Effect of Glycine on the Microcirculation in Rat Mesenteric Vessels

Podoprigora, G. I.; Nartsissov, Yaroslav R.

doi:10.1007/s10517-009-0498-y

Cited by 10 publications

(8 citation statements)

References 11 publications

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“…Несмотря на то что результаты исследований моделей ишемии головного мозга на животных указывают на важ-ную роль оксидантного стресса при реперфузион-ном повреждении, доказательства реперфузионного повреждения при инсульте у человека ограниченны. В некоторых исследованиях с применением магнит-но-резонансной томографии (МРТ) при инсульте у человека с использованием режима с подавлением сигнала свободной воды (FLAIR) и перфузионно-взвешенной МРТ (ПВ-МРТ) было показано, как реперфузия может быть связана с ранним повышени-ем проницаемости гематоэнцефалического барьера и, следовательно, с вторичным реперфузионным по-вреждением и неблагоприятным исходом [9,10].…”

Section: Study Limitationsunclassified

“…As an example in human stroke, some MRI studies using fluid-attenuated inversion recovery and perfusion-weighted images have shown how reperfusion could be linked to an early opening of the blood-brain barrier and consequently to secondary reperfusion injury and poor outcome. 9,10 ROS generated during ischemia/reperfusion can react with unsaturated lipids of biomembranes, thereby generating malondialdehyde (MDA), an end-product of lipid peroxidation. MDA could be a biomarker of tissue injury and reflect oxidative damage; indeed, several studies have shown increased MDA concentrations in acute stroke patients.…”

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confidence: 99%

“…Примечательно, что поскольку существует про-странственное распределение внешних условий и уровня метаболитов вокруг ишемического очага [8], различные вмешательства, корректирующие метабо-лизм нейронов, должны быть разнесены во времени в зависимости от предполагаемой зоны воздействия. Тем не менее применение метаболической терапии может быть наиболее эффективным именно на ран-них стадиях ишемии [9,10].…”

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Oxidative Stress After Thrombolysis-Induced Reperfusion in Human Stroke

Domı́nguez

Delgado

Vilches

et al. 2010

Stroke

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Background and Purpose-Animal models of transient ischemia suggest that oxygen-derived free radicals produced on reperfusion of ischemic brain could constitute the main cause of reperfusion injury. We aimed to determine the presence and role of lipid peroxidation and protein oxidation-related molecules after tissue plasminogen activator-induced recanalization in human stroke. Methods-A total of 160 patients with strokes involving the middle cerebral artery and treated with tissue plasminogen activator and 60 healthy controls were included. Blood samples, transcranial Doppler recordings, and National Institutes of Health Stroke Scale scores were obtained at baseline (pretreatment), 1 hour and 2 hours after tissue plasminogen activator bolus, and 12 hours and 24 hours after stroke onset. The main lipid peroxidation end-product malondialdehyde, advanced oxidation protein products, and plasma concentrations of myeloperoxidase were assessed. Results-At baseline, all oxidative stress biomarkers were higher than in control subjects (PϽ0.01 for all comparisons).Malondialdehyde remained high compared with controls during the study period, whereas myeloperoxidase concentrations were significantly raised at baseline, 1 hour after tissue plasminogen activator administration, and 12 hours after stroke onset. Malondialdehyde concentrations correlated with stroke severity and were associated with outcome and with hemorrhagic complications. Regarding recanalization, among those patients with middle cerebral artery recanalization by the end of tissue plasminogen activator infusion (44%) or anytime thereafter, no peaking of any of the studied molecules could be identified. Conclusions-Our study showed that systemic oxidative damage to lipids and proteins had already occurred at baseline in stroke. In contrast to animal studies, a relationship between free radical-mediated oxidative damage to lipids or proteins and reperfusion injury after arterial recanalization could not be established. (Stroke. 2010;41:653-660.)Key Words: stroke Ⅲ thrombolysis Ⅲ oxidative stress Ⅲ MDA Ⅲ AOPPs Ⅲ MPO O xidative stress, resulting from an imbalance in redox state in which pro-oxidants overwhelm antioxidant capacity, has emerged as a potential mechanism implicated in the pathogenesis and disease progression of many unrelated pathological processes, including cardiovascular diseases, cancer, and diabetes, and may therefore contribute significantly to disease mechanisms; 1 however, increased oxidative stress may also result from pathological processes. 2 Reactive oxygen species (ROS) are continuously generated in the body as a consequence of aerobic metabolism or as part of the body's defense against microorganisms. ROS are highly reactive to any or all molecular targets: lipids, proteins, nucleic acids, or carbohydrates, 1 modifying their chemical structure and generating oxidation-derived products, markers of biomolecular oxidative damage. 3 Increased ROS production has been demonstrated in ischemic stroke, both during ischemia and reperfusion, o...

