-
Scientific Reports Apr 2023Malignant ventricular arrhythmias (VA) after acute myocardial infarction remain a major threat. Aim of this study was to characterize the electrophysiological and...
Malignant ventricular arrhythmias (VA) after acute myocardial infarction remain a major threat. Aim of this study was to characterize the electrophysiological and autonomic sequelae of cardiac ischemia and reperfusion (I/R) in mice during the first week post incident. Left ventricular function was serially assessed using transthoracic echocardiography. VA were quantified by telemetric electrocardiogram (ECG) recordings and electrophysiological studies on the 2nd and 7th day after I/R. Cardiac autonomic function was evaluated by heart rate variability (HRV) and heart rate turbulence (HRT). Infarct size was quantified by planimetric measures. I/R caused significant myocardial scarring and diminished left ventricular ejection fraction. The ECG intervals QRS, QT, QT, and JT were prolonged in I/R mice. Both spontaneous VA scored higher and the inducibility of VA was raised in I/R mice. An analysis of HRV and HRT indicated a relative reduction in parasympathetic activity and disturbed baroreflex sensitivity up to 7 days after I/R. In summary, during the first week after I/R, the murine heart reflects essential features of the human heart after myocardial infarction, including a greater vulnerability for VA and a decreased parasympathetic tone accompanied by decelerated depolarization and repolarization parameters.
Topics: Humans; Animals; Mice; Stroke Volume; Ventricular Function, Left; Myocardial Ischemia; Electrocardiography; Coronary Artery Disease; Myocardial Infarction; Arrhythmias, Cardiac; Myocardial Reperfusion; Heart Rate
PubMed: 37029160
DOI: 10.1038/s41598-023-32346-5 -
Journal of Cellular Physiology Aug 2019Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI.... (Review)
Review
Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumulation, disruption of mitochondrial membrane potential, the formation of reactive oxygen species, and so forth. One of the processes that gets activated in response to I/R injury is autophagy. Indeed, autophagy acts as a "double-edged sword" in the pathology of myocardial I/R injury and there is a controversy about autophagy being beneficial or detrimental. On the basis of the autophagy effect and regulation on myocardial I/R injury, many studies targeted it as a therapeutic strategy. In this review, we discuss the role of autophagy in I/R injury and its targeting as a therapeutic strategy.
Topics: Animals; Autophagy; Cardiovascular Agents; Humans; Myocardial Reperfusion Injury; TOR Serine-Threonine Kinases
PubMed: 30807647
DOI: 10.1002/jcp.28345 -
Molecular Immunology Feb 2021At present, studies have focused on microRNAs (miRNAs) in myocardial ischemia-reperfusion injury (MI/RI). But the specific role of miR-30e hasn't been fully explored....
AIM
At present, studies have focused on microRNAs (miRNAs) in myocardial ischemia-reperfusion injury (MI/RI). But the specific role of miR-30e hasn't been fully explored. Thus, this study is to uncover the mechanism of miR-30e in MI/RI.
METHODS
MI/RI models of rats and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established. Rats were injected with miR-30e and SRY-related high mobility group-box gene 9 (SOX9)-related oligonucleotides or vectors to explore their roles in MI/RI. H9C2 cardiomyocytes were transfected with restored miR-30e and depleted SOX9 to decipher their function in H/R injury. miR-30e and SOX9 expression in myocardial tissues and cardiomyocytes were detected. Online website prediction and luciferase activity assay were applied to validate the targeting relationship between miR-30e and SOX9.
RESULTS
Decreased miR-30e and increased SOX9 were found in myocardial tissues of MI/RI rats and H/R-treated cardiomyocytes. miR-30e targeted SOX9. miR-30e up-regulation or SOX9 down-regulation reduced cardiac function damage and suppressed oxidative stress, inflammation, cardiomyocyte apoptosis and myocardial enzymes in myocardial tissues of MI/RI rats. Restoring miR-30e or silencing SOX9 energized cell viability and inhibited apoptosis of H/R-treated cardiomyocytes. Down-regulating SOX9 reversed the effects of miR-30e down-regulation on myocardial injury, ventricular remodeling, cardiomyocyte damage and apoptosis in MI/RI.
