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Articles de revues sur le sujet « Ischemia »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 25 juillet 2025

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1

Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (2022): 5096. http://dx.doi.org/10.3390/ijms23095096.

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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe tran

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Park, Kwon Moo, Ang Chen, and Joseph V. Bonventre. "Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury and JNK, p38, and MAPK Kinase Activation by Remote Ischemic Pretreatment." Journal of Biological Chemistry 276, no. 15 (2001): 11870–76. http://dx.doi.org/10.1074/jbc.m007518200.

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MAPK activities, including JNK, p38, and ERK, are markedly enhanced after ischemiain vivoand chemical anoxiain vitro. The relative extent of JNK, p38, or ERK activation has been proposed to determine cell fate after injury. A mouse model was established in which prior exposure to ischemia protected against a second ischemic insult imposed 8 or 15 days later. In contrast to what was observed after 30 min of bilateral ischemia, when a second period of ischemia of 30- or 35-min duration was imposed 8 days later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtrat

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Lee, H. Thomas, and Charles W. Emala. "Protective effects of renal ischemic preconditioning and adenosine pretreatment: role of A1 and A3receptors." American Journal of Physiology-Renal Physiology 278, no. 3 (2000): F380—F387. http://dx.doi.org/10.1152/ajprenal.2000.278.3.f380.

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Renal ischemia and reperfusion during aortic and renal transplant surgery result in ischemic-reperfusion injury. Ischemic preconditioning and adenosine infusion before ischemia protect against ischemic-reperfusion injury in cardiac and skeletal muscle, but these protective phenomena have not been demonstrated in the kidney. Rats were randomized to sham operation, 45-min renal ischemia, ischemic preconditioning with four cycles of 8-min renal ischemia and 5-min reperfusion followed by 45-min renal ischemia, systemic adenosine pretreatment before 45-min renal ischemia, or pretreatments with sele

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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.

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The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models,

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Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.

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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral

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Li, Chuanfu, Race L. Kao, Tuanzhu Ha, Jim Kelley, I. William Browder та David L. Williams. "Early activation of IKKβ during in vivo myocardial ischemia". American Journal of Physiology-Heart and Circulatory Physiology 280, № 3 (2001): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1264.

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We have demonstrated that in vitro brief ischemia activates nuclear factor (NF)-κB in rat myocardium. We report in vivo ischemia-reperfusion (I/R)-induced NF-κB activation, IκB kinase -β (IKKβ) activity, and IκBα phosphorylation and degradation in rat myocardium. Rat hearts were subjected to occlusion of the coronary artery for up to 45 min or occlusion for 15 min followed by reperfusion for up to 3 h. Cytoplasmic and nuclear proteins were isolated from ischemic and nonischemic areas of each heart. NF-κB activation was increased in the ischemic area (680%) after 10 min of ischemia and in the n

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Zhan, Xinhua, Bradley P. Ander, Glen Jickling, et al. "Brief Focal Cerebral Ischemia That Simulates Transient Ischemic Attacks in Humans Regulates Gene Expression in Rat Peripheral Blood." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (2009): 110–18. http://dx.doi.org/10.1038/jcbfm.2009.189.

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Blood gene expression profiles of very brief (5 and 10 mins) focal ischemia that simulates transient ischemic attacks in humans were compared with ischemic stroke (120 mins focal ischemia), sham, and naïve controls. The number of significantly regulated genes after 5 and 10 mins of cerebral ischemia was 39 and 160, respectively (fold change ⩾∣1.5∣ and P<0.05). There were 103 genes common to brief focal ischemia and ischemic stroke. Ingenuity pathway analysis showed that genes regulated in the 5 mins group were mainly involved in small molecule biochemistry. Genes regulated in the 10 mins gr

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KAKOKI, MASAO, YASUNOBU HIRATA, HIROSHI HAYAKAWA, et al. "Effects of Tetrahydrobiopterin on Endothelial Dysfunction in Rats with Ischemic Acute Renal Failure." Journal of the American Society of Nephrology 11, no. 2 (2000): 301–9. http://dx.doi.org/10.1681/asn.v112301.

