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Peripheral Vascular Disease
Published in Gozie Offiah, Arnold Hill, RCSI Handbook of Clinical Surgery for Finals, 2019
Complications of Reperfusion➢ Reperfusion injury.➢ Rhabdomyolysis: Elevated K+, elevated CPK, renal impairment, myoglobinuria.Treat with aggressive IV fluids, diuresis with Mannitol, alkalinisation of urine.➢ Compartment syndrome - prevent and treat with 4-compartment fasciotomy
Therapy of acute myocardial infarction
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Joshua M. Stolker, Michael W. Rich
The findings of these randomized trials are also supported by subgroup analysis from a systematic overview of 22 randomized trials comparing PCI with fibrinolytic therapy in 6763 patients with acute MI (165). Overall, PCI was associated with a significant 37% reduction in 30-day mortality, and the absolute benefit was greater in patients over age 65 than in younger patients. Moreover, the absolute benefit of PCI increased progressively with age, from 1.0% in patients <65 years to 4.2%, 5.1%, and 6.9% in patients of ages 65–74, 75–84, and 85 or older, respectively (5). By comparison, among 1126 patients who did not undergo reperfusion therapy (mean age 80 years), in-hospital and 1-year mortality were 53% and 69%, respectively (170).
The heart
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Surgical reperfusion: Percutaneous coronary intervention (PCI)—may involve placing a balloon catheter in the affected coronary artery to restore blood flow. A spring-loaded metal stent is often placed in the vessel to help keep it open. Stents may be coated with drugs such as sirolimus that release slowly over time to prevent local cellular proliferation and reocclusion of the vesselCoronary artery bypass grafting (CABG)—the procedure involves replacing occluded coronary arteries with graft vessels taken from elsewhere in the bodyWith both PCI and CABG, reocclusion of coronary arteries may still occur over time
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].
Empagliflozin alleviates myocardial I/R injury and cardiomyocyte apoptosis via inhibiting ER stress-induced autophagy and the PERK/ATF4/Beclin1 pathway
Published in Journal of Drug Targeting, 2022
Cuan-Cuan Wang, Ying Li, Xiao-Qian Qian, Hui Zhao, Dong Wang, Guo-Xing Zuo, Kuan Wang
Ischaemic heart disease, also known as coronary artery disease, is a very severe problem in the heart resulted from limited supply of blood and oxygen, which ranks no. 1 leading cause of death in many regions [1,2]. Myocardial ischaemia is characterised by decreased blood flow to the myocardium and accompanying supply–demand imbalance of oxygen, usually leading to severe symptoms including arrhythmias, heart dysfunction and infarction, and even sudden death [3,4]. Therefore, effective treatments, such as thrombolytic medications and percutaneous coronary intervention, have been established to restore blood and oxygen supply to the ischaemic heart [5]. However, the restoration of blood flow, known as reperfusion, causes injury including myocardial stunning, cardiomyocyte damage and death, which is named myocardial ischaemia–reperfusion (I/R) injury [6–8]. Detrimental effects caused by reperfusion need to be well-controlled for improving clinical outcomes.
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.