Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats.

The small intestine is an organ with very well developed immunological activity, responsible for synthesis of specific inflammatory mediators that participate in causing the systemic inflammation that can occur after ischemia-reperfusion injury. The aim of our work was to study mRNA expression and protein concentration of inflammatory cytokines IL-10 and TNFα in the jejunal wall after intestinal ischemia-reperfusion injury (IRI). Cytokine concentration levels confirmed the direct effect of IRI on the inflammation process.

Impact of alanyl-glutamine dipeptide on proliferative and inflammatory changes in jejunal mucosa after acute mesenteric ischemia.

Purpose: The aim of our study was to determinate the impact of dipeptide (alanyl-glutamine) administration on inflammatory and proliferative changes in jejunal mucosa after acute mesenteric ischemia.

Methods: Male Wistar rats (n=30) were divided into three groups: ischemia/reperfusion (IR) group which undergoes 60min of mesenteric ischemia and 1 or 24h of reperfusion (IR1, IR24, n=12). Groups with dipeptide administration (D+IR1, D+IR24, Dipeptiven con inf.

Immunohistochemical expression of MPO, CD163 and VEGF in inflammatory cells in acute respiratory distress syndrome: a case report.

Acute respiratory distress syndrome (ARDS) is a serious medical condition occurring in patients with polytrauma, pulmonary or non-pulmonary sepsis, pneumonia and many other circumstances. It causes inflammation of the lung parenchyma leading to impaired gas exchange with a systemic release of inflammatory mediators, causing consequential lung tissue injury, hypoxemia and frequently multiple organ failure. The aim of current study was to describe expression of inflammatory markers (myeloperoxidase, CD163 and vascular endothelial growth factor) by the cells in acute phase of ARDS.

Trehalase as a possible marker of intestinal ischemia--reperfusion injury.

Background: Different pathological affections of the small intestine cause corresponding morphological and functional changes. The present study was aimed to assess intestinal trehalase activities during ischemia and following reperfusion, correlate them with the pathological changes and determine whether trehalase could be used as a biochemical marker of the intestinal ischemia, ischemia - reperfusion injury.

Material And Methods: Wistar rats, randomly divided into 5 experimental groups (IR) (each n=15), were subjected to one hour mesenteric ischemia followed by 0, 1, 4, 12 and 24 hours of reperfusion.

Intravenous administration of tetramethylpyrazine reduces intestinal ischemia-reperfusion injury in rats.

Intestinal ischemia-reperfusion injury (IIRI) is a life-threatening condition requiring prompt medical intervention. Tetramethylpyrazine (TMP) is a biologically active alkaloid isolated from Ligusticum wallichii. Previously, it was shown that TMP causes vasodilatation and inhibition of platelet aggregation as well as exhibits significant antioxidant effects.

Immunohistochemical study of jejunal graft mucosa cell populations during the initial adaptation phase in the host body in rats.

The character of the changes in cell populations within the jejunal graft mucosa during the initial adaptation phase in the host body was investigated. 24 adult male Wistar rats underwent intestinal heterotopic allotransplantation. Aorto-aortal and porto-caval anastomoses were performed using the end-to-side microsurgery technique.

The relationship between morphology and disaccharidase activity in ischemia- reperfusion injured intestine.

Background: Questions regarding functional markers characterizing injured intestines remain unanswered. Brush border disaccharidases are crucial for the functioning of the intestines.

Aims: The study was designed to assess changes in disaccharidase activity (DA) following intestinal injury and to compare them with morphological changes.

Intestinal ischemia-reperfusion injury - the histopathological status of remote vital organs in acute and subacute phases.

Background: Improvement of graft recovery and function follows current trends in intestinal transplantation; however, the alteration of remote organs (RO) predicts complicated systemic rejection. This study was conceived to describe the histopathological status of RO arising in both acute and subacute stages after intestinal ischemia-reperfusion injury (IIR) injury.

Material/methods: Wistar rats (n=54) were divided into 7 experimental groups (n=7 each).

Mesenteric ischemia-reperfusion injury: specific impact on different cell populations within the jejunal wall in rats.

The progress of jejunal damage and recovery in the course of mesenteric ischemia-reperfusion injury in rats at different time periods was investigated. Mesenteric ischemia lasting 1h followed by 1h of reperfusion caused a significant disintegration of the mucosa, reduction of the muscular layer and diminution of the wall thickness. The loss of epithelium included enterocytes, goblet cells and Paneth cells.

Different ischemic preconditioning regimens affecting preservation injury of intestines.

Decreasing ischemia-reperfusion injury in intestinal transplantation is of paramount importance for improving graft recovery and function. This study explores the ability of two ischemic preconditioning (IPC) regimens to reduce preservation injury. Sprague-Dawley rats were divided into 3 groups (n = 11 each).

Morphological and apoptotic changes in the intestinal mucosa and lung parenchyma after ischaemic/reperfusion injury of the jejunum.

Ischaemic/reperfusion (IR) injury of the small intestine may lead to the development of multiple organ failure. Little is known about the morphological changes occurring in the organs during the subacute course of this syndrome. The objective of this study was to observe histopathological features and the role of apoptosis in the jejunal mucosa and lung parenchyma after intestinal IR injury in a long-term experiment.

Expression of adrenergic receptors in mouse preimplantation embryos and ovulated oocytes.

Epinephrine and norepinephrine can play an important role in basic developmental processes such as embryogenesis and morphogenesis, regulating cell proliferation, differentiation and migration. We showed that beta-adrenergic receptors can mediate the effects of catecholamines on preimplantation embryos in our previous work. In the present study, we designed specific oligonucleotide primers which can distinguish among all members of the alpha-adrenergic receptor family, and showed (using RT-PCR) that the alpha2C-adrenergic receptor is transcribed in ovulated oocytes, 8- to 16-cell morulae and expanded blastocysts.

Expression of beta adrenergic receptors in mouse oocytes and preimplantation embryos.

Accumulating evidence indicates the role of endogenous catecholamines in mammalian embryogenesis. We searched public databases containing nucleotide sequences derived from mouse preimplantation cDNA libraries and found a partial sequence homology between a cDNA clone from mouse blastocysts and the mouse beta 2-adrenergic receptor sequence. No significant sequence homology was found for other mouse adrenergic and dopamine receptors.

Serotonin localization and its functional significance during mouse preimplantation embryo development.

Serotonin is a neurotransmitter functioning also as a hormone and growth factor. To further investigate the biological role of serotonin during embryo development, we analysed serotonin localization as well as the expression of specific serotonin 5-HT1D receptor mRNA in mouse oocytes and preimplantation embryos. The functional significance of serotonin during the preimplantation period was examined by studying the effects of serotonin on mouse embryo development.