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The role of nitric oxide (NO) in ischemic renal injury is still controversial. NO release was measured in rat kidneys subjected to ischemia and reperfusion to determine whether (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), a cofactor of NO synthase (NOS), reduces ischemic injury. Twenty-four hours after bilateral renal arterial clamp for 45 min, acetylcholine-induced vasorelaxation and NO release were reduced and renal excretory function was impaired in Wistar rats. Administration of BH4 (20 mg/kg, by mouth) before clamping resulted in a marked improvement of those parameters (10-8 M acetylcholin

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Kim, Gyung W., Taku Sugawara, and Pak H. Chan. "Involvement of Oxidative Stress and Caspase-3 in Cortical Infarction after Photothrombotic Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (2000): 1690–701. http://dx.doi.org/10.1097/00004647-200012000-00008.

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Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected

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Rivera, Maria Jesus, Monica Cavia-Saiz, Pilar Muñiz, María A. Risalde, and Angélica Martínez-Delgado. "Ischemic Preconditioning on Secondary Arterial and Venous Ischemia in Pedicled Axial Flaps in Wistar Rats." Journal of Reconstructive Microsurgery Open 10, no. 01 (2025): e19-e31. https://doi.org/10.1055/a-2624-2776.

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Abstract Background Microvascular complications, particularly secondary arterial and venous ischemia, pose significant challenges in reconstructive surgery. This study investigates the potential protective effects of ischemic preconditioning on flap survival, anatomopathological alterations, and immunological responses in pedicled axial flaps subjected to secondary ischemia. Methods Adult male Wistar rats underwent arterial or venous ischemia, with and without ischemic preconditioning. Histological assessments, immunohistochemistry studies, and biochemical analyses were conducted to evaluate t

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Pan, Hui-Lin, Shao-Rui Chen, Gloria M. Scicli, and Oscar A. Carretero. "Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (2000): H116—H121. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h116.

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Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardi

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Nishimura, Masaki, Toshiyuki Sugino, Kazuhiko Nozaki, et al. "Activation of p38 Kinase in the Gerbil Hippocampus Showing Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 23, no. 9 (2003): 1052–59. http://dx.doi.org/10.1097/01.wcb.0000084251.20114.65.

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Ischemic tolerance is a phenomenon in which brief episodes of ischemia protect against the lethal effects of subsequent periods of prolonged ischemia. The authors investigated the activation of p38 mitogen-activated protein kinase (p38) in the gerbil hippocampus by Western blotting and immunohistochemistry to clarify the role of p38 kinase in ischemic tolerance. After the 2-minute global ischemia, immunoreactivity indicating active p38 was enhanced at 6 hours of reperfusion and continuously demonstrated 72 hours after ischemia in CA1 and CA3 neurons. Pretreatment with SB203580, an inhibitor of

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Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (2017): 877–83. http://dx.doi.org/10.17750/kmj2017-877.

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Aim. To study clinical features, functional and neuroimaging characteristics of the brain of patients with ischemic brain disease and epileptic seizures. Methods. 772 patients with acute and chronic cerebral ischemia (265 stroke patients with epileptic seizures and 174 patients with seizures on the background of chronic cerebral ischemia, and 203 patients with stroke and 130 patients with chronic cerebral ischemia without seizures) were comprehensively examined. The clinical neurological examination, electroencephalography, magnetic resonance imaging, ultrasound duplex scanning of extra- and i

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Schwartz, Ilsa, Michel Babajanian, Wen X. Zhang, et al. "Prolongation of Secondary Critical Ischemia Time of Experimental Skin Flaps Using UW Solution as a Normothermic Perfusate." Otolaryngology–Head and Neck Surgery 108, no. 2 (1993): 149–55. http://dx.doi.org/10.1177/019459989310800207.