CONCLUSION
It is concluded that miR-30e elevation alleviated cardiac function damage and promoted ventricular remodeling via SOX9 repression.
Topics: Animals; Cells, Cultured; Male; MicroRNAs; Myocardial Reperfusion Injury; Myocytes, Cardiac; RNA Interference; Rats; Rats, Sprague-Dawley; SOX9 Transcription Factor; Up-Regulation; Ventricular Remodeling
PubMed: 33293097
DOI: 10.1016/j.molimm.2020.11.009 -
The American Journal of Chinese Medicine 2022Cardiovascular disease is a global health problem. Previous studies revealed that it involves acute myocardial infarction and ischemia-reperfusion (I/R) injury. The...
Cardiovascular disease is a global health problem. Previous studies revealed that it involves acute myocardial infarction and ischemia-reperfusion (I/R) injury. The mechanism of myocardial I/R injury is complex. But recognizing its mechanisms will bring important clinical significance. Lupeol is widely found in Chinese medicinal herbs and has been shown to have a variety of bio-activities. However, the pharmacological action of lupeol in the progress of myocardial ischemia-reperfusion injury (MIRI) is unclear. This study used a rat myocardial I/R model and the morphological changes in myocardium were determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The expression levels of IL-10, IL-1[Formula: see text], TNF-[Formula: see text], and IL-6 were assessed by quantitative real-time PCR (qRT-PCR) and ELISA. The expression levels of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) level and inflammatory cytokines were quantified using ELISA. The cellular apoptotic rate was determined by TUNEL staining. The findings showed that lupeol significantly decreased myocardial infarction after I/R and ameliorated I/R-induced myocardial inflammation, apoptosis, and oxidative stress. Furthermore, our results suggested that lupeol protected against MIRI-induced myocardial infarction through modulation of NF-[Formula: see text]B and Nrf2 signaling pathways. In summary, this study first clarified the cardioprotective effects of lupeol against I/R-induced myocardial infarction in rats, which could be due to its anti-oxidant, anti-inflammatory, and anti-apoptotic activities. Our study also highlighted a mechanism of NF-[Formula: see text]B and Nrf2 signaling, through which lupeol could be a promising agent in protecting against I/R-induced myocardial infarction.
Topics: Animals; Apoptosis; Myocardial Infarction; Myocardial Reperfusion Injury; NF-E2-Related Factor 2; Pentacyclic Triterpenes; Rats; Rats, Sprague-Dawley
PubMed: 35670060
DOI: 10.1142/S0192415X22500525 -
Texas Heart Institute Journal Apr 2020Warm blood cardioplegia has been an established cardioplegic method since the 1990s, yet it remains controversial in regard to myocardial protection. This review will... (Review)
Review
Warm blood cardioplegia has been an established cardioplegic method since the 1990s, yet it remains controversial in regard to myocardial protection. This review will describe the physiologic and technical concepts behind warm blood cardioplegia, as well as outline the current basic and clinical research that evaluates its usefulness. Controversies regarding this technique will also be reviewed. A long history of experimental data indicates that warm blood cardioplegia is safe and effective and thus suitable myocardial protection during cardiopulmonary bypass surgeries.
Topics: Cardiac Surgical Procedures; Heart Arrest, Induced; Humans; Intraoperative Care; Myocardial Reperfusion Injury
PubMed: 32603472
DOI: 10.14503/THIJ-18-6909 -
Resuscitation Apr 2021The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce these post-resuscitation care...
The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce these post-resuscitation care guidelines for adults, which are based on the 2020 International Consensus on Cardiopulmonary Resuscitation Science with Treatment Recommendations. The topics covered include the post-cardiac arrest syndrome, diagnosis of cause of cardiac arrest, control of oxygenation and ventilation, coronary reperfusion, haemodynamic monitoring and management, control of seizures, temperature control, general intensive care management, prognostication, long-term outcome, rehabilitation, and organ donation.
