Добірка наукової літератури з теми "Myocardial reperfusion Complications Prevention"
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Статті в журналах з теми "Myocardial reperfusion Complications Prevention"
Kozlov, I. A. "PREVENTION OF COMPLICATIONS CAUSED BY MYOCARDIAL ISCHEMIA-REPERFUSION IN NONCARDIAC SURGICAL PROCEDURES." Bulletin of Siberian Medicine 15, no. 3 (July 1, 2016): 102–19. http://dx.doi.org/10.20538/1682-0363-2016-3-102-119.
Повний текст джерелаShved, M. I., and I. O. Yastremska. "PREVENTION OF COMPLICATIONS IN PATIENTS WITH MYOCARDIAL INFARCTION AND CONCOMITANT METABOLIC SYNDROME." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 4 (December 30, 2020): 101–7. http://dx.doi.org/10.31718/2077-1096.20.4.101.
Повний текст джерелаHashemi, Baran, Majid Maleki, Amir Darbandi Azar, Morteza Zare, Seyed Mohammad Mazloomi, and Nasim Naderi. "Prevention of kidney injury after myocardial ischemia reperfusion is achievable with short-term protein restriction." Journal of Renal Injury Prevention 8, no. 4 (September 15, 2019): 301–5. http://dx.doi.org/10.15171/jrip.2019.55.
Повний текст джерелаIskhakov, M. M., D. R. Tagirova, N. V. Gazizov, L. A. Nugaybekova, and R. G. Sayfutdinov. "«No-reflow» phenomenon: clinical aspects of reperfusion failure." Kazan medical journal 96, no. 3 (June 15, 2015): 391–96. http://dx.doi.org/10.17750/kmj2015-391.
Повний текст джерелаLiu, Yuezhu, Hua Zeng, and Junmei Xu. "Recent Advance on Drug Therapy Related to Myocardial Ischemia Reperfusion Injury." Journal of Biomaterials and Tissue Engineering 12, no. 2 (February 1, 2022): 299–305. http://dx.doi.org/10.1166/jbt.2022.2899.
Повний текст джерелаRadovanovic, Nebojsa, Mina Radosavljevic-Radovanovic, Milan Dobric, Nebojsa Antonijevic, and Predrag Mitrovic. "Acute myocardial infarction – timely management (chain of care)." Acta chirurgica Iugoslavica 63, no. 2 (2016): 9–13. http://dx.doi.org/10.2298/aci1602009r.
Повний текст джерелаGilyarov, M. Yu, I. I. Ivanov, E. V. Konstantinova, N. I. Raschetnova, and N. A. Shostak. "No-reflow phenomenon and reperfusion injury. Mechanisms and treatment." Clinician 15, no. 1-4 (March 5, 2022): 10–19. http://dx.doi.org/10.17650/1818-8338-2021-15-1-4-k645.
Повний текст джерелаMayasi, Yunis, and Romergryko G. Geocadin. "Updates on the Management of Neurologic Complications of Post–Cardiac Arrest Resuscitation." Seminars in Neurology 41, no. 04 (August 2021): 388–97. http://dx.doi.org/10.1055/s-0041-1731310.
Повний текст джерелаHeinen, André, Vera Welke, Friederike Behmenburg, Martin Stroethoff, Volker Stoldt, Till Hoffmann, Markus W. Hollmann, and Ragnar Huhn. "Haemotherapy with Fibrinogen for Perioperative Bleeding Prevention—A view on Arterial Thrombogenesis and Myocardial Infarction in the Rat In Vivo." Journal of Clinical Medicine 8, no. 6 (June 19, 2019): 880. http://dx.doi.org/10.3390/jcm8060880.
Повний текст джерелаZykov, M. V., V. V. Butsev, and R. R. Suleymanov. "Myocardial Infarction Complicated by Ischemic Stroke: Risk Factors, Prognosis, Unresolved Problems and Possible Methods of Prevention." Rational Pharmacotherapy in Cardiology 17, no. 1 (March 3, 2021): 73–82. http://dx.doi.org/10.20996/1819-6446-2021-02-09.