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A myriad of investigations have been published on the pharmacologic manipulation of flaps to enhance tolerance to ischemia. We recently reported a threefold increase in ischemic tolerance of the rat abdominal skin flap pedicle after 6 hours of primary ischemia and 12 hours of reperfusion. Flaps underwent normothermic perfusion washout with lactated Ringer's or U.W. solution, a newly developed organ preservation medium. Perfusion washouts were performed at one of three different points in the protocol: (1) onset of primary ischemia; (2) onset of secondary ischemia; or (3) 2 hours after onset of

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Zhou, An, Manabu Minami, Xiaoman Zhu, et al. "Altered Biosynthesis of Neuropeptide Processing Enzyme Carboxypeptidase E after Brain Ischemia: Molecular Mechanism and Implication." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (2004): 612–22. http://dx.doi.org/10.1097/01.wcb.0000118959.03453.17.

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In this study, using both in vivo and in vitro ischemia models, the authors investigated the impact of brain ischemia on the biosynthesis of a key neuropeptide-processing enzyme, carboxypeptidase E (CPE). The response to brain ischemia of animals that lacked an active CPE was also examined. Combined in situ hybridization and immunocytochemical analyses for CPE showed reciprocal changes of CPE mRNA and protein, respectively, in the same cortical cells in rat brains after focal cerebral ischemia. Western blot analysis revealed an accumulation of the precursor protein of CPE in the ischemic corte

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Zhang, Zheng G., Wayne Tsang, Li Zhang, Cecylia Powers, and Michael Chopp. "Temporal and spatial expression of neuropilin-1 in focal cerebral ischemic brain." Stroke 32, suppl_1 (2001): 317. http://dx.doi.org/10.1161/str.32.suppl_1.317-b.

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6 Neuropilin-1 is a receptor for vascular endothelial grow factor 165 isoform (VEGF 165 ) and plays roles in vasculogenesis and angiogenesis. Neuropilin-1 also binds to semaphorin III which is an inhibitor to axon guidance signal. To seek evidence that neuropilin-1 may play roles in ischemic brain, we examined the temporal and spatial profiles of its expression after focal cerebral ischemia. Male Wistar Rats (n=42) were subjected to 1h to 28 days of embolic middle cerebral artery (MCA) occlusion. Expression of neuropilin-1 was measured by Northern blot, in situ hybridization and immunohistoche

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Duarte, Sinésio Grace, Antônio Dorival Campos, and Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model." Arquivos de Neuro-Psiquiatria 61, no. 3B (2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.

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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESU

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Wang, Jian, and Song-Yuan He. "Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries." Journal of Investigative Medicine 68, no. 7 (2020): 1276–81. http://dx.doi.org/10.1136/jim-2020-001328.

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This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative

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Wu, Bin, Akifumi Ootani, Ryuichi Iwakiri, et al. "Ischemic preconditioning attenuates ischemia-reperfusion-induced mucosal apoptosis by inhibiting the mitochondria-dependent pathway in rat small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 4 (2004): G580—G587. http://dx.doi.org/10.1152/ajpgi.00335.2003.

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Ischemic preconditioning provides a way of protecting organs from damage inflicted with prolonged ischemia-reperfusion. In this study, we investigated the mechanism of ischemic preconditioning involved in inhibition of prolonged ischemia-reperfusion-induced mucosal apoptosis in rat small intestine. Ischemic preconditioning was triggered by a transient occlusion of the superior mesenteric artery followed by reperfusion. Ischemia-reperfusion was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion in the small intestine. Ischemia-reperfusion alone induced

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YAMAKI, IGOR NAGAI, RUY VICTOR SIMÕES PONTES, FELIPE LOBATO DA SILVA COSTA, et al. "Kidney ischemia and reperfunsion syndrome: effect of lidocaine and local postconditioning." Revista do Colégio Brasileiro de Cirurgiões 43, no. 5 (2016): 348–53. http://dx.doi.org/10.1590/0100-69912016005012.

