Ischemia/Reperfusion-Induced Leukocyte-Endothelial Interactions in Postcapillary Venules

Mj, Eppihimer; Granger, D. N.

doi:10.1097/00024382-199707000-00004

Cited by 112 publications

(72 citation statements)

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“…When Fe 2+ or other transition metals are present and CAT activity is decreased (as in this study), H 2 O 2 is reduced to a very highly oxidizing OH radical. The OH radical cannot be enzymatically detached from cells, but a free radical scavenger may detoxify it (7)(8)(9)(10). Additionally in our study, CAT activity was significantly increased with administration of vitamins C and E.…”

Section: Discussionsupporting

confidence: 53%

“…I/R is the main cause of posttraumatic organ deficiency in these disciplines (7). Holding of white blood cells to the surrounding capillary endothelium is a critical pathophysiologic stage, regardless of the type of the I/R injury (8,9). As a result of adherence to endothelial cells, the neutrophils release proteases and oxygen radicals (10), which damages the endothelial layer.…”

Section: Introductionmentioning

confidence: 99%

“…However, in situations such as oxidative stress, where ROS production is out of control, damage to biomolecules such as protein, DNA, RNA, and lipids and cell structures is very likely (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Sirmali¹,

Armağan²,

Öktem³

et al. 2015

Turk J Med Sci

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Background/aim: To compare the protective efficacy of erdosteine and vitamins C and E against renal injury caused by hind limb ischemia-reperfusion (I/R).Materials and methods: Rats were split into 4 groups: group I as the control, group II as I/R, group III as I/R + erdosteine, and group IV as I/R + vitamins C and E. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) tissue levels were determined.Results: MDA levels were found comparable with the control group in groups II and III. However, they were considerably decreased in group IV when compared to group II (P < 0.01). Additionally, SOD, CAT, and GSH-Px activities were considerably (P < 0.05) decreased in group II. While CAT and GSH-Px activities were restored (P < 0.01) by vitamin E and C treatment, SOD activity was not significantly affected. While GSH-Px activities were higher (P < 0.05) with erdosteine administration, SOD and CAT activities were unchanged. Conclusion:The protective effect of vitamins C and E is higher than that of erdosteine treatment in reducing the oxidative stress after renal ischemia in this animal model.

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

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Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Sirmali¹,

Armağan²,

Öktem³

et al. 2015

Turk J Med Sci

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“…9,10,[12][13][14][15][16][19][20][21][32][33][34][35] Infiltrating neutrophils have been implicated as key mediators of I-R injury associated with numerous organs, including the intestine, heart, brain, skeletal muscle, and liver. 21,[36][37][38][39] The neutrophil is thought to have a central role, given the evidence that neutrophil elimination with vinblastin or blocking of neutrophil activity with mAb appears to be cytoprotective in the setting of I-R. 20,21 Our central hypothesis therefore was that RES dysfunction after I-R also was neutrophil dependent, at least to some degree.…”

Section: Discussionmentioning

confidence: 99%

“…A major component of I-R injury is caused by the generation of reactive oxygen intermediates (ROIs) and consequent neutrophil accumulation and activation, which induces secondary endothelial cell injury. [9][10][11] Studies have shown that leukocyte accumulation is a critical determinant of hepatic I-R injury, [12][13][14][15][16] and P-selectin has an important role in leukocyte adhesion after hepatic I-R. 15,16 The leukocyte-endothelial cell interaction that occurs after I-R injury has been shown to be a causative factor in the development of microvascular dysfunction and release of such cytotoxic mediators as ROIs and a variety of proteases. 10,[17][18][19] The importance of neutrophils in this pathophysiologic process is emphasized by the observation that neutropenia (induced with vinblastin and/or an antineutrophil monoclonal antibody [mAb]) results in markedly decreased hepatic cell damage after I-R. 20,21 Alterations in hepatic RES function have been variably modulated under conditions of cold or warm I-R. Caldwell-Kenkel et al 22 reported increased KC activity after cold I-R. 23 Rao et al 23 suggested that the reperfusion injury to the liver that occurs after cold ischemic preservation damages endothelial cells and activates KCs, which, in turn, initate a self-perpetuating injury pathway).…”

mentioning

confidence: 99%

Hepatic reticuloendothelial system dysfunction after ischemia-reperfusion: Role of P-selectin-mediated neutrophil accumulation