Повний текст джерелаДисертації з теми "Myocardial reperfusion Complications Prevention"
Van, Vuuren Derick. "The role of Protein Phosphatase 2A (PP2A) in myocardial ischaemia/reperfusion injury." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86397.
Повний текст джерелаENGLISH ABSTRACT: Ischaemic heart disease is a major contributor to global morbidity and mortality rates. Manoeuvres such as ischaemic preconditioning confer cardioprotection against ischaemia/reperfusion (I/R) injury by activating several intracellular signalling pathways. These pathways have been defined solely in terms of the kinases involved, despite the realization in recent years that protein phosphatase activity also contributes significantly to the attributes of the propagated signal. Protein phosphatase 2A (PP2A) is a heteromultimeric enzyme involved in an array of phosphatase reactions. We hypothesized that PP2A is an important participant in the myocardial response to I/R by regulating intracellular signalling. This project aimed to (i) characterize PP2A during myocardial I/R; (ii) determine the importance of its contribution to the cellular response to I/R; and (iii) investigate its role in the signalling pathways mediated by PKB/Akt, GSK-3β, ERK p42/p44 and p38 MAPK. Two models were used to characterize PP2A during I/R: (i) H9c2 cells exposed to simulated ischaemia (SI) buffer in conjunction with hypoxia (0.5% O2) for a maximum of 2 hours, followed by reoxygenation in standard growth medium for up to 30 minutes; and (ii) isolated working rat hearts exposed to a maximum of 20 minutes global ischaemia and 10 minutes reperfusion. In both models samples were collected at several time points during I/R for Western blotting analysis. PP2A-C (the catalytic subunit) accumulated in the nucleus during early ischaemia, but later redistributed to the cytosol. At the end of ischaemia there was an elevation of PP2A-C relative to PP2A-A in the unfractionated whole cell preparation concomitant with an increase in the inhibitory phosphorylation of PP2A-C. The impact of PP2A activity was evaluated by either inhibiting PP2A using okadaic acid (OA, 10 nM) or activating it by administering FTY720 (1 μM) in an isolated working rat heart model exposed to either 35 minutes of regional ischaemia (RI) with infarct size (IFS) as primary end-point, or 20 minutes global ischaemia (GI) with functional recovery as end-point. The results showed that the pre-ischaemic administration of OA or FTY720 reduced or exacerbated IFS respectively, indicating that PP2A activation during I/R favours cell death. OA and FTY720 were also employed to assess the contribution of PP2A to intracellular signalling in an isolated working rat heart exposed to I/R. Samples were collected at several timepoints and analyzed using Western Blotting. Pre-ischaemic administration of OA enhanced the phosphorylation of PKB/Akt, ERK p42/p44 and GSK-3β at the onset of reperfusion, while FTY720 given before ischaemia reduced the phosphorylation of GSK-3β, p38 MAPK and PKB/Akt at the end of ischaemia and onset of reperfusion. In summary, PP2A is part of an early nuclear-based response to ischaemia, while long-term ischaemia induces an increase in PP2A-C. A portion of this PP2A-C is stored in an inactive form, while an active portion acts as a regulator of the pro-survival signalling components PKB/Akt, GSK- 3β and ERK p42/p44 at the end of ischaemia and the onset of reperfusion. PP2A is therefore an important component of the myocardial response to I/R by regulating pro-survival signalling.
