Relevant bibliographies by topics / Modello ischemia in vitro

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Academic literature on the topic 'Modello ischemia in vitro'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Modello ischemia in vitro"

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Pelliccioli, G. P., P. F. Ottaviano, C. Gambelunghe, G. Mariucci, G. Bruschelli, G. Bartoli, and M. V. Ambrosini. "Ischemia cerebrale sperimentale nei gerbillo." Rivista di Neuroradiologia 6, no. 3 (August 1993): 325–30. http://dx.doi.org/10.1177/197140099300600313.

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Il gerbillo (Meriones unguiculatus), avendo il circolo di Willis incompleto per la mancanza delle arterie comunicanti, è considerato il modello animale di elezione per lo studio dell'ischemia cerebrale. L'assenza di connessioni tra circolo carotideo e vertebro-basilare garantisce infatti l'induzione di un'ischemia cerebrale mediante occlusione delle arterie carotidi comuni (ACC). È stata osservata tuttavia una certa variabilità nel sistema vascolare cerebrale del gerbillo, che spiegherebbe la differente risposta individuale alla legatura delle ACC. In letteratura sono stati descritti i deficit funzionali e le modificazioni comportamentali secondari ad un'ischemia cerebrale, correlabili post mortem a definiti quadri istopatologici. Raramente sono stati applicati metodi certi di valutazione in vivo degli esiti di un'ischemia cerebrale sperimentale e/o dell'efficacia di eventuali interventi terapeutici. Un contributo alle indagini in vivo sull'ischemia cerebrale sperimentale potrebbe derivare dallo studio con risonanza magnetica. La nostra indagine ha avuto lo scopo di valutare alla RM, l'evoluzione e la gravità del danno prodotto nel gerbillo: a) dall'occlusione di entrambe le ACC per 5 mine (b) dalla legatura permanente di una ACC. Lo studio parenchimale ed angiografico è stato condotto utilizzando apparecchiature da 1,5 Tesla. Gli animali sono stati esaminati a tempi diversi dall'ischemia. L'iperintensità del segnale rilevata in alcuni casi con le sequenze spin echo a TR lungo a carico dell'ippocampo non era semprecorrelabile al tipo di ischemia indotta. In un 20% dei casi si è apprezzato un aumento di volume del sistema ventricolare, confermato dall'esame anatomo-patologico. Lo studio istologico ha dimostrato che l'aumento di intensità del segnale non era obbligatoriamente associato a severi danni del parenchima. I risultati di questo studio, seppure preliminare, sosterrebbero la validità della tecnica RM nello studio delle ischemie cerebrali sperimentali, poiché essa consente di individuare un edema nel tessuto ischemico anche in assenza di grave sofferenza e/o necrosi cellulare. Le differenti risposte del gerbillo all'ischemia cerebrale potrebbero essere dovute ad una variabilita sia anatomica che biologica.
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Visocchi, M., M. Meglio, D. Cabezas Cuevas, B. Cioni, P. Carducci, G. Mastroianni, T. Tartaglione, G. Di Lella, and C. Colosimo. "Sensibilità e specificità della RM in un nuovo modello di ictus ischemico acuto sperimentale «collaterale»." Rivista di Neuroradiologia 9, no. 1 (February 1996): 21–23. http://dx.doi.org/10.1177/197140099600900102.

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Al fine di valutare la precocità e la sensibilità diagnostica della RM, unitamente alla eventuale ripetibilità degli eventi, abbiamo voluto sperimentare un nuovo modello di ischemia, che abbiamo definito «collaterale», poichè secondaria ad occlusione di due o più vasi pre - Willisiani. Per l'analogia con il circolo cerebrale umano sono stati studiati 12 conigli albini New Zealand (4–5 Kg) che venivano sottoposti ad anestesia generale. Per tutta la durata dell'esperimento si procedeva al monito-raggio della pressione arteriosa sistemica media, della frequenza cardiaca del pH e dell'emogas. L'ischemia veniva indotta con tecnica microchirurgica in 8 animali mediante chiusura di entrambe le carotidi comuni al collo (durata da un minimo di 2 h ad un massimo di 24 h) ed in altri 4 mediante chiusura dei vasi epiaor-tici a livello dell'arco aortico (durata da un minimo di 2 h ad un massimo di 4h). L'animale veniva sacrifi-cato senza previa riperfusione. Veniva quindi eseguito in tutti gli animali uno studio RM. In un caso (#12) il danno non è stato valutabile per la scarsa qualità iconografica. In otto casi sono state chiaramente iden-tificate incostanti e sfumate immagini lesionali lineari e/o puntiformi, prevalentemente monolaterali e a sede variabile. In analogia con quanto dimostrato in alcuni modelli di ischemia «terminale» studiati con RM, nel nostro gruppo di animali il danno ischemico «collaterale» è già evidente entro le prime due ore sia con chiusure di entrambe le carotidi che dell'arco aortico. La povertà dei reperti ottenuti, la aspecificità degli stessi, forse legata ad una vulnerabilità selettiva al-Pipossia di alcune strutture cerebrali mesiali e la scarsa ripetibilità degli stessi, scoraggia l'impiego del modello in oggetto per uno studio sistematico sperimentale dell'ischemia e quindi dell'efficacia di trials tera-peutici, sebbene la stessa negatività dello studio RM non possa escludere completamente un danno ischemico neuronale.
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Chen, Timothy, and Gordana Vunjak-Novakovic. "In Vitro Models of Ischemia-Reperfusion Injury." Regenerative Engineering and Translational Medicine 4, no. 3 (May 11, 2018): 142–53. http://dx.doi.org/10.1007/s40883-018-0056-0.