Topics: Adult; Cardiopulmonary Resuscitation; Consensus; Critical Care; Heart Arrest; Humans; Myocardial Reperfusion
PubMed: 33773827
DOI: 10.1016/j.resuscitation.2021.02.012 -
International Journal of Molecular... Mar 2021Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via... (Review)
Review
Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.
Topics: Adenosine Triphosphate; Animals; Cell Death; Humans; Ischemic Preconditioning, Myocardial; Mitochondria; Mitochondrial Dynamics; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Myocytes, Cardiac; Oxidative Phosphorylation; Oxidative Stress; Regeneration; Signal Transduction; Translational Research, Biomedical
PubMed: 33810024
DOI: 10.3390/ijms22063224 -
Cell Biochemistry and Function Mar 2021Cardiovascular diseases are known to be the most fatal diseases worldwide. Ischaemia/reperfusion (I/R) injury is at the centre of the pathology of the most common... (Review)
Review
Cardiovascular diseases are known to be the most fatal diseases worldwide. Ischaemia/reperfusion (I/R) injury is at the centre of the pathology of the most common cardiovascular diseases. According to the World Health Organization estimates, ischaemic heart disease is the leading global cause of death, causing more than 9 million deaths in 2016. After cardiovascular events, thrombolysis, percutaneous transluminal coronary angioplasty or coronary bypass surgery are applied as treatment. However, after restoring coronary blood flow, myocardial I/R injury may occur. It is known that this damage occurs due to many pathophysiological mechanisms, especially increasing reactive oxygen types. Besides causing cardiomyocyte death through multiple mechanisms, it may be an important reason for affecting other cell types such as platelets, fibroblasts, endothelial and smooth muscle cells and immune cells. Also, polymorphonuclear leukocytes are associated with myocardial I/R damage during reperfusion. This damage may be insufficient in patients with co-morbidity, as it is demonstrated that it can be prevented by various endogenous antioxidant systems. In this context, the resulting data suggest that optimal cardioprotection may require a combination of additional or synergistic multi-target treatments. In this review, we discussed the pathophysiology, experimental models, biomarkers, treatment and its relationship with genetics in myocardial I/R injury. SIGNIFICANCE OF THE STUDY: This review summarized current information on myocardial ischaemia/reperfusion injury (pathophysiology, experimental models, biomarkers, genetics and pharmacological therapy) for researchers and reveals guiding data for researchers, especially in the field of cardiovascular system and pharmacology.
Topics: Animals; Antioxidants; Biomarkers; Humans; Models, Biological; Myocardial Infarction; Myocardial Reperfusion Injury; Oxidative Stress; Reactive Oxygen Species; Troponin
PubMed: 32892450
DOI: 10.1002/cbf.3587 -
International Journal of Biological... Feb 2024Reperfusion therapy is the most effective treatment for acute myocardial infarction. However, reperfusion itself can also cause cardiomyocytes damage. Pyroptosis has... (Review)
Review
Reperfusion therapy is the most effective treatment for acute myocardial infarction. However, reperfusion itself can also cause cardiomyocytes damage. Pyroptosis has been shown to be an important mode of myocardial cell death during ischemia-reperfusion. Non-coding RNAs (ncRNAs) play critical roles in regulating pyroptosis. The regulation of pyroptosis by microRNAs, long ncRNAs, and circular RNAs may represent a new mechanism of myocardial ischemia-reperfusion injury. This review summarizes the currently known regulatory roles of ncRNAs in myocardial ischemia-reperfusion injury and interactions between ncRNAs. Potential therapeutic strategies using ncRNA modulation are also discussed.
Topics: Humans; Myocardial Reperfusion Injury; Pyroptosis; MicroRNAs; RNA, Untranslated; Myocardial Infarction
PubMed: 38048927
DOI: 10.1016/j.ijbiomac.2023.128558 -
Arquivos Brasileiros de Cardiologia Jul 2021
Topics: Humans; Myocardial Infarction; Myocardial Reperfusion; Thrombolytic Therapy
PubMed: 34320082
DOI: 10.36660/abc.20210500