AFRIKAANSE OPSOMMING: Iskemiese hartsiekte is een van die belangrikste komponente wat bydra tot globale morbiditeit en mortaliteit. Ingrepe soos iskemiese prekondisionering aktiveer veelvoudige intrasellulêre seintransduksiepaaie om kardiobeskerming teen iskemie/herperfusie (I/H)-besering te ontlok. Die kinases betrokke in hierdie seintransduksiepaaie is reeds deeglik nagevors, terwyl die potensiële belang van die proteïenfosfatases in seintransduksie tot onlangs misken is. Ons hipotese was dat Proteïenfosfatase 2A (PP2A), wat in ‘n wye verskeidenheid fosfatase reaksies betrokke is, ‘n belangrike rolspeler in die miokardiale reaksie op I/H-besering is, deur deelname aan die regulering van intrasellulêre seintransduksie. Hierdie projek het ten doel gehad om (i) PP2A te karakteriseer tydens miokardiale I/H; (ii) die belang van PP2A in die sellulêre reaksie op I/H-besering te bepaal; en (iii) PP2A se rol in die seintransduksiepaaie, gemedieer deur PKB/Akt, GSK-3β, ERK p42/p44 en p38 MAPK, te evalueer. Twee modelle is aangewend om PP2A tydens I/H te karakteriseer: (i) H9c2-selle blootgestel aan ‘n simuleerde iskemiebuffer tesame met hipoksie (0.5% O2) vir ‘n maksimum van 2 uur gevolg deur heroksiginasie in standaardgroeimedium vir verskillende tydsperiodes tot ‘n maksimum van 30 minute; en (ii) geïsoleerde, werkende rotharte blootgestel aan ‘n maksimum van 20 minute globale iskemie en 10 minute herperfusie. In beide modelle is monsters op verskillende tye versamel vir Western-kladanalise. Tydens vroeë iskemie het PP2A-C in die kern toegeneem, waarna dit met verloop van tyd na die sitosol herversprei het. Teen die einde van iskemie was daar ‘n toename in die vlakke van PP2A-C relatief tot PP2A-A in ongefraksioneerde weefselhomogenate, tesame met ‘n toename in die inhibitoriese fosforilering van PP2A-C. Die belang van PP2A-aktiwiteit is ondersoek deur die effek te bepaal van die inhibisie of aktivering daarvan op infarktgrootte (IFS) en funksionele herstel in ‘n geïsoleerde werkende rothartmodel, blootgestel aan onderskeidelik 35 minute streeksiskemie (RI) of 20 minute globale iskemie. Preiskemiese toediening van die PP2A-inhibitor okadaïensuur (OA, 10 nM), of aktiveerder FTY720 (1 μm) het infarktgrootte respektiewelik beperk of vergroot. PP2A-aktivering tydens I/H is dus nadelig. OA en FTY720 is ook aangewend om die bydrae van PP2A tot I/H-verwante, intrasellulêre seintransduksie in die geïsoleerde, werkende rothart te bepaal. Monsters is op verskeie tydintervalle versamel en ontleed deur gebruik te maak van die Western-kladtegniek. Preiskemiese toediening van OA het die fosforilering van PKB/Akt, ERK p42/p44 en GSK-3β by die aanvang van herperfusie bevoordeel, terwyl pre-iskemiese toediening van FTY720, die fosforilering van GSK-3β, p38 MAPK en PKB/Akt aan die einde van iskemie en die begin van herperfusie verminder het. Ter opsomming: PP2A is deel van ‘n vroeë gelokaliseerde kerngebaseerde reaksie op iskemie, terwyl langdurige iskemie ‘n toename in PP2A-C relatief tot PP2A-A induseer. ‘n Deel van hierdie PP2A-C is onaktief, terwyl die res funksioneer in die regulering van die seintransduksiekomponente PKB/Akt, GSK-3β en ERK p42/p44 wat oorlewing fasiliteer met die aanvang van herperfusie. PP2A is dus ‘n belangrike komponent in die miokardiale reaksie op I/H deurdat dit tot die beheer van seintransduksiepaaie bydra.
Esterhuyse, Adriaan Johannes. "Dietary red palm oil-supplementation offers cardioprotection against Ischaemia/Reperfusion injury : possible cellular mechanisms involved." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/16514.