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Dugan, Laura L., and Jeong-Sook Kim-Han. "Astrocyte Mitochondria in In Vitro Models of Ischemia." Journal of Bioenergetics and Biomembranes 36, no. 4 (August 2004): 317–21. http://dx.doi.org/10.1023/b:jobb.0000041761.61554.44.

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Lee, Won Hee, Sungkwon Kang, Pavlos P. Vlachos, and Yong Woo Lee. "A novel in vitro ischemia/reperfusion injury model." Archives of Pharmacal Research 32, no. 3 (March 2009): 421–29. http://dx.doi.org/10.1007/s12272-009-1316-9.

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Tanaka, E., S. Yasumoto, G. Hattori, S. Niiyama, S. Matsuyama, and H. Higashi. "Mechanisms Underlying the Depression of Evoked Fast EPSCs Following In Vitro Ischemia in Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 86, no. 3 (September 1, 2001): 1095–103. http://dx.doi.org/10.1152/jn.2001.86.3.1095.

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The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 ± 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 μM) did not change in amplitude during in vitro ischemia. In a normoxic medium, a pair of fast EPSCs was elicited by paired-pulse stimulation (40-ms interval), and the amplitude of the second fast EPSC increased to 156 ± 24% of the first EPSC amplitude. The ratio of paired-pulse facilitation (PPF ratio) increased during in vitro ischemia. Pretreatment of the slices with adenosine 1 (A1) receptor antagonist, 8-cyclopenthyltheophiline (8-CPT) antagonized the depression of the fast EPSCs, in a concentration-dependent manner: in the presence of 8-CPT (1–10 μM), the amplitude of the fast EPSCs decreased by only 20% of the control during in vitro ischemia. In addition, 8-CPT antagonized the enhancement of the PPF ratio during in vitro ischemia. A pair of presynaptic volleys and excitatory postsynaptic field potentials (fEPSPs) were extracellularly recorded in a proximal part of the stratum radiatum in the CA1 region. The PPF ratio for the fEPSPs also increased during in vitro ischemia. On the other hand, the amplitudes of the first and second presynaptic volley, which were abolished by TTX (0.5 μM), did not change during in vitro ischemia. The maximal slope of the Ca2+-dependent action potential of the CA3 neurons, which were evoked in the presence of 8-CPT (1 μM), nifedipine (20 μM), TTX (0.5 μM), and tetraethyl ammonium chloride (20 mM), decreased by 12 ± 6% of the control 4 min after the onset of in vitro ischemia. These results suggest that in vitro ischemia depresses the evoked fast EPSCs mainly via the presynaptic A1 receptors, and the remaining 8-CPT–resistant depression of the fast EPSCs is probably due to a direct inhibition of the Ca2+ influx to the axon terminals.
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Ke, Yong-Sheng, He-Gui Wang, De-Guo Wang, and Gen-Bao Zhang. "Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro." Canadian Journal of Physiology and Pharmacology 82, no. 6 (May 1, 2004): 402–8. http://dx.doi.org/10.1139/y04-041.

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Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na+-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K+-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts. Heart rate (HR), left ventricular developed pressure (LVDP), and its first derivative (±dp/dtmax) were recorded. The endoxin contents, intramitochondrial Ca2+ contents, and the Na+/K+-ATPase activity in myocardial tissues were measured. Myocardial damages were evaluated by electron microscopy. The endoxin and intramitochondrial Ca2+ contents in myocardial tissues were remarkably higher, myocardial membrane ATPase activity was remarkably lower, the cardiac function was significantly deteriorated, and myocardial morphological damages were severe in myocardial ischemia reperfusion group vs. control. Anti-digoxin antiserum (10, 30 mg/kg) caused a significant improvement in cardiac function (LVDP and ±dp/dtmax), Na+/K+-ATPase activity, and myocardial morphology, and caused a reduction of endoxin and intramitochondrial Ca2+ contents in myocardial tissues. In the present study, the endoxin antagonist, anti-digoxin antiserum, protected the myocardium against the damages induced by ischemia reperfusion in isolated rat hearts. The results suggest that endoxin might be one of main factors mediating myocardial ischemia reperfusion injury.Key words: endoxin, anti-digoxin antiserum, myocardial reperfusion injury, morphological evaluation, Na+/K+-exchanging ATPase.
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Joshi, Dhiraj, Hemanshu Patel, Daryll M. Baker, Xu Shiwen, David J. Abraham, and Janice C. Tsui. "Development of an in vitro model of myotube ischemia." Laboratory Investigation 91, no. 8 (May 23, 2011): 1241–52. http://dx.doi.org/10.1038/labinvest.2011.79.