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ABSTRACT Objective: to evaluate the effects of blocking the regulation of vascular tone on the ischemia and reperfusion syndrome in rats through the use of lidocaine in the postconditioning technique. Methods: we randomized 35 rats into seven groups of five animals: Group 1- Control; Group 2- Ischemia and Reperfusion; Group 3- Ischemia, Reperfusion and Saline; Group 4- Ischemic Postconditioning; Group 5- Ischemic Postconditioning and Saline; Group 6- Lidocaine; Group 7- Ischemic Postconditioning and Lidocaine. Except for the control group, all the others were submitted to renal ischemia for 30

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Sorimachi, Takatoshi, Hiroshi Abe, Shigekazu Takeuchi, and Ryuichi Tanaka. "Neuronal damage in gerbils caused by intermittent forebrain ischemia." Journal of Neurosurgery 91, no. 5 (1999): 835–42. http://dx.doi.org/10.3171/jns.1999.91.5.0835.

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Object. The purpose of this study was to investigate the possibility of preventing cumulative neuronal damage after repetitive severe ischemia.Methods. The authors monitored ischemic depolarization in the gerbil hippocampus, which has recently been shown to be a good experimental model of the effects of brief ischemia on the brain, and evaluated neuronal damage in the CA1 subregion 7 days after the ischemic insult. In a single-ischemia paradigm, the results indicate that induction of ischemia-induced neuronal damage depended on the duration of ischemic depolarization. Neuronal damage can be de

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Sapmaz, Ali, A. Tulga Ulus, Nilüfer N. Turan, et al. "Which type of conditioning method protects the spinal cord from the ischemia–reperfusion injury in 24 hours?" Vascular 23, no. 6 (2015): 614–21. http://dx.doi.org/10.1177/1708538114568702.

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Objective This study was designed to test the effects of different types of preconditioning and postconditioning methods on spinal cord protection following aortic clamping. Methods The animals (rabbits) were divided into sham-operated, ischemic preconditioning, remote ischemic preconditioning, simultaneous aortic and ischemic remote preconditioning, and ischemic postconditioning groups. After neurological evaluations, ultrastructural analysis and immunohistochemical staining for caspase-3 were evaluated after 24 h following ischemia. Results The neurological outcomes of the remote ischemic pr

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POP, Lacramioara-Eliza, Dana POP, and Cristina PANTELEMON. "Ambulatory electrocardiographic monitoring as a diagnostic tool for ischemic heart disease in women." Balneo Research Journal 11, Vol.11, no.3 (2020): 409–16. http://dx.doi.org/10.12680/balneo.2020.370.

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Introduction. Ischemic heart disease(IHD) is currently the leading cause of mortality in women. In this study we aimed to evaluate ambulatory electrocardiographic monitoring(AECGm) as a diagnostic test for IHD in women. Material and method. The study included 225 female who underwent AECGm divided into 2 groups: 136 previously diagnosed with IHD(IHD+) and 89 controls(IHD-). The IHD+ group was subdivided into AECGm ischemia subgroup(I+) and AECGm non-ischemia subgroup(I-). AECGm was assessed for presence of myocardial ischemia (ST segment depression >5mm), duration and ischemic load (the per

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Bosnjak, Zeljko J., and Zhi-Dong Ge. "The application of remote ischemic conditioning in cardiac surgery." F1000Research 6 (June 16, 2017): 928. http://dx.doi.org/10.12688/f1000research.11018.1.

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Perioperative myocardial ischemia and infarction are the leading causes of morbidity and mortality following anesthesia and surgery. The discovery of endogenous cardioprotective mechanisms has led to testing of new methods to protect the human heart. These approaches have included ischemic pre-conditioning, per-conditioning, post-conditioning, and remote conditioning of the myocardium. Pre-conditioning and per-conditioning include brief and repetitive periods of sub-lethal ischemia before and during prolonged ischemia, respectively; and post-conditioning is applied at the onset of reperfusion.

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Lakshmanan, Rajesh, Gopi Ukani, Muhammad Tipu Rishi, and Nilanjana Maulik. "Trimodal rescue of hind limb ischemia with growth factors, cells, and nanocarriers: fundamentals to clinical trials." Canadian Journal of Physiology and Pharmacology 95, no. 10 (2017): 1125–40. http://dx.doi.org/10.1139/cjpp-2016-0713.