Повний текст джерелаENGLISH ABSTRACT: Activation of the NO-cGMP pathway is associated with myocardial protection against ischaemia/reperfusion injury. However, high-cholesterol diets alter function of this pathway and these alterations have been implicated in both ischaemic/reperfusion injury and the development of ischaemic heart disease. Little is known about the effects of supplements such as Red Palm Oil (RPO) on the myocardial NO-cGMP-signalling pathway. RPO consists of saturated, mono-unsaturated and poly-unsaturated fatty acids and is rich in antioxidants such as β-carotene and Vitamin E (tocopherols and tocotrienols). The aims of this study were: 1) to determine whether dietary RPO-supplemention protects against ischaemia/reperfusion injury in rats fed a standard rat chow (control) and cholesterol-enriched diets and 2) if so, to investigate possible mechanisms for this protection. Male Long-Evans rats were fed a standard rat chow or a standard rat chow plus cholesterol and/or RPO-supplementation for 6 weeks. Myocardial functional recovery was measured and hearts were freeze-clamped for determination of myocardial phospholipid, cAMP/cGMP concentrations, total myocardial nitric oxide concentrations, lipid hydroperoxide production and superoxide dismutase- and nitric oxide synthase activity in isolated rat hearts subjected to 25 minutes of normothermic total global ischaemia. In addition, the degree of phosphorylation of extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal protein kinase (JNK) and protein kinase B (PKB/Akt) was investigated. Furthermore, the effect of RPO-supplementation on caspase-3 activation and poly (ADP-ribose) polymerase (PARP)-cleavage in hearts subjected to ischaemia and reperfusion was also investigated. Our data show that dietary RPO-supplementation protects the hearts of rats on a standard rat chow (control) and hypercholesterolaemic diet against ischaemia/reperfusion injury as reflected by improved aortic output recovery. Increased intracellular cardiomyocyte NO concentrations as observed in control hearts supplemented with RPO after 120 minutes hypoxia may contribute to the elevated cGMP concentration and may confer some of the cardioprotection to the ischaemic/reperfused heart. Although improved functional recovery with RPO-supplementation of a high-cholesterol diet was also associated with an increase in intracellular cardiomyocyte NO production after hypoxia compared to the non-hypoxic conditions, it could not be linked to increased NO-cGMP signalling. These data are in agreement with other studies, which showed that high-cholesterol diet impairs NO-cGMP signalling and confirms our hypothesis that elevated cGMP concentrations may not be the only mechanism of protection. We have also shown that RPOsupplementation caused increased phosphorylation of p38 and PKB, reduced phosphorylation of JNK and attenuation of PARP cleavage, which may contribute to the protection of the cell against apoptosis. Based on our results we propose that the myocardial protection offered by RPO-supplementation of rats on a normal and hypercholesterolaemic diet may be associated with either its antioxidant characteristics and/or changes in the fatty acid composition of the myocardium during ischaemia/reperfusion. Furthermore, we demonstrated for the first time that RPO-supplementation protects the isolated perfused working rat heart during reperfusion from ischaemia/reperfusion-induced injury through a MAPK-dependent pathway.
AFRIKAANSE OPSOMMING: Aktivering van die NO-cGMP sein transduksie pad word geassosieer met miokardiale beskerming teen isgemie/herperfusie skade. Hoë cholesterol diëte verander egter die funksie van die pad en hierdie veranderings speel ‘n rol in beide isgemie/herperfusie besering en die ontwikkeling van isgemiese hartsiekte. Daar is egter min inligting beskikbaar oor die uitwerking van aanvullings soos rooi palm olie (RPO) op die miokardiale NO-cGMP sein transduksie pad. RPO bevat versadigde, mono-onversadigde en poli-onversadigde vetsure en is ryk aan anti-oksidante nl. β-karotene en vitamien E (tokoferole en tokotriënole). Die doelwitte van hierdie studie was: 1) om vas te stel of ‘n RPO-aanvulling beskerming bied teen isgemie/herperfusie besering in rotte wat gevoed is met ‘n standaard rotmengsel (kontrole) en cholesterol-verrykte dieet en 2) indien wel, om moontlike meganismes van beskerming te ondersoek. Long-Evans manlike rotte is vir 6 weke gevoer met ‘n standaard rotmengsel of ‘n standaard rotmengsel plus cholesterol en/of RPO-aanvulling. Miokardiale funksionele herstel is gemeet en harte is gevriesklamp vir die bepaling van miokardiale fosfolipied, cAMP/cGMP, totale stikstofoksied, lipied hidroperoksied, superoksied dismutase en stikstofoksied sintase in geïsoleerde rotharte wat vir 25 minute onderwerp was aan normotermiese totale globale isgemie. Hiermee saam is die graad van fosforilering van ekstrasellulêre sein gereguleerde kinase (ERK), p38 mitogeen-geaktiveerde proteïen kinase (p38 MAPK), c-Jun-N-terminale proteïenkinase (JNK) en proteïen kinase B (PKB/Akt) ondersoek, asook kaspase-3 aktivering en poli (ADP-ribose) polimerase (PARP) kliewing in harte blootgestel aan isgemie en herperfusie. Ons resultate toon dat RPO-aanvulling van rotte op ‘n normale en hipercholesterolemiese dieet die hart beskerm soos getoon deur verbeterde herstel van aortiese uitset. Verhoogde intrasellulêre miokardiale NO vlakke in kontrole harte met ‘n RPO-aanvulling wat blootgestel was aan 120 minute hipoksie, mag bygedra het tot die verhoogde cGMP vlakke en beskerming van die hart tydens isgemie en herperfusie. Alhoewel verbeterde funksionele herstel met RPO-aanvulling van ‘n hoë cholesterol dieet ook geassosieer is met ‘n toename in intrasellulêre miokardiale NO produksie ná hipoksiese toestande, kon dit nie verbind word met verhoogde aktivering van die NOcGMP sein transduksie pad nie. Hierdie resultate stem ooreen met ander studies wat aangetoon het dat hoë-cholesterol diëte die NO-cGMP seinpad onderdruk. Hierdie bevinding bevestig ons hipotese dat verhoogde cGMP vlakke moontlik nie die enigste beskermingsmeganisme is nie. Ons resultate het ook gewys dat RPO-aanvulling fosforilering van p38 en PKB/Akt verhoog, fosforilering van JNK verminder en PARP kliewing onderdruk. Dit dui op beskerming van die sel teen apoptose. Ons resultate dui aan dat die miokardiale beskerming wat RPO-dieet aanvulling bied moontlik geassosieer kan word met sy anti-oksidant eienskap en/of veranderinge in die vetsuur samestelling van die miokardium tydens isgemie/herperfusie. Ons het ook vir die eerste keer bewys dat RPO-aanvulling die geïsoleerde geperfuseerde werkende rothart gedurende herperfusie beskerm teen isgemie/herperfusie besering deur die aktivering en/of deaktivering van die MAPK afhanklike pad.
Yamazaki, Kazuhiro. "Prevention of myocardial reperfusion injury by poly(ADP-ribose) synthetase inhibitor, 3-aminobenzamide, in cardioplegic solution : in vitro study of isolated rat heart model." Kyoto University, 2007. http://hdl.handle.net/2433/135743.
Повний текст джерелаMaarman, Gerald Jerome. "The effect of CPT-1 inhibition on myocardial function and resistance to ischemia/reperfusion injury in a rodent model of the metabolic syndrome." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5354.
Повний текст джерелаENGLISH ABSTRACT: Background: Obesity is associated with dyslipidemia, insulin resistance and glucose intolerance and together these components characterise the metabolic syndrome (Dandona et al. 2005). In the state of obesity, there are high levels of circulating free fatty acids and increased rates of fatty oxidation which inhibit glucose oxidation. This: (i) reduce the heart‘s contractile ability, (ii) exacerbates ischemic/reperfusion injury and (iii) decreases cardiac mechanical function during reperfusion (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Aim: The aim of our study was to investigate the effect of inhibiting fatty acid oxidation, with oxfenicine (4-Hydroxy-L-phenylglycine), on (i) cardiac mechanical function, (ii) mitochondrial respiration, (iii) myocardial tolerance to ischemia/reperfusion injury, (iv) CPT-I expression, MCAD expression, IRS-1 activation, total GLUT- 4 expression and (v) the RISK pathway (ERK42/44 and PKB/Akt). Methods: Male Wistar rats were fed a control rat chow diet or a high calorie diet (HCD) for 16 weeks. The HCD caused diet induced obesity (DIO). The animals were randomly divided into 4 groups [Control, DIO, Control + oxfen and DIO + oxfen]. The drug was administered for the last 8 weeks of feeding (200mg/kg/day). Animals were sacrificed and the hearts were perfused on the Langendorff perfusion system. After being subjected to regional ischemia and two hours of reperfusion, infarct size was determined. A separate series of animals were fed and/or treated and hearts were collected after 25 minutes global ischemia followed by 30 min reperfusion for determination of GLUT- 4, CPT-1, IRS -1, MCAD, ERK (42/44) and PKB/Akt expression/phosphorylation using Western blot analysis. A third series of hearts were excised and used for the isolation of mitochondria. Results: In the DIO rats, chronic oxfenicine treatment improved cardiac mechanical function by improving mitochondrial respiration. Oxfenicine inhibited CPT-1 expression but had no effect on MCAD or GLUT- 4 expression. Oxfenicine decreased IRS-1 iv expression, but not IRS-1 activation. Oxfenicine also improved myocardial tolerance to ischemia/reperfusion without activation of the RISK pathway (ERK & PKB). In the control rats, chronic oxfenicine treatment worsened cardiac mechanical function by adversely affecting mitochondrial respiration. Oxfenicine also worsened myocardial tolerance to ischemia/reperfusion in the control rats without changes in the RISK pathway (ERK & PKB). Oxfenicine had no effect on CPT-1, MCAD or GLUT- 4 expression. Oxfenicine increased IRS-1 expression, but not IRS-1 activity. Conclusion: Chronic oxfenicine treatment improved cardiac mechanical function and myocardial resistance to ischemia/reperfusion injury in obese animals, but worsened it in control animals. The improved cardiac mechanical function and tolerance to ischemia/reperfusion injury may be due to improvement in mitochondrial respiration.
