Role of Vasoactive Intestinal Peptide in Myocardial Ischemia Reperfusion Injury
Sami I. Said in Proinflammatory and Antiinflammatory Peptides, 2020
Ischemia, by definition, represents a phenomenon in which tissue is deprived of either partial or total blood flow in conjunction with hypoxia. Clinically this can occur during thrombolytic therapy and angioplasty, in which blood flow is temporarily interrupted (23). Prolonged myocardial ischemia can occur during open-heart surgery, when the heart must be arrested in order to permit surgical manipulations (24,25). Thus, ischemic insult may occur regionally or globally, either for a short period of time or for relatively longer periods, depending on the clinical setting. While short-term ischemia (usually less than 20 min) causes reversible tissue injury which may be completely restored, prolonged myocardial ischemia (more than 30 min) can lead to irreversible cellular injury, resulting from energy depletion, lactic acidosis, and inhibition of both glucose and fatty acid utilization (26,27).
Disorders in tHemostasis System and Changes in the Rheological Properties of the Blood in Ischemic Heart Disease and Diabetes Mellitus Patients
E.I. Sokolov in Obesity and Diabetes Mellitus, 2020
A change in the function of a cell (in particular of a thrombocyte) may occur under the effect of hypoxia, ischemia, a progressing hyperfunction, a deficiency of energy, and disturbance of the information relation with the environment [534]. The development of ischemia in a cell may cause depolarization of a membrane with the corresponding loss by the cell of one of the forms of “free energy”, i.e. the energy of the transmembrane potential. In this case, homeostasis of the cell is disturbed with a limited possibility of utilizing the energy, substrates, and adequately perceiving the information received. A state appears that in physiology is customarily called metabolic disorders. Here the intracellular regulation of homeostasis suffers. Three main components determine the functional viability of a cell: the exchange of substances, energy, and an exchange of information. These processes under the influence of ischemia, cold, toxicosis, or the action of pharmacological preparations may alter qualitatively and quantitatively.
Specific Arterial Disease
Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos in McDonald's Blood Flow in Arteries, 2022
Aging (Chapter 15), hypertension (Chapter 16), atherosclerosis (Chapter 19), diabetes (Chapter 21) and renal failure (Chapter 21) are the most common causes of altered arterial hemodynamics and of disturbed blood flow in the arteries of human subjects. A number of other conditions can do likewise but are either less common or less potent in their effect. These are discussed here. As for the more common causes of arterial dysfunction, these act through either narrowing or occluding an artery and/or stiffening the artery, and/or creating abnormal reflection, and/or causing the artery to rupture. Effects can be manifest as ischemia of tissues downstream, as increased load on the heart and arteries upstream, or (through rupture) as disturbance of surrounding tissues or loss of blood. Importantly, another ill effect of arterial stiffening is the damage to the micro-vasculature in the brain and kidney, which can be attributed to funneling of flow pulsations into the beds of these high-flow organs, when such pulsations cannot be absorbed in the aorta and large arteries (O'Rourke and Safar, 2005). This has been described as “pulse-wave encephalopathy” by neuroradiologists (Bateman, 2002; Henry-Feugeas et al., 2005), while basic researchers comment that small cerebral arteries “are destroyed by the pulse” (Stone et al., 2015).
The effect of desloratadine on ischemia reperfusion induced oxidative and inflammatory renal injury in rats
Published in Renal Failure, 2020
Huseyin Kocaturk, Fevzi Bedir, Mehmet Sefa Altay, Ebubekir Bakan, Bahadir Suleyman, Gulce Naz Yazici, Mukadder Sunar, Zeynep Suleyman, Halis Suleyman
Ischemia is a condition where the tissue is deprived of oxygen when there is a decrease or completely no blood flow to the tissue [1]. In tissue ischemia, a series of chemical events progressing to cellular dysfunction and cell necrosis are seen. Therefore, the first intervention in ischemic tissue is to ensure reperfusion of the tissue [2]. Reoxygenation in reperfusion leads to the formation of reactive oxygen species (ROS) [3]. These ROS are known as reperfusion mediators oxidize cell membrane lipids and they, produce toxic products such as aldehyde and malondialdehyde (MDA) from lipids [4]. ROS also increases proinflammatory cytokine nuclear factor-κB (NF-κB) production [5]. NF-κBs have been shown to stimulate the secretion of proinflammatory interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and other inflammation mediators [6]. Briefly, ischemia-reperfusion (I/R) injury is a complex pathological process that begins with deoxygenation of tissue and continues with the production of free oxygen radicals and expands with the inflammatory response [2]. The relevant literature data showed the value of antioxidant and anti-inflammatory therapy in I/R tissue damage.
Current Status of Liver Transplantation Using Marginal Grafts
Published in Journal of Investigative Surgery, 2020
Amr Badawy, Toshimi Kaido, Shinji Uemoto
Prolonged cold ischemia time usually exacerbates the hepatic ischemia/reperfusion injury leading to increased risk of primary nonfunction, delayed graft function, ischemic cholangiopathy and graft loss [60,79]. In 2018, Pan et al. [80] conducted a retrospective analysis using the United Network for Organ Sharing (UNOS) database. They analyzed the data of 67,426 recipients and observed that CIT between 9 and 16 h was associated with increased risk of graft loss. However, a study by Grat et al. [81] found that prolonged CIT (≥9 h) had no effect on 5-year graft survival in low MELD recipients (<10), while it was an independent risk factor for poor 5-year graft survival in high MELD recipients (>20). Also, they noticed that older donor age (>46 years) provoked the negative effect of prolonged CIT on graft survival in recipients with MELD score between 10 and 20. Therefore, it was suggested by several studies that prolonged CIT if associated with other donor or recipient risk factors such as older donors, graft steatosis, recipient high MELD score, obesity, and diabetes mellitus would significantly increase the risk of graft loss [79,81–83].
Transplantation in highly sensitized patients: challenges and recommendations
Published in Expert Review of Clinical Immunology, 2018
Sebastiaan Heidt, Frans H.J. Claas
While an increase in transplantation rates for highly sensitized patients is a very favorable result, an increased number of organs is shipped over longer distances, thereby increasing cold ischemia times. In the first year, the proportion of organs sent to highly sensitized patients with a cold ischemia time of over 24 h increased from 21.4% to 29.2% with the accompanying increase in delayed graft function rates [16]. While 6-month graft survival was not affected, the effect on the longer term needs to be determined. With long-term graft survival data not available for the coming years, it is of importance to note that we have recently shown that allocation of organs to highly sensitized patient based on the absence of unacceptable antigens leads to relatively poor 10-year graft survival rates, indicating that merely providing priority to highly sensitized patients in regular allocation may not be sufficient [19]. Additionally, the rate of zero HLA-A, -B, -DR and zero -DR mismatches significantly declined in the new KAS, increasing the chance of HLA immunization in case of graft loss [16].
Related Knowledge Centers
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- Metabolism
- Hypoxia
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