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Peripheral artery disease is a severe medical condition commonly characterized by critical or acute limb ischemia. Gradual accumulation of thrombotic plaques in peripheral arteries of the lower limb may lead to intermittent claudication or ischemia in muscle tissue. Ischemic muscle tissue with lesions may become infected, resulting in a non-healing wound. Stable progression of the non-healing wound associated with severe ischemia might lead to functional deterioration of the limb, which, depending on the severity, can result in amputation. Immediate rescue of ischemic muscles through revascula

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Kolocassides, K. G., M. Galinanes, and D. J. Hearse. "Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (1995): H1415—H1420. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1415.

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We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') bef

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Hoshida, S., T. Kuzuya, H. Fuji, et al. "Sublethal ischemia alters myocardial antioxidant activity in canine heart." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 1 (1993): H33—H39. http://dx.doi.org/10.1152/ajpheart.1993.264.1.h33.

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We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared wi

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Zhan, Ren-Zhi, Hideyoshi Fujihara, Hiroshi Baba, Tomohiro Yamakura, and Koki Shimoji. "Ischemic Preconditioning Is Capable of Inducing Mitochondrial Tolerance in the Rat Brain." Anesthesiology 97, no. 4 (2002): 896–901. http://dx.doi.org/10.1097/00000542-200210000-00022.

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Background Preconditioning to ischemia is a phenomenon whereby a brief episode of sublethal ischemia and other nonlethal stressors produce protection against a subsequent detrimental ischemic insult. As mitochondrial dysfunction is related to necrotic and apoptotic neuronal death after cerebral ischemia, the authors examined if ischemic preconditioning is capable of inducing mitochondrial tolerance. Methods Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 8 min in Wistar rats (275-300 g). A 3-min ischemic episode performed 48 h befor

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Manabe, Hiroaki, David O. Okonkwo, John L. Gainer, Ryon H. Clarke, and Kevin S. Lee. "Protection against focal ischemic injury to the brain by trans-sodium crocetinate." Journal of Neurosurgery 113, no. 4 (2010): 802–9. http://dx.doi.org/10.3171/2009.10.jns09562.

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Object Ischemic injury is a potential complication in a variety of surgical procedures and is a particular impediment to the success of surgeries involving highly vulnerable neural tissue. One approach to limiting this form of injury is to enhance metabolic supply to the affected tissue. Trans-sodium crocetinate (TSC) is a carotenoid compound that has been shown to increase tissue oxygenation by facilitating the diffusivity of small molecules, such as oxygen and glucose. The present study examined the ability of TSC to modify oxygenation in ischemic neural tissue and tested the potential neuro

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Hearse, David J., and Fiona J. Sutherland. "Catecholamines and preconditioning: studies of contraction and function in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (1999): H136—H143. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h136.

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The aims of this study were to determine whether 1) like ischemic preconditioning, transient exposure to norepinephrine before ischemia exacerbates contracture during ischemia and 2) protection afforded by norepinephrine is stereospecific (receptor mediated). Isolated perfused rat hearts were randomized into five groups ( n = 6/group): 1) ischemic preconditioning (3 min of ischemia + 3 min of reperfusion + 5 min of ischemia + 5 min of reperfusion), 2) untreated control, 3) vehicle control (ascorbic acid), 4) substitution of preconditioning ischemia by perfusion with d-norepinephrine, and 5) su

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Ala, Alireza, Jafar Ghobadi, Haleh Yaghubi, and Ali Adib. "The prognostic values of platelet to lymphocyte ratio for predicting mortality in patients with acute mesenteric ischemia: a cross-sectional study." Journal of Research in Clinical Medicine 10 (December 24, 2022): 29. http://dx.doi.org/10.34172/jrcm.2022.029.

