scholarly journals Leukotrienes in Atherosclerosis: New Target Insights and Future Therapy Perspectives

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Graziano Riccioni ◽  
Alessandra Zanasi ◽  
Nicola Vitulano ◽  
Barbara Mancini ◽  
Nicolantonio D'Orazio
Keyword(s):  
Vascular Wall ◽  
Lipid Mediators ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Morphological Alterations ◽  
Beneficial Effects ◽  
Coronary Syndrome ◽  
Atherosclerotic Lesions ◽  
Leukotriene Receptor ◽  
Future Therapy

Atherosclerosis represents an important chronic inflammatory process associated with several pathophysiological reactions in the vascular wall. The arachidonic acid, released by phospholipase A2, is an important substrate for the production of a group of lipid mediators known as leukotrienes, which induce proinflammatory signaling through the activation of specific BLT and CysLT receptors. The interaction of these substances in the vascular wall determines important morphological alterations like the early lipid retention and the accumulation of foam cells, the development of intimal hyperplasia, and advanced atherosclerotic lesions, and it plays an important role in the rupture of atherosclerotic plaque. Many studies regarding myocardial ischemia and reperfusion show that leukotriene signaling may be involved in the development of ischemic injury. For these, reasons both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested for inducing beneficial effects at different stages of the atherosclerosis process and may represent a new therapeutic target in the treatment of atherosclerotic vessel diseases, in particular in acute coronary syndrome.

scholarly journals Morphological illustration of alterations in the arterial endothelium in ischemic and reperfusion injuries

2018 ◽  
Vol 26 (2) ◽  
pp. 184-194
Author(s):  
Alexander S. Pshennikov ◽  
Roman V. Deev
Keyword(s):  
Vessel Wall ◽  
Vascular Wall ◽  
General Purpose ◽  
Laboratory Animals ◽  
Synthetic Activity ◽  
Ischemia And Reperfusion ◽  
Morphological Alterations ◽  
Ischemic And Reperfusion Injury ◽  
Main Components ◽  
Arterial Endothelium

Background. Reperfusion syndrome is an inevitable event in recovery of the blood flow after a longstanding ischemia. The article is dedicated to the study of the expressiveness of this condition. Aim – to compare the depth of morphological alterations of the arterial endothelium in ischemic and reperfusion injury in experiment. Materials and Мethods. The work was conducted on 90 laboratory animals – rats of Wistar line. Models of ischemia and reperfusion were obtained by compression of the abdominal part of the aorta (1st group) with further conditioning (2nd group). The animals were withdrawn from the experiment and the vessel wall was taken on the 1st, 3d, 5th, 7th day. Preparations were studied in a transmission electron microscope «Libra 120» with automatic scanning of images. Results. Comparison of pathomorphological data obtained in examination of the aortas and iliac arteries of the two groups of animals («ischemia» and «reperfusion») showed that the cascade of pathomorphological changes includes several main stages. Transient ischemia leads to injury (alteration) of the main components of the vessel wall. Under action of this factor endotheliocytes exhibit a nonspecific response changing their synthetic activity that was manifested by a complex of morphological signs in the nucleus, karyolemma, cytoplasm and plasmalemma. In some cells the changes took an irreversible character and were accompanied by rupture of mitochondrial membranes, of general purpose organelles and of plasmalemma. Such endotheliocytes died and were desquamated. Because of short duration of ischemia these changes were insignificant. Subendothelial structures underwent edema which is logical in view of derangement of the barrier function of the epithelium and presence of a mild inflammatory component (in response to death of a part of endotheliocytes and cells of the vascular wall stroma). Examination of the ultrastructure of the vessel wall in the ischemiareperfusion group revealed adaptive and pathological changes in the endothelial cells. Data were obtained that evidence a significant disorder in microhemodynamics in tissues in reperfusion. Conclusion. No significant structural and ultrastructural differences in injuries and reactive changes in «ischemia» and «reperfusion» groups were found. In view of this, for subtle differentiation of pathomorphogenesis of these two conditions it is reasonable to use examination methods with higher resolution.

Beneficial effects of the PAF antagonist UR-12460 in myocardial ischemia and reperfusion in rats

1995 ◽  
Vol 31 ◽  
pp. 236
Author(s):  
M. Giral ◽  
M. Merlos ◽  
D. Balsa ◽  
R. Ferrando ◽  
J. García-Rafanell ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Beneficial Effects

scholarly journals Morphological illustration of alterations in the arterial endothelium in ischemic and reperfusion injuries

2018 ◽  
Vol 26 (2) ◽  
pp. 184-194
Author(s):  
Alexander S. Pshennikov ◽  
Roman V. Deev
Keyword(s):  
Vessel Wall ◽  
Vascular Wall ◽  
General Purpose ◽  
Laboratory Animals ◽  
Synthetic Activity ◽  
Ischemia And Reperfusion ◽  
Morphological Alterations ◽  
Ischemic And Reperfusion Injury ◽  
Main Components ◽  
Arterial Endothelium