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Richard, Marc J. P., Tarek M. Saleh, Bouchaib El Bahh, and Jeffrey A. Zidichouski. "A novel method for inducing focal ischemia in vitro." Journal of Neuroscience Methods 190, no. 1 (June 2010): 20–27. http://dx.doi.org/10.1016/j.jneumeth.2010.04.017.

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Maher, Pamela, and Anne Hanneken. "Flavonoids protect retinal ganglion cells from ischemia in vitro." Experimental Eye Research 86, no. 2 (February 2008): 366–74. http://dx.doi.org/10.1016/j.exer.2007.11.009.

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Dissertations / Theses on the topic "Modello ischemia in vitro"

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BRESCHI, GIAN LUCA. "STUDIO ANATOMICO E FUNZIONALE DELLA REGIONE DI PENOMBRA IN UN MODELLO DI ISCHEMIA IN VITRO." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/215236.

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ANATOMICAL AND FUNCTIONAL STUDY OF THE PENUMBRA REGION IN AN IN VITRO MODEL OF FOCAL CEREBRAL ISCHEMIA Experimental data have shown that the ischemic brain region is characterized by a highly damaged core surrounded by a rim of reversibly altered tissue, commonly referred to as the ischemic penumbra. The core region is characterized by a severely compromised CBF, whereas in the penumbra CBF is reduced but cellular metabolism is still preserved (Hossmann, 2008). One possible approach to identify core and penumbra is based on the evaluation of both metabolism and perfusion of the cerebral tissue. In principle, MRI could be utilized to solve this issue. Still, the significance of the MRI changes observed in the early phase of focal cerebral ischemia is a matter of discussion (Neumann-Hafelin et al., 2000; Kidwell et al., 2003; Rivers et al., 2006). Understanding the functional and structural correlates of MRI findings will help to characterize the pathological status of brain tissue that continuously change during the early few hours that follow an ischemic stroke. The model of the isolated brain facilitates these objectives because permits to induce a highly reproducible infarction by the simple ligation of the MCA and allows to perform multiple fine electrophysiological recordings before, during and after occlusion. In the guinea pig the medial cerebral artery (MCA) supplies the entire piriform cortex (PC), the Olfactory Tubercle (OT) is perfused, also, by collaterals of the anterior cerebral artery, especially in its medial part. This vascular condition puts the lateral Olfactory Tubercle (l-OT) as an area of watershed between the ischemic core and the normally perfused tissue. We analyzed and correlated neurophysiological, morphological and MRI changes induced by transient (30-60 minutes) and permanent occlusion of the medial cerebral artery (MCAo) in the isolated guinea pig brain. Multi-site extracellular recordings demonstrated prolonged ischemic depolarizations (ID) and the abolition of evoked responses in the piriform cortex served by MCA, but not in the olfactory tubercle, supplied by the anterior cerebral artery. Here evoked responses were transiently reduced and brief peri-infarctual depolarizations (PID) could be observed during the transient MCA occlusion. Diffusion weighted images performed on brains fixed 4 hours after transient ischemia and immunostaining for a microtubule-associated protein, MAP-2, showed overlapping changes due to acute brain injury, restricted to the piriform cortex. Our compared analysis of neurophysiological, MR and anatomical data demonstrate that DW-MRI sequences underestimate the extension of brain tissue damage induced by focal ischemia and do not include the area of PIDs generation, namely the penumbra region Hence the penumbra is a region that maintains the capability to be excited. Hypothetically the ionic imbalance successive to the ischemic condition may prelude to a seizure that is frequent consequence of a stroke. In a consecutive study we verified whether anoxic ischemia per se, without intracranial hemorrhagic complication and in the absence of blood-borne elements responsible for brain infarction, is able to induce early changes in excitability that may prelude to the generation of seizures, and, ultimately could prime epileptogenesis. We used the multimodal approach herein described to identify the penumbra region in the very acute post-ischemic phase. To evaluate the effect of ischemia on cortical excitability we focused on ventral cortical structures (PC and OT) that have been extensively analyzed in this preparation (Biella & de Curtis, 1995; Carriero et al., 2009). The major input to these olfactory-limbic regions is carried by the lateral olfactory tract (LOT) that originates from neurons in the olfactory bulb (Haberly & Price, 1978). LOT is supplied by the medial cerebral artery (MCA). Since we aimed at evaluating synaptic excitability changes that occur acutely after ischemia, we needed to preserve the LOT as source of stimulation to evoke field responses in the olfactory cortex. Therefore, we chose to perform permanent bilateral occlusion of the anterior cerebral arteries (ACAo). We recorded, in olfactory cortices, slow potentials and evoked responses using specific patterns of stimulation in order to evaluate excitability changes in the acute phase after ischemia. The ACAo induces a core area located in the shell of nucleus accumbens and a region of penumbra in the underlying olfactory cortices, where characteristic slow potential shifts (i.e PIDs), but no reduction of diffusion tensor MR signal and MAP-2 immunostaining (typical of ischemic core) were observed. Recording of responses evoked by low- and high-frequency stimulations of the lateral olfactory tract showed no excitability changes in the early hours that follow ischemia in the olfactory cortical areas supplied by ACA. The absence of early hyperexcitability changes in an isolated whole brain model of ischemia, strongly suggests that brain anoxia per se does not contribute to the generation of early seizures. These findings support the view that blood-borne events (such as hemorrhage and inflammation) may play a major role in early post-ischemic seizures.
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BACIGALUPPI, SUSANNA. "Ruolo e potenziale delle cellule progenitrici endoteliali nel vasospamo cerebrale." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/27113.

