22 research outputs found

    The role of aldosterone inhibitors in cardiac ischemia–reperfusion injury

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    Myocardial ischaemia–reperfusion (I/R) injury is a well-known term for exacerbation of cellular destruction and dysfunction after the restoration of blood flow to a previously ischaemic heart. A vast number of studies that have demonstrated that the role of mineralocorticoids in cardiovascular diseases is based on the use of pharmacological mineralocorticoid receptor (MR) antagonists. This review paper aimed to summarize current knowledge on the effects of MR antagonists on myocardial I/R injury as well as postinfarction remodeling. Animal models, predominantly the Langendorff technique and left anterior descending coronary artery occlusion, have confirmed the potency of MR antagonists as preconditioning and postconditioning agents in limiting infarct size and postinfarction remodeling. Several preclinical studies in rodents have established and proved possible mechanisms of cardioprotection by MR antagonists, such as reduction of oxidative stress, reduction of inflammation, and apoptosis, therefore limiting the infarct zone. However, the results of some clinical trials are inconsistent, since they reported no benefit of MR antagonists in acute myocardial infarction. Due to this, further studies and the results of ongoing clinical trials regarding MR antagonist administration in patients with acute myocardial infarction are being awaited with great interest.This is the peer-reviewed version of the article: Dragasevic, N.; Jakovljevic, V.; Zivkovic, V.; Draginic, N.; Andjic, M.; Bolevich, S.; Jovic, S. The Role of Aldosterone Inhibitors in Cardiac Ischemia–Reperfusion Injury. Can. J. Physiol. Pharmacol. 2021, 99 (1), 18–29. [https://doi.org/10.1139/cjpp-2020-0276

    Показатели хемилюминесценции лейкоцитов у детей больных бронхиальной астмой, получавших ингаляции гиперкапнической гипоксической газовой смеси

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    The CO2 effect on phagocytal generation of reactive oxygen species was studied in 40 bronchial asthma infants obtaining therapy with hypercapnic hypoxic gas mixture (HHGM) inhalations. It was found that chemiluminescence intensity parameters were greater in that patients during the postattack period than in healthy infants. During the intermedia period, the parameters decreased but were significantly higher than in controls. The satisfactory leucocyte sensitivity to CO2 was found in 37.5% of patients, that well correlates with positive clinical effect. The lower effect from HHGM was noted in 62.5% of infants with the decreased reaction to CO2. The role of leukocytes in bronchoconstriction was shown.Изучено влияние СО2 на генерацию активных форм кислорода фагоцитами у больных бронхиальной астмой 40 детях, в лечении которых использовали ингаляции гиперкапнической гипоксической газовой смеси (ГГС). Выявлено, что в послеприступном периоде показатели интенсивности хемилюминесценции были вы ш е по сравнению с контрольной группой (здоровые дети). В межприступном периоде они снижаются, но превышаю т контрольные значения. Выялена у 37,5% больных хорошая чувствительность лейкоцитов к СО2, что хорош о коррелировало с клиническим положительным эффектом . У 62,5% детей со сниженной реакцией к СО2 отмечен меньший эффект от ГГС. Показана роль лейкоцитов в развитии бронхоконстрикции при бронхиальной астме у детей

    Use of perfluorocarbon based blood substitute perftoran in correction of hypoxia during acute anemia in animals [Upotreba zemene za krv zasnovane na perfluorokarbonu za korigovanje hipoksije tokom akutne anemije kod sisara]

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    The cause of acute and severe hypoxia of the organism is acute posthemorrhagic anemia. To eliminate posthemorrhagic anemia in animals, the perfluorocarbon blood substitute Perftoran (Russia) with a gas-transporting function was used. The aim of this study was to determine the clinical effectiveness of the perfluorocarbon based blood substitute Perftoran with a gas-carrying function in acute posthemorrhagic anemia in animals and reveal possible side effect of the blood substitute and remove them. In the study conducted in the Clinic of Veterinary Medicine of Pushchino Research Center (Russia) participated 20 cats of both sexes, who were admitted with internal bleeding as a result of injuries. The animals were divided into two groups: the control and the treatment groups (10 per group). All animals with anemia were examined according to the standard scheme: anamnesis vitae and anamnesis morbi, physical examination (basic methods of research were used), additional methods that were used: complete blood count (CBC) and biochemical analysis of blood (BA), microscopy of blood smears, abdominal ultrasonography. Based on the obtained results, we can conclude that the use of the gas-carrying substitute for donor blood Perftoran in the treatment group of animals with posthemorrhagic anemia, which resulted from polytrauma, eliminated tissue hypoxia; the treatment of the animals in the control group with standard solutions (by infusing Stabisol) without gas transport correction led to the development of persistent hypoxia, which persisted to the stage of reticulocyte crisis. © 2019, University of Kragujevac, Faculty of Science. All rights reserved