AFRIKAANSE OPSOMMING: Agtergrond: Vetsug word geassosieer met dislipidemie, insulien weerstandigheid en glukose intoleransie, wat saam die metaboliese sindroom karakteriseer (Dandona et al. 2005). Met vetsug is daar ‗n hoë sirkulasie van vetsure, sowel as verhoogde vertsuur oksidasie wat gevolglik glukose oksidasie onderdruk. Dit: (i) verlaag die hart se vermoë om saam te trek, (ii) vererger isgemiese/herperfusie skade en (iv) verlaag kardiale effektiwiteit gedurende herperfusie (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Doel: Die doel van die studie was om die effekte van vetsuur onderdrukking m.b.v. oksfenisien (4-Hidroksie-L-fenielglisien) op (i) meganiese hart funksie, (ii) mitokondriale respirasie, (iii) miokardiale toleransie teen isgemiese/herperfusie skade, (iv) CPT-I uitdrukking, MCAD uitdrukking, IRS-1 aktiwiteit, totale GLUT-4 uitdrukking en (v) die RISK pad (ERK42/44 en PKB/Akt) te ondersoek. Metodes: Manlike Wistar rotte was gevoer met ‗n kontrole rot dieet of ‗n hoë kalorie dieet (HKD) vir 16 weke. Die HKD lei tot dieet-geïnduseerde vetsug (DGV). Die diere was lukraak verdeel in 4 groepe [kontrole, DGV, kontrole + oksfen en DGV + oksfen]. Die behandeling met die middel was toegedien vir die laaste 8 weke van die voeding protokol (200mg/kg/dag). Die diere was geslag en die harte was geperfuseer op die Langendorff perfusie sisteem. Na blootstelling aan streeks- of globale isgemie en 2 ure herperfusie was infark groottes bepaal. ‗n Aparte reeks diere was gevoer en/of behandel en die harte was versamel na 25 minute globale isgemie gevolg deur 30 minute herperfusie vir die bepaling van GLUT-4, CPT 1, IRS -1, MCAD, ERK (42/44) en PKB/Akt uitdrukking/aktivering d.m.v. Western blot analise. ‗n Derde reeks diere was gebruik vir die isolasie van mitokondria. Resultate: In die DGV diere, het kroniese oksfenisien behandeling meganiese hart funksie verbeter d.m.v. die verbetering van mitokondriale respirasie. Oksfenisien het CPT-1 uitdrukking verlaag terwyl GLUT- 4 en MCAD uitdrukking nie geaffekteer was vi nie. Oksfenisien het IRS-1 uitdrukking verlaag, maar nie IRS-1 aktiwiteit nie. Oksfenisien het ook miokardiale weerstand teen isgemiese/herperfusie verbeter met sonder aktivering van die RISK pad (ERK & PKB). In die kontrole diere, het kroniese oksfenisien behandeling die meganiese hart funksie versleg d.m.v. negatiewe effekte op mitokondriale respirasie. Oksfenisien het die miokardiale weerstand teen isgemiese/herperfusie van die kontrole rotte versleg sonder veranderinge in die RISK pad (ERK & PKB). Oksfenisien het geen effek gehad op CPT-1, MCAD en GLUT-4 uitdrukking nie. Oksfenisien het IRS-1 uitdrukking verhoog, maar nie IRS-1 aktiwiteit nie. Samevatting: Kroniese oksfenisien behandeling het die meganiese hart funksie en miokardiale weerstand teen isgemiese/herperfusie skade in die vet diere verbeter, maar versleg in die kontrole diere. Hierdie verbetering van meganiese hart funksie en weerstand teen isgemiese/herperfusie skade kon dalk wees a.g.v. ‗n verbetering in mitokondriale respirasie.