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Title: Role and potential of endothelial progenitor cells in cerebral vasospasm Abstract: Background and aim: Despite many treatment approaches, cerebral vasospasm and delayed ischemic neuronal damage (DIND) still represent a serious threat to patients with subarachnoid haemorrhage (SAH). Endothelial progenitor cells (EPC) have been involved as prognostic indicators in several vascular diseases and mesenchymal stem cells already have shown some benefits in ischemic injury. Aim of this study was to investigate the therapeutic potential of endothelial progenitor cells (EPC) and mesenchymal stem cells (MSC) in attenuating or preventing vasospasm and DIND in patients with SAH. Methods: Given the emergent role of DIND as a result of multifactorial hypoperfusion stress in the outcome of SAH patients, the efficacy of EPC and MSC in reducing neuronal damage has been evaluated in an in vitro model of ischemia, namely the oxygen glucose deprivation (OGD), on primary rat cortical neuronal cultures. Further, we tested in a clinical observational study SAH patients with and without vasospasm for different recruitment patterns of circulating EPC. To this purpose arterial blood samples were collected at various timepoints from admission to discharge of the patients. On these samples real-time quantitative PCR (RT-qPCR) was performed to detect gene expression relative to EPCs, since cytofluorimetric analysis appeared not sensitive enough to detect this rare cell population. Results: Though present results need further confirmation, in vitro it was observed that both MSC and EPC treatment through conditioned medium or co-culture in transwell- although with some differences - mediate a survival advantage for OGD stressed neurons. Furthermore stem cell mediated treatment showed efficacy even when applied 24 hours after OGD stress induction. RT-qPCR results from a small sample of SAH patients might indicate an early mobilization of EPC related gene expression in subjects that do not develop vasospasm with a peak around day 4, whereas the expression of these genes remain invariably low in patients that develop vasospasm as in controls not affected by SAH. Conclusions: MSCs and EPCs seem to have an important potential role in preventing DIND in vitro as well as EPC recruitment might associate with lack of vasospasm in SAH patients. Further studies are needed to confirm these results and to prove a causal relationship between EPCs and vasospasm protection.
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Tsang, Hing-wai, and 曾慶威. "In vitro studies of hypoxic ischemic down-regulated 1 (HID-1) protein encoded by a novel gene down-regulated in neonatal hypoxic-ischemicencephalopathy in different cell death paradigms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45608192.

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Barandier, Christine. "Potentiel thérapeutique du manganèse et de l'un de ses dérivés synthétiques sur le système cardiovasculaire." Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10238.

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Le present travail qui s'inscrit dans le cadre general des etudes consacrees a la protection pharmacologique des tissus cardiaque et vasculaire au cours de la reperfusion post-ischemique, comprend deux parties principales. La premiere a ete realisee sur un modele d'ischemie/reperfusion myocardique sur un modele experimental de coeur isole de rat. Les resultats sont exprimes en termes de donnees fonctionnelles, metaboliques et ultrastructurales. La seconde partie est une etude pharmacologique menee sur un modele d'anneaux d'aorte isolee de rat et comporte essentiellement des mesures de contractilite vasculaire. Dans la premiere partie, nous avons etudie l'effet protecteur du chlorure de manganese sur la recuperation post-ischemique du myocarde. Nous avons demontre que le manganese, administre durant la phase precoce de la reperfusion, ameliore la recuperation metabolique et fonctionnelle, vraisemblablement par le biais d'une protection antioxydante de la membrane des cardiomyocytes. Nous avons egalement mis en evidence un effet protecteur du manganese administre avant la periode d'ischemie sur la fonction et l'ultrastructure du myocarde post-ischemique. Dans la seconde partie de notre travail, nous avons montre qu'euk8, un compose de type salen-manganese presentant de fortes activites sod et catalase, exerce in vitro un effet vasorelaxant dose-dependant, non medie par une simple protection antioxydante de no, mais essentiellement du a une activation de l'adenylate cyclase et de la guanylate cyclase soluble des cellules musculaires lisses vasculaires. Enfin, une etude des effets vasomoteurs du manganese nous a amenes a conclure qu'il induit une relaxation par le biais de mecanismes plus complexes qu'une simple protection antioxydante de no et qu'un simple effet antagoniste calcique direct sur les cellules musculaires lisses vasculaires.
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Pocar, M. "Perfusione spinale retrograda selettiva durante ischemia da clampaggio aortico: modello sperimentale nel suino." Doctoral thesis, Università degli Studi di Milano, 2000. http://hdl.handle.net/2434/195626.