    Laboratory Tests in Diagnosis of Mastocytosis: Literature Review and Case Report

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    Мastocytosis is a heterogeneous group of disorders characterized by abnormal growth and accumulation of mast cells (MCs) in the skin and/or other organ systems. Mastocytosis is a rare disease. The annual incidence is 5-10 cases per 1 million people. However, the majority of cases stay undiagnosed due to the lack of specific tests and a wide variety of clinical features of the disease. In mastocytosis, somatic mutations of KIT gene lead to autocrine dysregulation and constitutive c-KIT activation in the absence of its ligand SCF. Clinical symptoms of the disease are determined by MC mediator release and/or infiltration of tissues by MCs. According to the World Health Organisation classification updated in 2016 mastocytosis is divided to cutaneous mastocytosis (CM), indolent systemic mastocytosis (ISM), smoldering systemic mastocytosis (SSM), SM with an associated hematologic (non-MC-lineage) neoplasm (SMAHN), aggressive SM (ASM), MC leukemia (MCL) and MC sarcoma (MCS). The CM and ISM prognosis is excellent with (almost) normal life expectancy, unlike aggressive forms (ASM and MCL) with poor prognosis. In this paper the key aspects of clinical features and diagnostic criteria of mastocytosis are discussed. We present a case report of a patient with mastocytosis in the skin following psoralen plus ultraviolet A (PUVA) therapy with good response

    Pituitary hyperplasia, hormonal changes and prolactinoma development in males exposed to estrogens—an insight from translational studies

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    © 2020 by the authors. Licensee MDPI, Basel, Switzerland. Estrogen signaling plays an important role in pituitary development and function. In sensitive rat or mice strains of both sexes, estrogen treatments promote lactotropic cell proliferation and induce the formation of pituitary adenomas (dominantly prolactin or growth-hormone-secreting ones). In male patients receiving estrogen, treatment does not necessarily result in pituitary hyperplasia, hyperprolactinemia or adenoma development. In this review, we comprehensively analyze the mechanisms of estrogen action upon their application in male animal models comparing it with available data in human subjects. Sex-specific molecular targets of estrogen action in lactotropic (PRL) cells are highlighted in the context of their proliferative and secretory activity. In addition, putative effects of estradiol on the cellular/tumor microenvironment and the contribution of postnatal pituitary progenitor/stem cells and transdifferentiation processes to prolactinoma development have been analyzed. Finally, estrogen-induced morphological and hormone-secreting changes in pituitary thyrotropic (TSH) and adrenocorticotropic (ACTH) cells are discussed, as well as the putative role of the thyroid and/or glucocorticoid hormones in prolactinoma development, based on the current scarce literature

    Влияние СО2 на генерацию активных форм кислорода лейкоцитами крови у больных бронхиальной астмой

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    The purpose of the study was to investigate the features of CO2 inhibiting action on leukocytal generation of reactive oxygen species (ROS) in patients with bronchial asthma (BA). Sixty patients with BA and 20 healthy donors were examined. The CO2 action on leukocytal generation of ROS was estimated by luminol dependent and lucinogen dependent chemiluminescent (CL) methods before and after the CO2 action of 5.1%, 8%, and 20%. It was found that CO2 inhibites significantly the leukocytal CL. However, this inhibiting influence on generation of ROS is decreased in patients with BA in the exacerbation phase in comparison with healthy donors. The influence does not differ from normal values in 30% of the patients. In the remission phase, the inhibiting influence of CO2 on leukocytal generation of ROS is repaired partly or completely. Thus, on the one hand, CO2 is included into the BA pathogenesis thru the decrease of inhibiting influence on generation of ROS, and, on the other hand, only 30% of BA patients are prescribed to be treated with increased CO2 concentration inhalations.Целью настроящего исследования явилось выяснение особенностей ингибирующего влияния СО2 на генерацию активных форм кислорода (АФК) лейкоцитами крови у больных бронхиальной астмой (БА). Для этого было обследовано 60 больных БА и 20 здоровых доноров. Влияние СО2 на генерацию АФК лейкоцитами определяли люминолзависимым и люцигенинзависимым хемилюминесцентным (ХЛ) методами до и после воздействия 5,1%, 8% и 20% СС>2. Было выявлено, что у здоровых доноров все три концентрации СО2 значительно ингибируют ХЛ лейкоцитов. Однако у больных БА в фазе обострения по сравнению со здоровыми донорами снижается ингибирующее влияние 5,1%, 8% и 20% СО2 на генерацию АФК лейкоцитами. У 30% больных БА оно не отличается от нормы. В фазе ремиссии ингибирующее влияние СО2на генерацию АФК лейкоцитами частично или полностью восстанавливается. Таким образом, с одной стороны, СО2 включается в патогенез БА через снижения ингибирующего влияния на генерацию АФК лейкоцитами, а с другой — всего 30% больным БА показано лечение повышенными концентрациями СО2
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