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Introduction: Acute mesenteric ischemia (AMI) is a life-threatening disease that can cause multi-organ damage and ultimately lead to death. Early diagnosis and treatment significantly reduce morbidity and mortality rates in high-risk patients. This study aimed to explore the prognostic values of platelet to lymphocyte ratio (PLR) in predicting mortality in patients with mesenteric ischemia. Methods: This prospective study included 126 patients with a complaint of acute abdominal pain, suggesting mesenteric ischemia. Demographic data and measured variables were determined using a pre-designed q

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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. 2 (2022): 27–35. http://dx.doi.org/10.3897/rrpharmacology.8.75753.

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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; gro

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Sanada, Shoji, Issei Komuro, and Masafumi Kitakaze. "Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (2011): H1723—H1741. http://dx.doi.org/10.1152/ajpheart.00553.2011.

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Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioning-induced

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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. (2) (2022): 27–35. https://doi.org/10.3897/rrpharmacology.8.75753.

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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; group

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Duszczyk, Malgorzata, Apolonia Ziembowicz, Roman Gadamski, and And Lazarewicz. "Behavioral evaluation of ischemic damage to CA1 hippocampal neurons: Effects of preconditioning." Acta Neurobiologiae Experimentalis 66, no. 4 (2006): 311–19. http://dx.doi.org/10.55782/ane-2006-1620.

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In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly redu

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Packard, Amy E. B., Jason C. Hedges, Frances R. Bahjat, et al. "Poly-IC Preconditioning Protects against Cerebral and Renal Ischemia-Reperfusion Injury." Journal of Cerebral Blood Flow & Metabolism 32, no. 2 (2011): 242–47. http://dx.doi.org/10.1038/jcbfm.2011.160.

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Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is

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McCully, James D., Yoshiya Toyoda, Masahisa Uematsu, Robert D. Stewart, and Sidney Levitsky. "Adenosine-enhanced ischemic preconditioning: adenosine receptor involvement during ischemia and reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (2001): H591—H602. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h591.

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Adenosine-enhanced ischemic preconditioning (APC) extends the cardioprotection of ischemic preconditioning (IPC) by both significantly decreasing myocardial infarct size and significantly enhancing postischemic functional recovery. In this study, the role of adenosine receptors during ischemia-reperfusion was determined. Rabbit hearts ( n = 92) were used for Langendorff perfusion. Control hearts were perfused for 180 min, global ischemia hearts received 30-min ischemia and 120-min reperfusion, and IPC hearts received 5-min ischemia and 5-min reperfusion before ischemia. APC hearts received a b

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Santos, Carlos Henrique Marques dos, Otoni Moreira Gomes, José Carlos Dorsa Vieira Pontes, Luciana Nakao Odashiro Miiji, and Marco Aurélio Feltrin Bispo. "The ischemic preconditioning and postconditioning effect on the intestinal mucosa of rats undergoing mesenteric ischemia/reperfusion procedure." Acta Cirurgica Brasileira 23, no. 1 (2008): 22–28. http://dx.doi.org/10.1590/s0102-86502008000100005.

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PURPOSE: To evaluate the effect of the ischemic preconditioning and the ischemic postconditioning over the tissue injury in the intestinal mucosa of rats undergoing the procedure of mesenteric ischemia and reperfusion. METHODS: Thirty Wistar rats were studied, divided in three groups: group A, undergoing mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B, mesenteric ischemia and reperfusion preceded by ischemic preconditioning; group C, mesenteric ischemia and reperfusion and, before the beginning of reperfusion, the ischemic postconditioning was performed. At the end, a se

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Wang, Lei, Xu Zhang, Xiaoxing Xiong, et al. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke." Antioxidants 11, no. 12 (2022): 2377. http://dx.doi.org/10.3390/antiox11122377.

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcript

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Burda, Rastislav, Jozef Burda, and Radoslav Morochovič. "Ischemic Tolerance—A Way to Reduce the Extent of Ischemia–Reperfusion Damage." Cells 12, no. 6 (2023): 884. http://dx.doi.org/10.3390/cells12060884.