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Section: Study Limitationsunclassified

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Oxidative Stress After Thrombolysis-Induced Reperfusion in Human Stroke

Domı́nguez

Delgado

Vilches

et al. 2010

Stroke

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“…The fi rst studies demonstrated microcirculatory effect of glycine solution on mesenteric microvessels and on pial arterioles in laboratory rats [4][5][6]. A capacity of glycine to restore impaired microcirculation in the arterioles of the rat mesenterium under histamine induced infl ammatory alterations was shown revealing it's great, but little studied yet, antiinfl ammatory potential [5]. Effect of glycine on pial arterioles has been performed by using the original direct biomicroscopy with "open window" technique [6].…”

Section: Introductionmentioning

confidence: 99%

“…One of the tests used for an assessment of Glycine direct vasodilatory effect is an intravital biomicroscopy of pial microvessels in a brain of laboratory rats. The fi rst studies demonstrated microcirculatory effect of glycine solution on mesenteric microvessels and on pial arterioles in laboratory rats [4][5][6] …”

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Vasodilatory Effect of the Dissolved Glycine locally applied on Pial Microvessels

Es¹,

Ev²,

Yr³

et al. 2017

Ann Circ

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By the method of biomicroscopy it was shown that a single application of a dissolved glycine on the parietal region of the rat brain ("open window" technique) leads to a vasodilatation -an increase in arteriolar diameter about 1.5-2 times. There were no changes in the microcirculation when saline applied under similar conditions. It was also shown that there were no pH effects on the microvessels. For the testing of the vasodilatory effect of glycine in arteriol spastic conditions the adrenomimetic phenylephrine hydrochloride possessing the vasoconstrictor properties has been used as an agent for ischemic stroke modeling. Further work on the development of an adequate ischemic stroke models is the prospective task for the testing of antiischemic preparations. Research Article Vasodilatory Effect of the Dissolved IntroductionIn recent years, the increasing prevalence of ischemic diseases affecting the vitally important organs especially those of cardiovascular and central nervous system is observed. Ischemic brain injury is accompanied by the severe neurological disorders, such as cognitive deterioration, dysfunction of motor, verbal and other CNS functions. Stroke ranks fi rst among the causes of persistent disability. Correcting the imbalance of excitatory and inhibitory neurotransmitter systems is one of the most promising areas of neuroprotection and therapeutic target. Attention of researchers is attracted to a role of inhibitory neurotransmitter glycine in the mechanisms of acute cerebral ischemia [1]. The widespread use of the drug "Glycine" in patients with neurological disorders, as well as clinical observation of the positive therapeutic effect of the drug in ischemic stroke [2,3], suggest the existence of one or more fundamental biological mechanisms responsible for the neuroprotective effect of the amino acid at the molecular level. Since one of the important pathogenic mechanisms leading to the development of an ischemic stroke is a disturbance of blood supply to the brain, the effect of any drug that is expected to have clinical benefi t should be assessed in terms of possible normalization of microcirculation. One of the tests used for an assessment of Glycine direct vasodilatory effect is an intravital biomicroscopy of pial microvessels in a brain of laboratory rats. The fi rst studies demonstrated microcirculatory effect of glycine solution on mesenteric microvessels and on pial arterioles in laboratory rats [4][5][6]

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