Neutrophil-mediated microvascular dysfunction in postischemic canine skeletal muscle. Role of granulocyte adherence.

Carden, Donna L.; Smith, Jessica; Korthuis, Ronald J.

doi:10.1161/01.res.66.5.1436

Cited by 205 publications

(98 citation statements)

References 31 publications

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“…37,38 A strong argument that supports this hypothesis are the neutrophil depletion or CD11/CD18 blocking experiments that have been shown to attenuate vascular injury under inflammatory and ischemia-reperfusion conditions. [38][39][40][41] However, when microvascular permeability was measured simultaneously with leukocyte-endothelial interactions, local plasma leakage sites were distinct from those of leukocyte adhesion or transmigration. 4,5,[42][43][44][45] Moreover, several studies have shown that the timing of leukocyte adhesion and transmigration are not well correlated with the evoked permeability change during acute inflammation.…”

Section: Leukocyte Extravasation and Vascular Permeabilitymentioning

confidence: 99%

Leukocyte transendothelial migration: A local affair

2016

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Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens. It serves as a protective response that involves leukocytes, blood vessels and molecular mediators with the purpose to eliminate the initial cause of cell injury and to initiate tissue repair. Inflammation is tightly regulated by the body and is associated with transient crossing of leukocytes through the blood vessel wall, a process called transendothelial migration (TEM) or diapedesis. TEM is a close collaboration between leukocytes on one hand and the endothelium on the other. Limiting vascular leakage during TEM but also when the leukocyte has crossed the endothelium is essential for maintaining vascular homeostasis. Although many details have been uncovered during the recent years, the molecular mechanisms from the vascular part that drive TEM still shows significant gaps in our understanding. This review will focus on the local signals that are induced in the endothelium that regulate leukocyte TEM and simultaneous preservation of endothelial barrier function.

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Section: Leukocyte Extravasation and Vascular Permeabilitymentioning

confidence: 99%

Leukocyte transendothelial migration: A local affair

2016

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“…However, the ability of neutrophils and macrophages to induce injury in other cells in vitro [10][11][12] suggests that these early stages of muscle inflammation may also involve damage to muscle fibers caused by the invading cells. This possibility is supported by the ability of neutrophils to induce skeletal muscle injury during tissue reperfusion after ischemia [13,14].…”

Section: Introductionmentioning

confidence: 98%

Nitric oxide synthase inhibition reduces muscle inflammation and necrosis in modified muscle use

Pizza

Hernandez

Tidball

1998

Journal of Leukocyte Biology

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The objective of this study was to determine the role of nitric oxide in muscle inflammation, fiber necrosis, and apoptosis of inflammatory cells in vivo. The effects of nitric oxide synthase (NOS) inhibition on the concentrations of neutrophils, ED1 ؉ and ED2 ؉ macrophages, apoptotic inflammatory cells, and necrotic muscle fibers in rats subjected to 10 days of hindlimb unloading and 2 days of reloading were determined. Administration of NOS inhibitor N -nitro-L-arginine methyl ester (L-NAME) significantly reduced the concentrations of neutrophils, ED1 ؉ and ED2 ؉ macrophages, and necrotic fibers in soleus muscle relative to water-treated controls. The concentration of apoptotic inflammatory cells was also significantly lower for L-NAME-treated animals compared with watertreated controls. However, the proportion of the inflammatory cell population that was apoptotic did not differ between L-NAME-treated and control animals, suggesting that L-NAME treatment did not decrease inflammatory cell populations by increasing the frequency of apoptosis. Thus, nitric oxide or one of its intermediates promotes muscle inflammation and fiber necrosis during modified muscle use and plays no more than a minor role in the resolution of muscle inflammation by inducing apoptosis of inflammatory cells.

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“…When activated, PMNs increase in size and stiffness, which facilitates their trapping in alveolar capillaries and precapillary vessels (14,40,41). This may contribute to the no-reflow phenomenon, wherein a tissue fails to reperfuse despite restoration of adequate perfusion pressures (42)(43)(44). Current optimal clinical pulmonary preservation strategies, which consist of hypothermic lung storage in an electrolyte solution with no form of reperfusion therapy (45), miss the chance to mitigate deleterious PMN-endothelial adhesive interactions.…”

Section: Discussionmentioning

confidence: 99%

Failure to express the P-selectin gene or P-selectin blockade confers early pulmonary protection after lung ischemia or transplantation

Naka

Toda

Kayano

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Endothelial P-selectin expression contributes to the first wave of neutrophil (polymorphonuclear leukocyte; PMN) inf lux in several inf lammatory conditions. Although remote tissue ischemia, such as a crush injury to the hindlimb, may result in P-selectin-mediated pulmonary leukosequestration, it is not known whether the lungs exhibit a similar response after hypothermic preservation or when subjected to a direct ischemic insult. To determine if P-selectin may mediate early primary graft failure, left lungs harvested from male Lewis rats were preserved for 6 hr at 4؇C and transplanted orthotopically into isogeneic recipients. Recipients immunodepleted of PMNs before transplantation demonstrated improved graft function; pulmonary vascular resistance was reduced Ϸ6-fold, arterial oxygenation was increased Ϸ3-fold, and recipient survival was increased Ϸ4-fold (P < 0.05, 0.05, and 0.005, respectively). Administration of a blocking anti-P-selectin IgG 10 min before reperfusion diminished graft PMN infiltration and resulted in improved graft function and recipient survival compared with controls. To establish the role of P-selectin in normothermic pulmonary ischemia, mice were subjected to temporary left pulmonary artery ligation. After functional removal of the nonischemic right lung, mice deletionally mutant for the P-selectin gene (Pselectin ؊͞؊) exhibited reduced PMN infiltration (Ϸ2-fold), improved arterial oxygenation (Ϸ2-fold), and improved survival (Ϸ3-fold) compared with P-selectin ؉͞؉ control mice (P < 0.05, 0.01, and 0.05, respectively). These studies isolate and identify the central role of a single gene product (Pselectin) in early PMN recruitment and tissue injury after frank pulmonary ischemia and in the setting of lung transplantation after hypothermic preservation.

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Neutrophil-mediated microvascular dysfunction in postischemic canine skeletal muscle. Role of granulocyte adherence.

Cited by 205 publications

References 31 publications

Leukocyte transendothelial migration: A local affair

Leukocyte transendothelial migration: A local affair

Nitric oxide synthase inhibition reduces muscle inflammation and necrosis in modified muscle use

Failure to express the P-selectin gene or P-selectin blockade confers early pulmonary protection after lung ischemia or transplantation

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