China
Africa
Explore chapters and articles related to this topic
Role of Vasoactive Intestinal Peptide in Myocardial Ischemia Reperfusion Injury
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Dipak K. Das, Nilanjana Maulik, Richard M. Engelman
The scientific community has witnessed the development of the concept of ischemia reperfusion injury associated with the revascularization of ischemic tissue in a relatively short time. Despite the fact that the exact mechanism of reperfusion injury remains unknown, the importance of reperfusion injury in the biological system has become increasingly recognized and appreciated in recent years. It is generally believed that several interrelated factors are responsible for reperfusion injury; among them three are considered to be major: (a) free radical generation, (b) intracellular Ca2+ overloading, and (c) loss of membrane phospholipids.
The Role of Neutrophils and Reactive Oxygen Metabolites in Reperfusion Injury
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Barbara J. Zimmerman, D. Neil Granger
When a tissue is subjected to ischemia, a sequence of chemical reactions is initiated that may ultimately lead to cellular dysfunction and necrosis. Although no single process can be identified as the critical event in ischemia-induced tissue injury, most studies indicate that depletion of cellular energy stores and accumulation of toxic metabolites may contribute to cell death. It is undeniable that re-establishing blood flow is necessary in rescuing ischemic tissues; however, reperfusion of ischemic tissues also leads to a sequence of events that paradoxically injures tissues. Parks and Granger have shown that relatively little injury to the intestinal mucosa occurs during the ischemic period and that the majority of the injury occurs upon reperfusion.1 This observation implicated some reaction initiated by the return of oxygenated blood to the ischemic tissue, which led to the concept that reperfusion injury may be mediated, at least in part, through the formation of reactive oxygen metabolites.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
If reperfusion occurs before the onset of irreversible injury of myocytes, then all myocytes survive. In contrast, if reperfusion occurs after irreversible injury, then myocytes that are already necrotic are lost but myocytes that are reversibly injured may be salvaged, particularly at the edge of established infarcts, thus reducing the size of the infarct. However, despite salvage, the process of reperfusion may damage some myocytes that were not already dead when reflow occurred. This is termed ‘reperfusion injury’, which is mediated by toxic oxygen species that are over-produced on restoration of the oxygen supply. Reperfused infarcts are haemorrhagic and, if large, may result in terminal arrhythmia, rupture, and sudden death. Although, most often, myocardium that is viable at the time of reflow ultimately recovers, critical abnormalities in biochemistry and function may persist for several days as prolonged post-ischaemic ventricular dysfunction, known as ‘stunned’ myocardium. Decreased intercellular calcium or decreased calcium sensitivity of the contractile process is the most likely explanation. Preservation of the myocyte fraction is an important determinant of functional recovery after revascularization. A higher myocyte fraction is required to maintain contractile function after a period of hibernation of the myocardium.
Advances in research on the protective mechanisms of traditional Chinese medicine (TCM) in myocardial ischaemia-reperfusion injury
Published in Pharmaceutical Biology, 2022
Jiexin Zhang, Yonghe Hu, Han Wang, Jun Hou, Wenjing Xiao, Xudong Wen, Tingting Wang, Pan Long, Hezhong Jiang, Zhanhao Wang, Huawei Liu, Xin Chen
Nonetheless, the mechanisms of MI/R injury remain unclear, and the development of therapeutic approaches for reperfusion injury has been disappointing (Ibáñez et al. 2015). Many clinical trials have failed to demonstrate the existence of specific therapies that can reduce reperfusion injury (Fernández-Jiménez and Ibanez 2015; Jones et al. 2015). Although currently used drugs such as statins (Mensah et al. 2005) and ACE inhibitors (ACEIs) (Manning and Vehaskari 2005) have certain therapeutic effects on MI/R injury, synthetic drugs can cause side effects. The field of traditional Chinese medicine (TCM) has a history of more than 2000 years and features unique theories and abundant resources (Hao et al. 2015). Over the past several years, more than 100 TCM studies have been registered with ClinicalTrials.gov. Evidence from randomised controlled trials (Hao et al. 2017) and some other studies have indicated that TCMs can effectively relieve abnormal myocardial perfusion by acting on multiple pathways (Li et al. 2016) and controlling risk factors for cardiovascular disease. Moreover, the side effects of medicinal plants are usually mild (Sedighi et al. 2019). Therefore, it is feasible to treat MI/R injury with TCMs and their active compounds.
Devices for donor lung preservation
Published in Expert Review of Medical Devices, 2022
Cora R Bisbee, Curry Sherard, Jennie H. Kwon, Zubair A. Hashmi, Barry C. Gibney, Taufiek Konrad Rajab
Static cold storage, or preservation of organs in an ice cooler at 4°C, remains the most used system for clinical lung transplantation. Lungs are initially flushed with a low potassium, dextran preservation solution, then immersed into the solution and stored in an ice cooler at 0–4°C until transplantation. The hypothermic environment initiates the arrest of cell function, and the preservation solution reduces cellular metabolism and provides cytoprotection [10]. While SCS is simple and cost-effective, preservation time is limited as extended periods of cold exposure increase ischemia reperfusion injury (IRI) once transplanted into the recipient. Reperfusion injury may result in inflammation, vascular leakage, reactive oxygen species, and cell death, all contributing to graft dysfunction [9]. Additionally, the inhibition of cellular metabolism eliminates the possibility for reparative processes after donor organ injury but prior to recipient implantation [9]. Lung grafts subjected to longer periods of hypothermia during SCS experience tissue damage conferring worse survival and post-operative outcomes when compared to lungs subjected to shorter periods of cold storage [11]. This hypothermia-induced tissue damage reduces the flexibility for extended preservation times when using standard 4°C static cold storage devices. Furthermore, more recent studies point to better graft function for lungs in SCS preservation at 10°C for 12 hours compared to 4°C. Preservation at 10°C could become the standard of care for prolonged pulmonary preservation in SCS, providing benefits to both patients and transplant care teams [12–14].
Effects of stem cell-derived exosomes on neuronal apoptosis and inflammatory cytokines in rats with cerebral ischemia-reperfusion injury via PI3K/AKT pathway-mediated mitochondrial apoptosis
Published in Immunopharmacology and Immunotoxicology, 2021
Ying Zhang, Jun Yu, Jing Liu, Hongbiao Liu, Jing Li
Ischemic injury of the brain is one of the commonly diagnosed diseases in neurology. Cerebral ischemia can cause local brain damage, the severity of which is influenced by the duration of the ischemia. If symptoms of cerebral ischemia develop, reversible damage may be observed in the short term; however, prolonged ischemia and hypoxia can cause cerebral edema and neuronal necrosis [1]. Reperfusion injury is the tissue damage caused when the blood supply is restored in a tissue after experiencing ischemia or hypoxia. This restoration of the circulation results in inflammation and oxidative damage rather than, or along with, the restoration of normal function [2]. Clinical studies [3] have shown that free radicals, intracellular calcium overload, leukocyte adhesion and aggregation, and inadequate production of high-energy phosphate compounds are involved in the development of cerebral ischemia-reperfusion injury. In addition, a previous study [4] has shown that a large number of free radicals and inflammatory factors are often produced during cerebral ischemia-reperfusion injury and that the mitochondrial apoptotic pathway, regulated by the phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway, may participate in the induction of apoptosis [5,6] and worsen the ischemic damage.