Ischemia-reperfusion syndrome

Неймарк, М. И.

doi:10.17116/hirurgia202109171

Cited by 9 publications

(4 citation statements)

References 30 publications

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“…I-R injury caused by the interruption of oxygen flow and the consecutive restoration of oxygen concentration, which is known as reperfusion, is still poorly understood [ 279 ]. These therapeutic targets can be a great alternative for modulating I-R injury.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Rangel

García-Valdés

Villar

et al. 2022

Oxidative Medicine and Cellular Longevity

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Ischemia-reperfusion (I-R) injury is damage caused by restoring blood flow into ischemic tissues or organs. This complex and characteristic lesion accelerates cell death induced by signaling pathways such as apoptosis, necrosis, and even ferroptosis. In addition to the direct association between I-R and the release of reactive oxygen species and reactive nitrogen species, it is involved in developing mitochondrial oxidative damage. Thus, its mechanism plays a critical role via reactive species scavenging, calcium overload modulation, electron transport chain blocking, mitochondrial permeability transition pore activation, or noncoding RNA transcription. Other receptors and molecules reduce tissue and organ damage caused by this pathology and other related diseases. These molecular targets have been gradually discovered and have essential roles in I-R resolution. Therefore, the current study is aimed at highlighting the importance of these discoveries. In this review, we inquire about the oxidative damage receptors that are relevant to reducing the damage induced by oxidative stress associated with I-R. Several complications on surgical techniques and pathology interventions do not mitigate the damage caused by I-R. Nevertheless, these therapies developed using alternative targets could work as coadjuvants in tissue transplants or I-R-related pathologies

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Section: Discussionmentioning

confidence: 99%

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Rangel

García-Valdés

Villar

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…По результатам исследований уже было продемонстрировано и доказано его протективное воздействие на почки, сердце, головной мозг [5,6,8]. Во время ИК и ЦА длительная гипоперфузия в совокупности с ишемией-реперфузией приводят к повреждению клеток, оксидативному стрессу, ишемии интестинальных ворсинок, потере интестинального барьера с последующей резорбцией эндотоксинов и бактерий, запуску системного воспалительного ответа, который, в свою очередь, может привести к отдаленному повреждению органов и полиорганной недостаточности [9,10].…”

Section: результатыunclassified

Intestinal protection by nitric oxide supply in the simulation of artificial blood circulation and circulatory arrest: an experimental study

Podoksenov,

Churilina,

Kamenshchikov

et al. 2024

Pulʹmonologiâ (Mosk.)

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Cardiac surgery is associated with high risks of complications, and these risks increase when it comes to aortic surgery because of the technical complexity of the surgeries, the use of cardiopulmonary bypass (CPB) and “circulatory arrest” (CA) that leads to ischemia-reperfusion damage. Abdominal complications in cardiovascular surgery are not the most common complications but are associated with high mortality. Protecting the gastrointestinal (GI) organs from ischemia-reperfusion injury is still a serious problem. According to a study of the organoprotective properties of nitric oxide (NO), its effectiveness in the treatment of diseases of the cardiovascular system, lungs, and kidneys has been proven, and observational results have shown that patients who were administered NO were less prone to complications from the gastrointestinal tract.The aim of the study was to evaluate the protective properties of NO for the intestines during simulated surgery under CPB and hypothermic CA. Methods. The study was conducted on sheep (n = 24). The animals were divided into 4 groups: the “CPB” group with the standard CPB protocol, the “CPB + NO” group with CPB and NO administration, the “CPB + CA” group with the standard CPB and CA protocol, and the group “CPB + CA + NO” with CPB and CA and NO administration. Instrumental and laboratory parameters were monitored at all stages of the experiment to assess the effectiveness and safety of CPB and CA simulation. In intestinal biopsy samples, the changes in the defecation rate, the concentration of a biochemical marker of intestinal ischemia (intestinal enterocyte fatty acid binding protein – i-FABP), and tissue concentrations of adenosine triphosphate (ATP) and lactate were assessed.Results. A higher rate of defecation was established (p = 0.046) in the “CPB + NO” group after CPB compared to the “CPB” group. The concentration of i-FABP in the CPB + NO group after CPB was lower compared to that in the CPB group (p = 0.002), and it was lower in the “CPB + CA + NO” group compared to the “CPB + CA” group (p = 0.033). 1 hour after CPB, the tissue concentration of ATP in intestinal biopsies in the “CPB + NO” group was higher than in the CPB group (p = 0.005).Conclusion. When modeling CPB and CA in the experiment, a positive effect of NO therapy on the intestine was noted: the functional state improved, the concentration of i-FABP decreased, and the concentration of ATP in intestinal biopsies increased.

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“…This situation fully develops during cardiac arrest and subsequent resuscitation, but it also includes cases of successful treatment of a number of diseases ~ 27 ~ (Restoration of blood flow during embolectomy, surgeries in which artificial circulation is used, compartment syndrome, etc.) If ischemia lasts more than 40 minutes [12] . Brain damage with mental and neurological disorders in these cases is referred to as post hypoxic, post anoxic, post cardiac arrest, post resuscitation encephalopathy and is one of the components of the complex of pathophysiological processes that occur during cardiac arrest and subsequent reperfusion reaction and are called post cardiac arrest syndrome, repurphyseal syndrome, post-resuscitation illness [1,9,13,15] Mechanisms of brain damage at the biochemical, cellular, molecular levels are widely presented in the literature and show that at the stage of ischemia synaptic failure occurs (temporary, complete or partial depolarization of neuron membranes), their apoptosis activates within 72 hours after cardiac arrest, which is accompanied by a violation of intersystem and intrasystem relationships.…”

Section: Introductionmentioning

confidence: 99%

Mental disorder as an example of sequelae of cerebral hypoxia-ischemia in case of acute blood loss in forensic medicine

Yurievna,

Grand

2024

Int. J. Forensic Med.

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Defining the full range of injuries and their causes is one of the most important issues in forensic medicine. Particularly difficult and insufficiently developed is the assessment of injuries manifested in a mental disorder. Forensic diagnostics in this case requires knowledge of the mechanism of injury, the peculiarities of the formation of injuries, and their correlation with neuropathological disorders. Presented is the case in which a complex of processes in response to the primary injury and pathological processes attached to the injury led to structural and functional insufficiency of the brain (encephalopathy), the manifestation of which was an organic mental disorder. Its analysis contributes to the understanding of the process of decoding the information contained in the objects of expertise, assessing the elements of the cause-and-effect relationship and making scientifically based expert conclusions.

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Ischemia-reperfusion syndrome

Cited by 9 publications

References 30 publications

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Intestinal protection by nitric oxide supply in the simulation of artificial blood circulation and circulatory arrest: an experimental study

Mental disorder as an example of sequelae of cerebral hypoxia-ischemia in case of acute blood loss in forensic medicine

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