Cavalcante, Leonardo Pessoa. "Efeito da administração aguda de 17beta-estradiol ou de progesterona em modelo de isquemia-reperfusão medular em ratos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-06022017-103854/.
Повний текст джерелаBACKGROUND: Spinal cord ischemic injury remains a dreadful complication following thoracic and thoracoabdominal aortic interventions. Reports on gender-related neurological outcomes after ischemic and traumatic brain injuries have raised interest in hormonal influences, and have generated studies into neuroprotective effects of estrogen and progesterone. We hypothesized that the acute pre-operative administration of estradiol or of progesterone would prevent or attenuate spinal cord ischemic injury induced by transitory occlusion of the proximal descending thoracic aorta. OBJECTIVE: Evaluate the spinal cord effects of the acute administration of 17beta-estradiol or of progesterone in a spinal cord ischemia-reperfusion model. METHODS: Male rats were divided to receive 280ug/Kg of 17beta-estradiol (n=12) or 4mg/Kg of progesterone (n=8) or vehicle (control group) (n=12) 30 minutes before transitory occlusion of the proximal descending thoracic aorta, mean distal arterial blood pressure was maintained at 10mmHg during 12 minutes. Hind limb motor function was assessed at 1, 3, 5, 7 and 14 days after reperfusion. At the 14th day, a segment of the thoracolumbar spinal cord was harvested and prepared to histological and imunohistochemical analyses. RESULTS: There was an important hind limb motor function impairment initially in the 3 study groups, with partial improvement along time, but no difference was detected between groups during de observational period. Gray matter analysis showed scarce viable neurons and a marked cellular vacuolation in all three groups, but the number of viable neurons per section areas was not different between study groups at day 14th. Immunostaining of the spinal cord gray matter with antibodies anti-Bcl2 and anti-annexin V was similar among the 3 study groups. There was positive staining for the necrotic marker propidium iodide, with all groups presenting a similar staining pattern. CONCLUSION: We found that a single-dose administration of estradiol or of progesterone, 30 minutes before transitory occlusion of the proximal descending thoracic aorta of male rats, was not able to prevent spinal cord ischemic injury through analysis of functional and histological outcomes at 14 days of observation
Книги з теми "Myocardial reperfusion Complications Prevention"
A, Salerno Tomas, and Ricci Marco, eds. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.
Знайти повний текст джерелаS, Dhalla Naranjan, ed. Myocardial ischemia and preconditioning. Boston: Kluwer Academic, 2003.
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Знайти повний текст джерелаЧастини книг з теми "Myocardial reperfusion Complications Prevention"
Kuijt, Wichert J., Judson Williams, Christopher B. Granger, Mitchell W. Krucoff, and Matthew T. Roe. "Current Approaches to Prevention and Management of Reperfusion Injury." In Management of Myocardial Reperfusion Injury, 215–38. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9_10.
Повний текст джерелаHugenholtz, P. G., M. L. Simoons, P. W. Serruys, P. J. De Feyter, M. Van Den Brand, and P. Fioretti. "Late Results of Reperfusion with Intracoronary Streptokinase." In Secondary Prevention in Coronary Artery Disease and Myocardial Infarction, 315–26. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5024-5_33.
Повний текст джерелаRamrakha, Punit S., Kevin P. Moore, and Amir H. Sam. "Cardiac emergencies." In Oxford Handbook of Acute Medicine, 1–170. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198797425.003.0001.
