1998
DOI: 10.1016/s1078-5884(98)80089-0
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Neutrophil sequestration in the lung following acute aortic occlusion starts during ischaemia and can be attenuated by tumour necrosis factor and nitric oxide blockade

Abstract: Acute lung injury resulting from distal aortic occlusion starts during ischaemia. TNF and NO blockade decrease PMN chemotaxis and sequestration and attenuate the lung injury process.

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Cited by 26 publications
(12 citation statements)
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“…NO then modulates cell migration on a two-dimensional surface as well as cell migration through three-dimensional matrix, as encountered in the extraluminal environment of the vessel or in the soft tissue adjacent to a wound. In a rat model of acute lung injury, NOS blockade led to decreased polymorphic neutrophils (PMN) transmigration (Tassiopoulos et al, 1998). These data are consistent with our finding that NO enhances transendothelial cell migration of monocytes across a stimulated monolayer of endothelial cells.…”
Section: Cellular Responses To Nitric Oxidesupporting
confidence: 90%
“…NO then modulates cell migration on a two-dimensional surface as well as cell migration through three-dimensional matrix, as encountered in the extraluminal environment of the vessel or in the soft tissue adjacent to a wound. In a rat model of acute lung injury, NOS blockade led to decreased polymorphic neutrophils (PMN) transmigration (Tassiopoulos et al, 1998). These data are consistent with our finding that NO enhances transendothelial cell migration of monocytes across a stimulated monolayer of endothelial cells.…”
Section: Cellular Responses To Nitric Oxidesupporting
confidence: 90%
“…Various reperfusion techniques have been developed to modify or prevent the reperfusion damage, such as the limb washout technique using a roller pump [37], axillo-bifemoral grafting with intermittent perfusion of the lower limbs to control subsequent hyperkalemia [40], or the use of an oxygenator to reperfuse ischemic tissue [48]. In addition, numerous pathophysiological mechanisms and pharmacological treatments have been advocated for the management of reperfusion injury after acute limb ischemia, including steroids, lazaroids, barbiturates, papaverine, pentoxifylline, leukocyte-antibodies and radical scavenger just to mention a few [4,8,10,14,16,[20][21][22]24,32,33,39,44]. However, a stable reperfusion protocol has not evolved and the treatment of ischemiaperfusion of the lower limbs still consists in surgical revascularization, fasciotomy, excision of primary necrotic tissue, increase of urine output with urine alkalinization, treatment of hyperkalemia and, recently, the development of interventional treatment, e.g., for aortic saddle thrombus consisting in angioplasty and streptokinase 1 application [2,25].…”
Section: Discussionmentioning
confidence: 99%
“…Peroxynitrite has cytotoxic potential through reactions with protein and non-protein sulphydryls, oxidation of lipids, nitrosation of tyrosine and induction of single-strand breaks in DNA [32,33]. However, studies have also shown that NO may promote the chemotactic potential of neutrophils [34][35][36][37] and stimulate the production of proinflammatory agents [36].…”
Section: Discussionmentioning
confidence: 99%