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BACKGROUND. Spinal cord damage represents a devastating complication of thoracic and thoracoabdominal aortic surgery. Retrograde perfusion as an alternative route to protect the spinal cord has recently been investigated with controversial results. MEHODS. Ten juvenile pigs were divided into control and study groups (A and B, respectively). Through a lateral thoracotomy the distal aortic arch was cannulated and connected to a cardiotomy reservoir. All animals underwent 40-minute single cross-clamping of the proximal descending aorta while keeping proximal systolic arterial pressure above 100 mmHg. In group B, normothermic arterial blood was delivered retrogradely through the azygos vein, maintaining perfusion pressure within 25-30 mmHg. Animals were allowed to recover to perform a primary neurologic evaluation. RESULTS. Flaccid paraplegia was uniformly observed in group A. In group B, all animals showed mild-to-moderate voluntary hind limb movements on awakening. Controls also showed urine incontinence short after cross-clamping, and this was not observed in group B. A different veno-arterial oxygen step-down was observed in blood collected from the excluded aorta in the two groups. CONCLUSIONS. Preliminary results indicate that controlled retrograde normothermic perfusion alone through the azygos system provides some degree of protection from spinal cord ischemia. Bladder dysfunction may represent a simple test to detect massive cord damage intraoperatively. Retrograde spinal cord perfusion warrants further investigation.
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Poignet, Hervé. "Activites pharmacologiques des antagonistes du calcium sur differents modeles physiopathologiques utilises dans l'ischemie cerebrale experimentale : effets sur les atteintes fonctionnelles et neuronales." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21111.

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SAKAMOTO, NOBUO, TATSUAKI MATSUBARA, YOSHIHIRO KAKINUMA, and TATSUO HASHIMOTO. "MYOCARDIAL METABOLIC MARKERS OF TOTAL ISCHEMIA IN VITRO." Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/15927.

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ZAMBAITI, ELISA. "Organoidi gastrointestinali pediatrici e fetali: modello di cultura tridimensionale in vitro." Doctoral thesis, Università degli studi di Padova, 2022. http://hdl.handle.net/11577/3447317.

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Obiettivi Il COVID-19 è una malattia principalmente respiratoria nell’età adulta; nei bambini, al contrario, i sintomi gastrointestinali sono più frequenti. Inoltre, non si conoscono i meccanismi di infezione in epoca fetale, epoca in cui i pazienti sono raramente colpiti da COVID-19. Gli organoidi sono uno strumento relativamente nuovo per stabilire in vitro colture di lunga durata che assomigliano tridimensionalmente al tessuto di origine e possono sia mantenere la staminalità che differenziarsi completamente in tutti i tipi di cellule. Abbiamo quindi mirato a sviluppare un sistema di coltura per organoidi gastrointestinali (GIO) per studiare l'infezione da SARS-CoV-2 nell'epitelio gastrico lungo tutta la durata della vita. Metodi I GIO sono stati derivati da feti di 8-21 settimane e da tessuti pediatrici e adulti. Sono stati coltivati utilizzando un terreno chimicamente definito, per testare la loro capacità di mantenere la forma e di differenziarsi completamente. GIO sono stati analizzati in correlazione all'ECM circostante. Gli organoidi sono stati quindi indotti a differenziarsi nella forma a polarità cellulare inversa (RP-GO) e quindi incubati con SARS-CoV-2. Tutti gli esperimenti sono stati analizzati mediante qPCR, immunofluorescenza e analisi qualitativa a seconda dei casi. Risultati Gli organoidi gastrointestinali possono essere isolati da tutte le età gestazionali, dimostrando la normale morfologia dell'epitelio gastrico ed esprimendo tipi di cellule mature, comprese le cellule della nicchia, del villo/ghiandola e di tipo enteroendocrino. Queste colture possono essere mantenute indefinitamente in vitro e coltivate in condizioni conformi alle indicazioni GMP. Gli RP-GO mostrano polarità apicale, esponendo ACE2 sulla superficie esterna, ottimizzando le condizioni per l'infezione virale. La nucleoproteina virale è stata dimostrata nelle cellule in fase di apoptosi, con gli RP-GO pediatrici più suscettibili ed infettati in modo efficiente rispetto agli organoidi fetali e adulti. Conclusioni Abbiamo stabilito con successo un efficiente sistema di coltura di organoidi gastrointestinali per tutte le età, dalla vita fetale all'età adulta. La tecnologia basata sugli organoidi può essere utilizzata per modelli di malattie in vitro, test sui farmaci o terapia cellulare. L'applicazione di regole conformi alle GMP rende la traduzione clinica più vicina.
Aims Adult COVID-19 is mainly respiratory illness, but in children GI symptoms are more frequent. Furthermore, fetuses are rarely affected by COVID-19. Organoids are a relatively new tool to in vitro establish long-living culture that three-dimensionally resemble the tissue of origin and may both maintain the stemness and fully differentiate in all cell types. As a proof of concept, we aimed to develop a culture system for gastrointestinal organoids (GIOs) to investigate SARS-CoV-2 infection in gastric epithelium across the lifespan. Methods GIO were derived from 8-21 week fetuses and from pediatric and adult tissues. They were cultured using chemically-defined medium, to test their ability to maintain stemness and to fully differentiate. GIO were analyzed in correlation to the surrounding ECM. Reverse cellular polarity Organoids (RP-GOs) were induced and incubated with SARS-CoV-2. All experiments were analyzed by qPCR, immunofluorescence and qualitative analysis as appropriate. Results Gastrointestinal organoids can be isolated from all gestational ages, demonstrating normal gastric epithelial morphology and expressing mature gastric cell types including, the niche, secretive, and enteroendocrine cells. These cultures may be maintained indefinitely in vitro and cultured in GMP-compliant conditions. RP-GOs exhibit apical-out polarity, exposing ACE2 on the external surface, optimizing conditions for viral infection. Viral nucleoprotein was demonstrated in cells undergoing apoptosis, with pediatric RP-GOs most susceptible and efficiently infected compared to fetal and adult organoids. Conclusions We have successfully established an efficient gastrointestinal organoid culture systems for all ages, from fetal life to adulthood. Organoid-based technology can be used for in vitro disease modelling, drug testing or cell therapy. The application of GMP compliant rules makes the clinical translation closer.
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Zwaini, Zinah Dheyaa Razzaq. "In vitro and in vivo models of renal ischemia reperfusion injury." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39344.