Sakamoto

2003

Liver Transplantation

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The relationship between hepatic ischemia-reperfusion (I-R) and subsequent injury through neutrophil accumulation is well described. Although alterations in reticuloendothelial system (RES) function (specifically Kupffer cell function) after I-R have been delineated, the degree to which discrete components of RES function (phagocytosis and killing) are independently modulated under these conditions has not been quantified. A hepatic segmental I-R model was established in mice, in which blood supply to the left lateral lobe of the liver was occluded for 45 minutes, the liver was reperfused, and the laparotomy incision was closed. Experimental animals were pretreated with either vinblastin (1.5 mg/kg) to induce neutropenia or anti-P-selectin monoclonal antibody (mAb; 50 g/mice) 4 days and 5 minutes before ischemia, respectively. We previously reported that after intravenous injection of chromium 51 ( 51 Cr) and iodine 125 ( 125 I) double-labeled Escherichia coli, hepatic 51 Cr levels could be used to reliably quantify hepatic phagocytic clearance (HPC) of bacteria from blood, whereas the subsequent release of 125 I from the liver accurately paralleled hepatic bacterial killing efficiency (HKE). Using this double-label bacteria clearance assay, HPC and HKE were depressed after I-R, in association with hepatic neutrophil accumulation. Segmental I-R resulted in decreased HPC and HKE activity in both ischemic and nonischemic hepatic lobes. Depressions in HPC and HKE were attenuated by either vinblastin-induced neutropenia or blocking neutrophil adhesion to the hepatic endothelium with anti-Pselectin mAb. These findings support the hypothesis that I-R induces hepatic RES dysfunction, at least in part, through P-selectin-mediated neutrophil accumulation. The liver is the principle anatomic site of RES activity and is responsible for approximately 80% of total-body RES function. 2 During the past three decades, liver transplantation has evolved from an experimental attempt to salvage desperately ill patients dying of liver failure to preferred definitive therapy for a defined population of patients with acute or chronic liver disease. Despite advancements in preoperative, intraoperative, and postoperative patient management and refinements in immunosuppressive protocols that have resulted in improved patient survival, postoperative sepsis has been documented in the majority of liver recipients. 3 Infection remains the predominant cause of posttransplantation morbidity and mortality. [4][5][6] The risk for infectious complications after liver transplantation has been reported to be between 50% and 83%. 4-7 Proportionally, the incidence of septic events seems to be greater than in recipients of other types of transplanted organs (i.e., kidney or heart) who undergo similar or often more intensive regimens of systemic immunosuppression.We previously reported that hepatic RES function, quantified by the liver's capacity to phagocytose and kill circulating bacteria or fungi, is altered after liver transplantation in the rat. 7...

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The apoptosis of blood polymorphonuclear leukocytes in sickle cell disease

Özdoğu¹,

Boğa²,

Sozer³

et al. 2006

Cytometry Part B Clinical

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Background: The apoptosis of human polymorphonuclear leukocytes (PMNs) in patients with sickle cell disease (SCD) is not well understood. The goal of this study was to examine the apoptosis of PMNs in patients with SCD and in controls.Methods: Flow cytometric quantitation of PMN apoptosis was performed in 17 patients during and after sickle cell vasoocclusive crisis and in 17 healthy volunteers. Plasma nitric oxide concentrations were also measured in patients with SCD.Results: The mean of annexin-V and annexin-V/PI staining (early and late apoptotic cells) increased to a greater degree in patients with SCD than in healthy controls for patients with SCD during and after vasoocclusive crisis. The mean of PI staining showing dead cells was higher only in patients after SCD crisis than in healthy controls. In the SCD groups during and after vasoocclusive crisis, there was no difference between PMN apoptosis levels. Furthermore, plasma nitric oxide concentrations were not correlated with PMN apoptosis.Conclusions: There was an evidence that the alteration of blood PMN apoptosis could contribute to the pathogenetic mechanisms of vasoocclusion in patients with SCD. This can be attributed to the effects of numerous inflammatory mediators rather than simply the effects of nitric oxide. q 2006 International

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Ischemia/Reperfusion-Induced Leukocyte-Endothelial Interactions in Postcapillary Venules

Cited by 112 publications

References 0 publications

Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Hepatic reticuloendothelial system dysfunction after ischemia-reperfusion: Role of P-selectin-mediated neutrophil accumulation

The apoptosis of blood polymorphonuclear leukocytes in sickle cell disease

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