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Individual tissues have significantly different resistance to ischemia–reperfusion damage. There is still no adequate treatment for the consequences of ischemia–reperfusion damage. By utilizing ischemic tolerance, it is possible to achieve a significant reduction in the extent of the cell damage due to ischemia–reperfusion injury. Since ischemia–reperfusion damage usually occurs unexpectedly, the use of preconditioning is extremely limited. In contrast, postconditioning has wider possibilities for use in practice. In both cases, the activation of ischemic tolerance can also be achieved by the

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Gupta, Sachin, and Deeksha S. Tomar. "Ischemic Gut in Critically Ill (Mesenteric Ischemia and Nonocclusive Mesenteric Ischemia)." Indian Journal of Critical Care Medicine 24, S4 (2020): S157—S161. http://dx.doi.org/10.5005/jp-journals-10071-23611.

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Omae, Tsuyoshi, Matthew D. Silva, Orna Mayzel-Org, et al. "Temporal evolution of Diffusion / Perfusion Mismatch in a Rat Stroke Model." Stroke 32, suppl_1 (2001): 351. http://dx.doi.org/10.1161/str.32.suppl_1.351-c.

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P69 Background and Purpose: Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) can rapidly detect lesions in acute ischemic stroke. Studies show that lesions by PWI are sometimes larger than those of DWI in patients with acute ischemic stroke, suggests that the mismatch between DWI and PWI is potentially predictive of tissue at high risk for evolving into infarction. The aims of this study were to detect the evolution of the DWI/PWI mismatch in permanent focal experimental ischemia and transient focal experimental ischemia. Methods: Rats were subjected to permanent (n=8) and

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Daly, Hafedh. "Diagnosis and Management of Acute Limb Ischemia." Angiology & Vascular Surgery 7, no. 2 (2022): 1–6. http://dx.doi.org/10.24966/avs-7397/100089.

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Introduction: Acute limb ischemia is considered as a life threatening disease .After twelve hours of ischemia, chances of saving the ischemic limb are lower (78%), with higher mortality (31%) as well. Methods: A total of 54 patients who underwent surgery for acute non traumatic limb ischemia between January 2013 and December 2020 were retrospectively reviewed. Results: We included 30 women and 24 men; median age was 69 years. Twenty patients (37%) were presented with upper limb ischemia, where as 34 patients (63%) with lower limb ischemia. Mean delay between the onset of symptoms and hospital

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Zicola, Elisa, Elisa Arrigo, and Daniele Mancardi. "H2S Pretreatment Is Promigratory and Decreases Ischemia/Reperfusion Injury in Human Microvascular Endothelial Cells." Oxidative Medicine and Cellular Longevity 2021 (April 17, 2021): 1–13. http://dx.doi.org/10.1155/2021/8886666.

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Endothelial cell injury and vascular function strongly correlate with cardiac function following ischemia/reperfusion injury. Several studies indicate that endothelial cells are more sensitive to ischemia/reperfusion compared to cardiomyocytes and are critical mediators of cardiac ischemia/reperfusion injury. H2S is involved in the regulation of cardiovascular system homeostasis and can act as a cytoprotectant during ischemia/reperfusion. Activation of ERK1/2 in endothelial cells after H2S stimulation exerts an enhancement of angiogenesis while its inhibition significantly decreases H2S cardio

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Kato, Hiroyuki, Kyuya Kogure, Tsutomu Araki, Xiao-Hong Liu, Kanefusa Kato, and Yasuto Itoyama. "Immunohistochemical Localization of Superoxide Dismutase in the Hippocampus following Ischemia in a Gerbil Model of Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 15, no. 1 (1995): 60–70. http://dx.doi.org/10.1038/jcbfm.1995.7.