Повний текст джерелаRabai, Ferenc, Michol A. Cooper, and Derek B. Covington. "Postoperative Management of Vascular Surgery Patients and Complications." In Vascular Anesthesia Procedures, 241–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197506073.003.0017.
Повний текст джерелаHollenberg, Steven M. "Management of Complications." In Reperfusion Therapy for Acute Myocardial Infarction, 280–99. Informa Healthcare, 2008. http://dx.doi.org/10.3109/9781420019179.017.
Повний текст джерелаMariani, Serena, Francesco Formica, and Giovanni Paolini. "Mechanical Complications of Myocardial Infarction." In Coronary Artery Disease - Assessment, Surgery, Prevention. InTech, 2015. http://dx.doi.org/10.5772/61373.
Повний текст джерелаVasa-Nicotera, Mariuca, and Tony Gershlick. "Stent thrombosis." In Oxford Textbook of Interventional Cardiology, 503–24. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.029.
Повний текст джерелаPuerto, Elena, and Héctor Bueno. "Mechanical complications of myocardial infarction." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 513–30. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0041.
Повний текст джерелаPizarro, Gonzalo, Rodrigo Fernández-Jiménez, and Borja Ibanez. "Prevention of Microvascular Obstruction by Addressing Ischemia Reperfusion Injury—Part B." In Coronary Microvascular Obstruction in Acute Myocardial Infarction, 277–93. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-812528-1.00016-6.
Повний текст джерелаStiermaier, Thomas, Ingo Eitel, Domenico D’Amario, and Giampaolo Niccoli. "Prevention of Coronary Microvascular Obstruction by Addressing Ischemia Reperfusion Injury—Part A." In Coronary Microvascular Obstruction in Acute Myocardial Infarction, 255–76. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-812528-1.00015-4.
Повний текст джерелаТези доповідей конференцій з теми "Myocardial reperfusion Complications Prevention"
Egbring, R., C. Bethge, A. Behling, and R. A. Seitz. "ANTITHROMBIN III (AT III) REPLACEMENT FOR THE PREVENTION OF REOCCLUSION AFTER INTRACORONARY THROMBOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643677.
Повний текст джерелаMilazzotto, F., M. Carelli, C. Citone, G. Di Macro Tullio, G. C. Gambelli, P. Giampaolo, U. Malinconico, C. Polizzi, and U. Cornelli. "EFFECTIVENESS OF DEFIBROTIDE IN THE TREATMENT OF ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643146.
Повний текст джерелаAnderson, J., R. Rothbard, R. Hackworthy, S. Sorensen, P. Fitzpatrick, and V. Harder. "COMPARISON OF INTRAVENOUS ANISOYLATED PLASMINOGEN STREPTOKINASE ACTIVATOR COMPLEX (APSAC) AND INTRACORONARY STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643621.
Повний текст джерелаSchmitz-Huebner, U., H. Ostermann, D. G. Mathey, J. Schofer, Ch Diefenbach, and R. Erbel. "INFLUENCE OF RECOMBINANT PRO-UROKINASE ON THE HEMOSTATIC SYSTEM IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643572.
Повний текст джерелаLoerakker, Sandra, Anke Stekelenburg, Gustav J. Strijkers, Klaas Nicolay, Dan L. Bader, Frank P. T. Baaijens, and Cees W. J. Oomens. "Effect of Continuous and Intermittent Mechanical Loading on the Development of Skeletal Muscle Damage - A Combined Experimental/Numerical Approach." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206354.
Повний текст джерелаLiebert, Ann. "Translational research in the prevention of myocardial reperfusion injury by PBM: a review of molecular mechanisms and current research results (Conference Presentation)." In Mechanisms of Photobiomodulation Therapy XIII, edited by Michael R. Hamblin, James D. Carroll, and Praveen Arany. SPIE, 2018. http://dx.doi.org/10.1117/12.2292128.
Повний текст джерелаPoniewierski, M., M. Barthels, and H. Poliwoda. "THE SAFETY AND EFFICACY OF A LOW MOLECULAR WEIGHT HEPARIN (FRAGMIN) IN THE PREVENTION OF DEEP VEIN THROMBOSIS IN MEDICAL PATIENTS: A RANDOMIZED DOUBLE-BLIND TRIAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643224.
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