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Successful kidney transplantation is a life-saving procedure to patients with irreversible chronic renal failure. Despite the presence of various obstacles facing this surgery, preserving donor kidney and consequent ischemia reperfusion injury (IRI) are still major challenges affecting renal function as well as prognosis of transplant surgery. This study pursued two main aims: firstly, characterising changes in damage associated inflammatory gene expressions through developing, and analysis of an in vitro model of proximal tubular epithelial cells (PTEC) of normal human kidney mimicking renal IRI in vivo. The second aim was to simulate the concurrence of factors relevant to human intervention (renoprotective anaesthesia, peri- and postoperative analgesia, volume substitution) in mice deficient of properdin and congenic controls and to allow long-term observation of renal outcome after IRI. In this study, a reproducible and standardisable in vitro model was developed. It demonstrated the complexity of signalling where a multitude of factors affects the target cells. Secondly, the use of congenic properdin deficient mice showed that properdin has a significant role to play in renal injury (and recovery). There was significant impairment in renal function (and structure) compared to wildtype mice after IRI.
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Champattanachai, Voraratt. "Effects of hexosamine biosynthesis on an in vitro model of cardiac ischemia." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008d/champattanachai.pdf.

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Books on the topic "Modello ischemia in vitro"

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Drug Distribution in the Body: In Vitro Prediction and Physiological Interpretation/the Cat As an in Vivo Model for Myocardial Ischemia and Infarction ... in Pharmacology and Clinical Pharmacology). Vch Pub, 1989.

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Frantseva, Marina. Mechanisms of free radical formation and toxicity in an in vitro model of ischemia. 1999.

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Book chapters on the topic "Modello ischemia in vitro"

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Betz, E. L. "Inhibition of Atherogenesis In Vivo and In Vitro." In Cerebral Ischemia and Dementia, 77–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6_10.

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Waxham, M. N., S. A. Westgate, and M. D. Mauk. "In Vitro Ischemia in the Hippocampal Slice." In Cerebral Ischemia and Basic Mechanisms, 217–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_23.

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Fujiwara, Naoshi, Takashi Abe, Yoshiko Ebine, and Koki Shimoji. "Changes in Intracellular Ca2+ and pH of Hippocampal Slices in Response to Ischemia In Vitro." In Molecular Biology and Brain Ischemia, 115–27. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68467-1_8.

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Paakkari, I., R. Nevala, A. Peitola, and H. Vapaatalo. "Effect of Nitric Oxide Donors on Rat Bronchial Muscle in Vitro." In Mediators in the Cardiovascular System: Regional Ischemia, 207–11. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7346-8_30.

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Plesnila, N., E. Ringel, F. Staub, E. Stohr, C. C. Chang, and A. Baethmann. "In-Vitro Elucidation of Mechanisms Underlying Cell Swelling and Death of Nerve and Glial Cells." In Maturation Phenomenon in Cerebral Ischemia V, 167–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_16.

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Ryou, Myoung-gwi, and Robert T. Mallet. "An In Vitro Oxygen–Glucose Deprivation Model for Studying Ischemia–Reperfusion Injury of Neuronal Cells." In Methods in Molecular Biology, 229–35. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7526-6_18.

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Burke, Stephan P., and Charles P. Taylor. "Glutamale, Aspartate and Gaba Release from Hippocampal CA1 Slices During In Vitro Ischemia is Calcium-Independent." In The Role of Neurotransmitters in Brain Injury, 45–49. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3452-5_8.

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Urban, L., K. H. Neill, B. J. Crain, J. V. Nadler, and G. G. Somjen. "Effects of Transient Forebrain Ischemia in Area CA1 of the Gerbil Hippocampus: An in Vitro Study." In Excitatory Amino Acids and Neuronal Plasticity, 491–500. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_54.