Background. Reperfusion syndrome is an inevitable event in recovery of the blood flow after a longstanding ischemia. The article is dedicated to the study of the expressiveness of this condition. Aim – to compare the depth of morphological alterations of the arterial endothelium in ischemic and reperfusion injury in experiment. Materials and Мethods. The work was conducted on 90 laboratory animals – rats of Wistar line. Models of ischemia and reperfusion were obtained by compression of the abdominal part of the aorta (1st group) with further conditioning (2nd group). The animals were withdrawn from the experiment and the vessel wall was taken on the 1st, 3d, 5th, 7th day. Preparations were studied in a transmission electron microscope «Libra 120» with automatic scanning of images. Results. Comparison of pathomorphological data obtained in examination of the aortas and iliac arteries of the two groups of animals («ischemia» and «reperfusion») showed that the cascade of pathomorphological changes includes several main stages. Transient ischemia leads to injury (alteration) of the main components of the vessel wall. Under action of this factor endotheliocytes exhibit a nonspecific response changing their synthetic activity that was manifested by a complex of morphological signs in the nucleus, karyolemma, cytoplasm and plasmalemma. In some cells the changes took an irreversible character and were accompanied by rupture of mitochondrial membranes, of general purpose organelles and of plasmalemma. Such endotheliocytes died and were desquamated. Because of short duration of ischemia these changes were insignificant. Subendothelial structures underwent edema which is logical in view of derangement of the barrier function of the epithelium and presence of a mild inflammatory component (in response to death of a part of endotheliocytes and cells of the vascular wall stroma). Examination of the ultrastructure of the vessel wall in the ischemiareperfusion group revealed adaptive and pathological changes in the endothelial cells. Data were obtained that evidence a significant disorder in microhemodynamics in tissues in reperfusion. Conclusion. No significant structural and ultrastructural differences in injuries and reactive changes in «ischemia» and «reperfusion» groups were found. In view of this, for subtle differentiation of pathomorphogenesis of these two conditions it is reasonable to use examination methods with higher resolution.

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

scholarly journals Hydrocortisone decreases apoptosis in jejunum of horses subjected to experimental ischemia and reperfusion

2011 ◽  
Vol 31 (6) ◽  
pp. 471-476 ◽  
Author(s):  
Geraldo Eleno S. Alves ◽  
Heloisa M.F. Mendes ◽  
Tiago G.S. Alves ◽  
Rafael R. Faleiros ◽  
Anilton C. Vasconcelos ◽  
...  
Keyword(s):  
Cell Death ◽  
Time Course ◽  
Apoptotic Cell ◽  
Treated Group ◽  
Apoptotic Cell Death ◽  
Apoptotic Cells ◽  
Ischemia And Reperfusion ◽  
Beneficial Effects ◽  
Time Zero ◽  
Venous Ischemia

In order to evaluate the effect of hydrocortisone on apoptosis in the jejunum of horses subjected to ischemia and reperfusion, ten horses were paired and grouped into two groups - treated (n=5) and non treated (n=5). Segments of the jejunum were used as controls (C), or as venous ischemia (VIsc), which were subjected to 2h of ischemia followed by 2 or 12h of reperfusion. C samples were collected at time zero (prior to ischemia) and VIsc samples were collected at 2h of ischemia and at 2 and 12h of reperfusion. TUNEL positive apoptotic cells were counted in 10 microscopical fields in deep mucosa from each horse throughout the time course. After 12h of reperfusion, the number of apoptotic cells in treated group were significantly lower than in untreated animals, indicating that hydrocortisone inhibits apoptosis. These results indicate that hydrocortisone has a beneficial effects favoring the maintenance of jejunal integrity in horses with ischemia and reperfusion injuries by preventing apoptotic cell death.

scholarly journals Activation of signaling pathways and regulatory mechanisms of mRNA translation following myocardial ischemia-reperfusion

2006 ◽  
Vol 101 (2) ◽  
pp. 576-582 ◽  
Author(s):  
Stephen J. Crozier ◽  
Xueqian Zhang ◽  
Jufang Wang ◽  
Joseph Cheung ◽  
Scot R. Kimball ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Myocardial Ischemia ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Mrna Translation ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Mechanisms ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Mitogen Activated Protein

Protein expression in the heart is altered following periods of myocardial ischemia. The changes in protein expression are associated with increased cell size that can be maladaptive. There is little information regarding the regulation of protein expression through the process of mRNA translation during ischemia and reperfusion in the heart. Therefore, the purpose of this study was to identify changes in signaling pathways and downstream regulatory mechanisms of mRNA translation in an in vivo model of myocardial ischemia and reperfusion. Hearts were collected from rats whose left main coronary arteries had either been occluded for 25 min or reversibly occluded for 25 min and subsequently reperfused for 15 min. Following reperfusion, both the phosphoinositide 3-kinase and mitogen-activated protein kinase pathways were activated, as evidenced by increased phosphorylation of Akt (PKB), extracellular signal-regulated kinase 1/2, and p38 mitogen-activated protein kinase. Activation of Akt stimulated signaling through the protein kinase mammalian target of rapamycin, as evidenced by increased phosphorylation of two of its effectors, the ribosomal protein S6 kinase and the eukaryotic initiation factor eIF4E binding protein 1. Ischemia and reperfusion also resulted in increased phosphorylation of eIF2 and eIF2B. These changes in protein phosphorylation suggest that control of mRNA translation following ischemia and reperfusion is modulated through a number of signaling pathways and regulatory mechanisms.

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