experiment

Modern medicine faces the problem of the growth of cardiovascular pathology. Given the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods to prevent or weaken ischemic myocardial damage and mechanisms for their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to determine the significance of hyperlactatemia in the realization of the infarct-limiting effect of remote ischemic postconditioning (RIPostC) in rat myocardial ischemia-reperfusion in the experiment. The study revealed that after 15-minute RIPostC, which was performed 10 minutes after 30-minute acute myocardial ischemia followed by 120-minute reperfusion, the plasma lactate level in rats increased 1.87 times (87.7 %, p &lt; 0.05) compared with intact animals. It was established that the introduction of L-lactate into the left common jugular vein at a dose of 10 μg/kg, which was carried out 25 minutes after the onset of reperfusion under the conditions of myocardial ischemia (30 minutes) and next reperfusion (120 minutes) and RIPostC (10 minutes after the onset of reperfusion), which was reproduced by ischemia of these limbs, have a heart attack-limiting effect. The increase of the level of blood lactate (hyperlactatemia) after RIPostC in myocardial ischemia-reperfusion is of significance in the implementation of its infarct-limiting effect.

No Added Neuroprotective Effect of Remote Ischemic Postconditioning and Therapeutic Hypothermia After Mild Hypoxia-Ischemia in a Piglet Model.

Introduction: Hypoxic ischemic encephalopathy (HIE) is a major cause of death and disability in children worldwide. Apart from supportive care, the only established treatment for HIE is therapeutic hypothermia (TH). As TH is only partly neuroprotective, there is a need for additional therapies. Intermittent periods of limb ischemia, called remote ischemic postconditioning (RIPC), have been shown to be neuroprotective after HIE in rats and piglets. However, it is unknown whether RIPC adds to the effect of TH. We tested the neuroprotective effect of RIPC with TH compared to TH alone using magnetic resonance imaging and spectroscopy (MRI/MRS) in a piglet HIE model.Methods: Thirty-two male and female piglets were subjected to 45-min global hypoxia-ischemia (HI). Twenty-six animals were randomized to TH or RIPC plus TH; six animals received supportive care only. TH was induced through whole-body cooling. RIPC was induced 1 h after HI by four cycles of 5 min of ischemia and 5 min of reperfusion in both hind limbs. Primary outcome was Lac/NAA ratio at 24 h measured by MRS. Secondary outcomes were NAA/Cr, diffusion-weighted imaging (DWI), arterial spin labeling, aEGG score, and blood oxygen dependent (BOLD) signal measured by MRI/MRS at 6, 12, and 24 h after the hypoxic-ischemic insult.Results: All groups were subjected to a comparable but mild insult. No difference was found between the two intervention groups in Lac/NAA ratio, NAA/Cr ratio, DWI, arterial spin labeling, or BOLD signal. NAA/Cr ratio at 24 h was higher in the two intervention groups compared to supportive care only. There was no difference in aEEG score between the three groups.Conclusion: Treatment with RIPC resulted in no additional neuroprotection when combined with TH. However, insult severity was mild and only evaluated at 24 h after HI with a short MRS echo time. In future studies more subtle neurological effects may be detected with increased MRS echo time and post mortem investigations, such as brain histology. Thus, the possible neuroprotective effect of RIPC needs further evaluation.

The Effect of Remote Ischemic Postconditioning on miRNA-145 and Troponin I levels in STEMI patients undergoing primary percutaneous coronary intervention

Background: Primary Percutaneous Coronary Intervention Procedure (PPCI) results in reperfusion injury which will result in more extensive infarction. Remote Ischemic Postconditioning (RIPC) is a protective strategy to reduce the increase in the area of ​​infarction. miRNA-145 also plays a role in the protective effect of IPC and RIPC.&#x0D; &#x0D; Research Methods: This study uses a pre and post test approach only with control group design with experimental research designs. Data is taken at the Integrated Heart Services Installation RSUP Dr. M. Djamil Padang from July to November 2019, 40 patients with ST-segment elevation myocardial infarction (STEMI) performed RIPC. Bivariate analysis was performed to determine differences in levels of miRNA-145 and troponin I in STEMI patients underwent PPCI with and without RIPC using the Wilcoxon test and the Mann Whitney test.&#x0D; &#x0D; Results:A total of 40 patients who underwent the PPCI procedure were divided into two groups PPCI + RIPC (n = 20) and PPCI without RIPC (n = 20). There were no significant differences in the basic characteristics between the two groups. There were no significant difference in escalation of median expression of miRNA-145 in PPCI+ RIPC [pre test 36.33 (27.44-52.39), post test 34.83 (27.65-65.26), p = 0.765] compared to PPCI without RIPC [pre test 31.66 (26.31-43.28), post test 33.43 (26.83-64.97), p = 0.765]. There were an increase in median troponin I levels in both groups, PPCI+ RIPC [pretest 4,104.70 (67.30-40,000.00), post test 30,448.50 (120.00-16.3192.20), p = 0.001] and PPCI without RIPC [pretest 826.50 (17.00-48.259.00), post test 42.784.50 (2,119.00-162.897.00), p = &lt;0.001].&#x0D; &#x0D; Conclusion:There were no significant difference in median expression of miRNA-145 in STEMI patients before and after (48 hours) underwent PPCI+RIPC and PPCI without RIPC. There were a significant difference in median levels of troponin I in STEMI patients before and after (48 hours) underwent PPCI+RIPC and PPCI without RIPC.&#x0D; Keywords: Remote Ischemic Postconditioning, miRNA-145, troponin I