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Produit-Zengaffinen, Nathalie, Tatiana Favez, Constantin J. Pournaras, and Daniel F. Schorderet. "JNK Inhibition Reduced Retinal Ganglion Cell Death after Ischemia/Reperfusion In Vivo and after Hypoxia In Vitro." In Retinal Degenerative Diseases, 677–83. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_90.

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Tanguy, Stéphane, Madhumathy Jeyaraman, Bradley W. Doble, Zhisheng Jiang, Robert R. Fandrich, and Elissavet Kardami. "Effects of Ischemia on Cardiomyocyte Connexin-43 Distribution and Phosphorylation Studied in in vivo and in vitro Models." In Pathophysiology of Cardiovascular Disease, 257–68. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4615-0453-5_19.

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Conference papers on the topic "Modello ischemia in vitro"

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Burmistrov, D. E., M. I. Krivonosov, T. A. Mishchenko, M. V. Ivanchenko, M. V. Vedunova, and E. V. Mitroshina. "Network features of consolidated astrocytic response in modeled ischemia-like conditions in vitro." In 2020 4th Scientific School on Dynamics of Complex Networks and their Application in Intellectual Robotics (DCNAIR). IEEE, 2020. http://dx.doi.org/10.1109/dcnair50402.2020.9216830.

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Korkmaz-Icöz, S., M. Schwär, S. Loganathan, K. Wächter, A. Sayour, P. Kraft, T. Mayer, et al. "Nutritional Extracts Protect Rats’ Vascular Grafts from In Vitro Ischemia/Reperfusion Injury." In 51st Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742851.

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Ding, Q., S. Loganathan, P. Brlecic, A. A. Sayour, M. Ruppert, T. Radovits, B. Korkmaz, M. Karck, G. Szabó, and S. Korkmaz-Icöz. "ALPHA-1-Antitrypsin Protects Vascular Grafts of Brain-Dead Rats against In Vitro Ischemia/Reperfusion Injury." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725680.

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Soethoff, J., S. Korkmaz-Icöz, G. Szabó, and G. Veres. "Comparison of Two Graft Storage Solutions (DuraGraft and TiProtec) in an In Vitro Model of Ischemia-Reperfusion Using Arterial Grafts." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705432.

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Xiao, Min, Annie Bailey, and Olga Pierrakos. "In-Vitro Modeling of Heart Failure in the Presence of a Prosthetic Heart Valve Using Particle Image Velocimetry." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53788.

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It is well-known that cardiovascular disease, affecting millions of people, is the number one killer in the US and worldwide. Current trends indicate that cardiovascular disease (CVD) will claim approximately 20 million victims in 2020 as the leading cause of death worldwide and will be responsible for over a billion deaths between 2000 and 2050 [1]. According to the American Heart Association, one in three American adults have one or more types of heart disease. Economically, the total and indirect costs due to cardiovascular diseases in 2009 were estimated at $475.3 billion. The spectrum of cardiac disease encompasses a broad range of disorders, varying from myocardial ischemia, valvular disease, diastolic dysfunction, congestive heart failure (which is projected to affect 20 million people by 2020), etc. Most of these disorders initiate and are associated to the left side of the heart, which is the workhorse and also the focus of our research herein.
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Korkmaz-Icöz, S., C. Kocer, A. A. Sayour, M. I. Benker, S. Abulizi, S. Loganathan, P. Brlecic, et al. "The Sodium-Glucose Cotransporter-2 Inhibitor Canagliflozin Alleviates Endothelial Dysfunction of Vascular Grafts Submitted to In-Vitro Ischemia/Reperfusion Injury in Nondiabetic Rats." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725601.

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Wallentin, Lars, Ingyar Nyman, ULF Berglund, and Eva Swahn. "HEPARIN AND ACETYLSALICYLIC ACID (ASA) 75 MG/DAY IN UNSTABLE CORONARY ARTERY DISEASE - EFFECTS ON PLATELET REACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643009.

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In unstable coronary artery disease (UCAD), i.e. unstable angina pectoris (UAP) or non-Q-myocardial infarction (NMI), treatment with heparin or ASA have given encouraging results. The present study attempts to verify the effects of i.v. heparin (5 days) and to evaluate the utility of ASA 75 mg/day (one year). Patients, admitted because of chest pain, who either develops NMI or signs of ischemia in resting or exercise ECG.s are included. Within 72 hours patients are randomized to obtain Heparin+ASA, Heparin+Placebo, Placebo + ASA or Placebo+Placebo . Platelet reactivity is studied in vitro in platelet rich plasma (PRP) in a subgroup of patients.The aggregation response is studied after addition of collagen and ADP and after preincubation with prostacyclin before aggregation with ADP. The figures present results from 85 randomized patients tested before, 5 days, one month and one year after start of therapy.Conclusion: In patients with unstable CAD long term treatment with ASA 75 mg/day inhibits collagen induced platelet aggregation and hampers the ADP response. I.v. heparin tends to raise platelet reactivity and reduce the inhibitory effect of prostacyclin. Heparin induced platelet activation is reduced by simultaneous ASA therapy.
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Alessandri, C., F. Violi, M. Rasura, C. Caliendo, and P. Pelaia. "BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643169.