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Pretreatment of the gerbil brain with a 2-min period of sublethal ischemia protects against neuronal damage following a subsequent 3-min period of ischemia, which normally destroys pyramidal neurons in the CA1 region of the hippocampus. To clarify the role of superoxide dismutase (SOD) in this ischemic tolerance, we immunohistochemically investigated the alterations in copper-zinc SOD (CuZnSOD) and manganese SOD (MnSOD) in the gerbil hippocampus following 3-min ischemia with or without the first mild ischemia. Normal hippocampus showed an intense CuZnSOD immunostaining in pyramidal neurons but

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Yagita, Yoshiki, Kazuo Kitagawa, Naoki Oyama, et al. "Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (2013): 1532–39. http://dx.doi.org/10.1038/jcbfm.2013.112.

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Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177

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Tian, Guo-Feng, and Andrew J. Baker. "Protective Effect of High Glucose Against Ischemia-Induced Synaptic Transmission Damage in Rat Hippocampal Slices." Journal of Neurophysiology 88, no. 1 (2002): 236–48. http://dx.doi.org/10.1152/jn.00572.2001.

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Cerebral ischemic damage is an important cause of morbidity and mortality. However, there is conflicting evidence regarding the effect of the extracellular glucose concentration in focal and global ischemic injury. This study was designed to investigate this effect in ischemia-induced synaptic transmission damage in rat hippocampal slices. Slices were superfused with artificial cerebrospinal fluid (ACSF) containing various concentrations of glucose before and after ischemia. The evoked somatic postsynaptic population spike (PS) and dendritic field excitatory postsynaptic potential (fEPSP) were

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Liu, Shimin, Honglian Shi, Wenlan Liu, Takamitsu Furuichi, Graham S. Timmins, and Ke Jian Liu. "Interstitial pO2 in Ischemic Penumbra and Core are Differentially Affected following Transient Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 24, no. 3 (2004): 343–49. http://dx.doi.org/10.1097/01.wcb.0000110047.43905.01.

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Stroke causes heterogeneous changes in tissue oxygenation, with a region of decreased blood flow, the penumbra, surrounding a severely damaged ischemic core. Treatment of acute ischemic stroke aims to save this penumbra before its irreversible damage by continued ischemia. However, effective treatment remains elusive due to incomplete understanding of processes leading to penumbral death. While oxygenation is central in ischemic neuronal death, it is unclear exactly what actual changes occur in interstitial oxygen tension (pO2) in ischemic regions during stroke, particularly the penumbra. Usin

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Danielisová, Viera, Miroslava Némethová, and Jozef Burda. "Iron Deposition in the Brain Following the Ischemia in a Rat Model of Ischemic Tolerance." Acta Medica (Hradec Kralove, Czech Republic) 47, no. 4 (2004): 285–88. http://dx.doi.org/10.14712/18059694.2018.107.

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Preconditioning of the brain by short-term ischemia increases brain tolerance to the subsequent severer ischemia. In this study, we investigated iron deposition in the cerebral cortex and the ischemic tolerance in a rat model of cerebral ischemia. Forebrain ischemia was induced by four-vessel occlusion for 5 min as ischemic preconditioning. Two days after preconditioning or after the sham-operation, the second ischemia was induced for 20 min. Changes in the cerebral cortex were examined after 1 to 8 weeks of recirculation following 20 min ischemia with or without preconditioning using the iron

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Pluta, Ryszard, Janusz Kocki, Jacek Bogucki, Anna Bogucka-Kocka, and Stanisław J. Czuczwar. "LRP1 and RAGE Genes Transporting Amyloid and Tau Protein in the Hippocampal CA3 Area in an Ischemic Model of Alzheimer’s Disease with 2-Year Survival." Cells 12, no. 23 (2023): 2763. http://dx.doi.org/10.3390/cells12232763.

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Explaining changes at the gene level that occur during neurodegeneration in the CA3 area is crucial from the point of view of memory impairment and the development of post-ischemic dementia. An ischemic model of Alzheimer’s disease was used to evaluate changes in the expression of genes related to amyloid transport in the CA3 region of the hippocampus after 10 min of brain ischemia with survival of 2, 7 and 30 days and 12, 18 and 24 months. The quantitative reverse transcriptase PCR assay revealed that the expression of the LRP1 and RAGE genes involved in amyloid transport was dysregulated fro

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