Remote ischemic postconditioning attenuates damage in rats with chronic cerebral ischemia by upregulating the autophagolysosome pathway via the activation of TFEB

The transcription factor EB (TFEB) is known for its role in lysosomal biogenesis, and it coordinates this process by driving autophagy and lysosomal gene expression during ischemia. In the present study, we aimed to explore the role of the TFEB-regulated autophagolysosome pathway (ALP) in rats with chronic cerebral ischemia (CCI) that were treated with remote ischemic postconditioning (RIPC). A modified 2-vessel occlusion (2-VO) method was utilized to establish the CCI rat model, and the CCI rats were identified by the Morris water maze test and histological staining. After the CCI rats were treated with RIPC, the damage to the rat cortex and hippocampal tissues and the status of the ALP were determined. Western blot analysis and immunofluorescence assays were performed to observe the nuclear translocation of TFEB. The rats were injected with TFEB siRNA via the lateral ventricle to investigate the effect of TFEB siRNA on the RIPC-treated CCI rats. The results suggested that RIPC of the CCI rats alleviated nerve injury, induced TFEB translocation into the nucleus, upregulated autophagy-related protein expression, and activated ALP machinery. Furthermore, TFEB siRNA decreased the levels of TFEB and impaired the neuroprotective effects of RIPC on the CCI rats. Collectively, we highlighted that RIPC attenuates damage in CCI rats via the activation of the TFEB-mediated ALP.

Short-term outcomes of remote ischemic postconditioning 1 h after perinatal hypoxia-ischemia in term piglets.

We aimed to assess remote ischemic postconditioning (RIPC) as a neuroprotective strategy after perinatal hypoxia-ischemia (HI) in a piglet model. Fifty-four newborn piglets were subjected to global HI for 45 min. One hour after HI, piglets were randomized to four cycles of 5 min of RIPC or supportive treatment only. The primary outcome was brain lactate/N-acetylaspartate (Lac/NAA) ratios measured by magnetic resonance spectroscopy at 72 h. Secondary outcomes included diffusion-weighted imaging and neuropathology. RIPC was associated with a reduction in overall and basal ganglia Lac/NAA ratios at 72 h after HI, but no effect on diffusion-weighted imaging, neuropathology scores, neurological recovery, or mortality. The selective effect of RIPC on Lac/NAA ratios may suggest that the metabolic effect is greater than the structural and functional improvement at 72 h after HI. Further studies are needed to address whether there is an add-on effect of RIPC to hypothermia, together with the optimal timing, number of cycles, and duration of RIPC. RIPC after HI was associated with a reduction in overall and basal ganglia Lac/NAA ratios at 72 h, but had no effect on diffusion-weighted imaging, neuropathology scores, neurological recovery, or mortality. RIPC may have a selective metabolic effect, ameliorating lactate accumulation without improving other short-term outcomes assessed at 72 h after HI. We applied four cycles of 5 min RIPC, complementing existing data on other durations of RIPC. This study adds to the limited data on RIPC after perinatal HI and highlights that knowledge gaps, including timing and duration of RIPC, must be addressed together with exploring the combined effects with hypothermia.

Peripheral M-choline-reactive systems in the infarct-limited effect implementation of remote ischemic postconditioning during ischemia-reperfusion of myocardium in experiment

The search for new effective methods to prevent or mitigate ischemic myocardial damage and the mechanisms for their realization is an important task of modern experimental and clinical medicine. The aim of the study was to elucidate the significance of peripheral M-choline-reactive systems in the realization of the cardioprotective effects of remote ischemic postconditioning (RIPostC) during ischemia-reperfusion of myocardium in experiment. The study revealed that RIPostC has an infarct-limiting effect during ischemia-reperfusion of myocardium in young and old rats, but under the conditions of systemic action of atropine (2 mg/kg), the infarct-limiting effect of RIPostC remained only in old rats. It seems that the activity of peripheral M-choline-reactive systems is important in the mechanisms of realization of the cardioprotective effects of RIPost in young, but not in old rats.