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Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a neutrophil oxidase able to convert,in vitro, adrenaline to adrenochrome.Aim of present study was to evaluate if neutrophil activation can be observed in patients with brain hemor ragie (BH) also.Six patients (females 1,males 5;age 68-79 years) suffering from BH and 15 patients (females 5, Males 10;age 58-86 years) affected by brain infarction (BI) were studied within 20-48 hours from acute episode.Diagnosis of stroke was made by computerized tomography.Neutrophil activation was studied in plasma evaluating the oxidation of adrenaline to adrenochrome according to Matthews and Campbell method.20 matched for age and sex healthy subjects were studied as control.A significant rise of plasma adrenaline oxidase activity was observed in patients with BI.This preliminary investigation suggests that neutrophil activation could be restricted to patients with BI.In fact,patients with BH had plasma oxidase activity similar to controls.Clinical data should be necessary to evaluate if a relation between leucocyte activation and the natural course of cerebral ischemia does exist.
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Fayssal, Iyad, and Fadl Moukalled. "A Numerical Analysis of the Hemodynamic Functionality of Human Coronary Stenosis Under Different Physiologic Conditions and Boundary Condition Formulations." In ASME-JSME-KSME 2019 8th Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/ajkfluids2019-4820.

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Abstract Coronary artery disease (CAD) is among the foremost causes for human death worldwide. This study aims at investigating the performance of different boundary condition model types to characterize CAD functional significance. In addition, alternate models to estimate FFR using any different combination of boundary conditions at inlet and outlet were analyzed. In the first type of boundary condition, an outflow resistance model is used combined with a fixed pressure at inlet. In the second model of boundary conditions, constant pressure values are imposed at the domain inlet and outlet/s sections. In the third model, a zero diffusion flux is applied at outlet with a pre-specified flow rate at inlet. Numerical simulations performed on healthy and stenosed idealized and physiological arterial models revealed the superiority of the first type of boundary condition to directly capture the level of ischemia in diseased arteries. However, in this model, special numerical treatment at the outflow boundary is needed to dampen pseudo numerical reflections entering the computational domain. Alternative simple methods are developed to tackle the problem incurred in the second and third types of boundary condition types. The alternate models are effective for carrying extensive parametric studies with minimal computational effort. The new developed methods allow results generated via generic simulations under any specified boundary condition type to correctly estimate CAD functional significance. The obtained surrogate models account for the effects of the patient-specific physiologic parameters and can be easily incorporated without modifying existing CFD codes. Moreover, where it is unfeasible to experimentally incorporate the downstream effects of a given diseased arterial segment, an important aspect the alternative models provide is that they can be easily adopted by experimentalists through building in-vitro arterial models to assess the functional significance of the obstruction caused by the disease and its relation to any given patient specific physiologic parameter.
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Shatos, M., J. Doherty, D. Allen, and J. Hoak. "ALTERATIONS IN VASCULAR ENDOTHELIAL CELL FUNCTION BY OXYGEN-FREE RADICALS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643365.

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The vascular endothelium is a target for oxidant-induced damage in many disease states including hyperoxia, inflammation, ischemia and reperfusion injury. However, little is known concerning oxidant injury to endothelial cells and its relationship to hemostasis. Our studies have focused on the ability of oxygen free radicals to injure and/or alter selected vascular endothelial cell functions pertinent to the regulation of hemostasis. Xanthine and xanthine oxidase, a well-characterized generating system for the production of the superoxide anion radical (O− 2) was used to sublethally injure human umbilical vein endothelial cells (HUVE) in vitro. We examined the effects of a 15 min exposure of HUVE cells to xanthine (50μM), and xanthine oxidase (2.5-100mU) (previously determined to be non-toxic using trypan blue dye exclusion) on platelet adherence, and prostacyclin release using established assays. The antioxidant enzymes superoxide dismutase (SOD) 200μg/ml and catalase 50μg/ml were added to endothelium incubation systems to evaluate any protective effects upon O− 2-induced alterations. All experiments were conducted in a serum-free HEPES-Tyrode's buffer, pH 7.4 incubation system. Our results show that exposure of HUVE cells to sublethal concentrations of oxygen free radical generating systems causes significant enhancement of platelet adherence (65%) to injured endothelium. A 12-fold increase in prostacyclin release resulted after a 15 min treatment with xanthine and xanthine oxidase. The addition of exogenous PGI2 (150nM) to platelet-endothelial systems did not completely prevent the enhanced platelet adherence suggesting that lack of prostacyclin was not completely responsible for the adherence of platelets to O− 2 injured cells. When SOD and catalase, scavengers of O− 2 and H2O− 2, were added to treated cells, platelet adherence decreased by 42-77% and prostacyclin release approached that of control cultures. These data implicate an active participation of activated metabolites of molecular oxygen in the alteration of vascular endothelial cell function.
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