Kinetics of P-Selectin Expression in Regional Vascular Beds After Resuscitation of Hemorrhagic Shock: A Clue to the Mechanism of Multiple System Organ Failure

Fm, Akgür; Gb, Zibari; Jc, McDonald; Dn, Granger; Mf, Brown

doi:10.1097/00024382-200013020-00008

Cited by 16 publications

(12 citation statements)

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“…Body temperature was monitored and maintained at 37°C. After 3 h, mice were resuscitated with the shed blood plus a volume of lactated Ringer solution corresponding to 50% of the shed blood volume, which was infused with a syringe pump over 30 min (3,4). Adequacy of resuscitation was determined by the restoration of blood pressure.…”

Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lehnert¹,

Uehara²,

Bradford³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation. Am J Physiol Gastrointest Liver Physiol 291: G456 -G463, 2006. First published May 18, 2006 doi:10.1152/ajpgi.00480.2005.-Hemorrhagic shock and resuscitation cause endotoxemia and hepatocellular damage. Because lipopolysaccharide-binding protein (LBP) enhances cellular responses to endotoxin, our aim was to determine whether LBP contributes to hemorrhage/resuscitation-induced injury by comparing LBP knockout and wild-type mice. Under pentobarbital anaesthesia, wild-type and LBP-deficient mice were hemorrhaged to 30 mmHg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer solution. Serum alanine aminotransferase (ALT) necrosis, neutrophil infiltration, and 4-hydroxynonenal by histology/ cytochemistry and stress kinase activation by immunoblot analysis were then determined. ALT in wild-type mice was 2,461 Ϯ 383 and 1,418 Ϯ 194 IU/l (means Ϯ SE), respectively, at 2 and 6 h after resuscitation versus sham ALT of 102 Ϯ 6 IU/l. In LBP-deficient mice, ALT was blunted at both time points to 1,108 Ϯ 340 and 619 Ϯ 171 IU/l (P Ͻ 0.05). Liver necrosis after 6 h was also attenuated from 3.5 Ϯ 0.8% in wild-type mice to 1.3 Ϯ 0.5% in LBP-deficient mice (P Ͻ 0.05). After hemorrhage/resuscitation, neutrophil infiltration increased 71% more in wild-type than LBP knockout mice. Similarly, hepatic 4-hydroxynonenal staining, indicative of lipid peroxidation, decreased from 33.8 Ϯ 4.5% in wild-type mice to 11.6 Ϯ 1.9% in knockout mice (P Ͻ 0.05).

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Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lehnert¹,

Uehara²,

Bradford³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…P-Selectin expression in multiple organs displayed a dual peak following resuscitation of hemorrhagic shock; the first peak at 30 min and the second peak at 5 h [49]. The magnitude of the second peak was more striking compared with the first peak [49].…”

Section: Fig 1-continuedmentioning

confidence: 97%

“…Using a modification of this technique [48], we studied the time course of P-selectin expression after hemorrhagic shock [49]. P-Selectin expression in multiple organs displayed a dual peak following resuscitation of hemorrhagic shock; the first peak at 30 min and the second peak at 5 h [49]. The magnitude of the second peak was more striking compared with the first peak [49].…”

Section: Fig 1-continuedmentioning

confidence: 99%

Effects of Dextran and Pentoxifylline on Hemorrhagic Shock-Induced P-Selectin Expression

Akgür¹,

Zibari²,

McDonald³

et al. 1999

Journal of Surgical Research

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“…P-selectin is one of the first cell surface molecules to be expressed on the endothelial cell in response to inflammatory stimuli and triggers initial neutrophil rolling along the microvascular endothelium (1,10,23,25,31,38,46). Its expression on the endothelial cell luminal surface in response to circulating mediators such as thrombin is bimodal, with an early peak occur-ring within minutes and a late peak occurring after 4-6 h (1).…”

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confidence: 99%

Rapid upregulation of endothelial P-selectin expression via reactive oxygen species generation

Takano

Meneshian

Sheikh

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Rapid upregulation of endothelial P-selectin expression via reactive oxygen species generation. Am J Physiol Heart Circ Physiol 283: H2054-H2061, 2002. First published July 26, 2002 10.1152/ ajpheart.01011.2001.-Endothelial cell ICAM-1 upregulation in response to TNF-␣ is mediated in part by reactive oxygen species (ROS) generated by the endothelial membrane-associated NADPH oxidase and occurs maximally after 4 h as the synthesis of new protein is required. However, thrombin-stimulated P-selectin upregulation is bimodal, the first peak occurring within minutes. We hypothesize that this early peak, which results from the release of preformed P-selectin from within Weibel-Palade bodies, is mediated in part by ROS generated from the endothelial membraneassociated xanthine oxidase. We found that this rapid expression of P-selectin on the surface of endothelial cells was accompanied by qualitatively parallel increases in ROS generation. Both P-selectin expression and ROS generation were inhibited, dose dependently, by the exogenous administration of disparate cell-permeable antioxidants and also by the inhibition of either of the known membrane-associated ROSgenerating enzymes NADPH oxidase or xanthine oxidase. This rapid, posttranslational cell signaling response, mediated by ROS generated not only by the classical NADPH oxidase but also by xanthine oxidase, may well represent an important physiological trigger of the microvascular inflammatory response.

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Kinetics of P-Selectin Expression in Regional Vascular Beds After Resuscitation of Hemorrhagic Shock: A Clue to the Mechanism of Multiple System Organ Failure

Cited by 16 publications

References 0 publications

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Effects of Dextran and Pentoxifylline on Hemorrhagic Shock-Induced P-Selectin Expression

Rapid upregulation of endothelial P-selectin expression via reactive oxygen species generation

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