Literature DB >> 15889591

Very early increase in nitric oxide formation and oxidative cell damage associated with the reduction of tissue oxygenation is a trait of blast casualties.

Gordana Zunić1, Predrag Romić, Marina Vueljić, Olivera Jovanikić.   

Abstract

BACKGROUND: In our previous experimental studies, we found evidence for the increase of nitric oxide (NO) formation immediately after blast injury. In the present study we investigated whether NO overproduction was a trait for the period immediately after blast injury in humans. Concomitant metabolic disturbances were also studied, and compared to the alterations in other traumatized patients.
METHODS: Blast casualties (group B, n = 13), surgical patients with the hip replacement or fractures, not exposed to blast effects (group S, n = 7) and healthy volunteers as controls (group C, n = 10), were examined. Both arterial and venous blood samples were taken within 6 hours, and 24 hours after blast injuries or surgical procedures, respectively. Plasma levels of nitrite/nitrate (NOx), superoxyde anion (O2-), sulfhydrils (SH), malondialdehyde (MDA) as well as acid-base status and other biochemical parameters (glucose, urea, creatinine, total proteins, albumin) were measured.
RESULTS: Significant, but transient increase in plasma NOx levels occurred only in group B. It was associated with the significant increase of hemoglobin oxygen (sO2) saturation of the venous blood and the concomitant decrease of its arterial--venous difference. In group S the venous sO2 decreased, its arterial--venous difference increased, while NOx levels were within the control limits. In both groups, other parameters of arterial acid-base status were kept within the control limits throughout the examined period. The decrease of SH levels were similar in the examined groups, while the increase of O2- was greater in group B.
CONCLUSION: Early NO overproduction was a trait of blast injuries in humans, contributing to the reduction of tissue the oxygenation and intensifying the oxidative cell damage that had to be considered in the therapy of casualties with blast injuries. These alterations were different from those observed in other surgical patients without blast injuries.

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Year:  2005        PMID: 15889591     DOI: 10.2298/vsp0504273z

Source DB:  PubMed          Journal:  Vojnosanit Pregl        ISSN: 0042-8450            Impact factor:   0.168


  4 in total

1.  Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury.

Authors:  Kabhilan Mohan; Helga Kecova; Elena Hernandez-Merino; Randy H Kardon; Matthew M Harper
Journal:  Invest Ophthalmol Vis Sci       Date:  2013-05-15       Impact factor: 4.799

Review 2.  Blast injury research models.

Authors:  E Kirkman; S Watts; G Cooper
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2011-01-27       Impact factor: 6.237

Review 3.  Characterization of the response to primary blast injury.

Authors:  E Kirkman; S Watts
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2011-01-27       Impact factor: 6.237

4.  Noradrenalin effectively rescues mice from blast lung injury caused by laser-induced shock waves.

Authors:  Hiroki Miyawaki; Daizoh Saitoh; Kohsuke Hagisawa; Midori Noguchi; Shunichi Sato; Manabu Kinoshita; Hiromi Miyazaki; Yasushi Satoh; Nahoko Harada; Toshihisa Sakamoto
Journal:  Intensive Care Med Exp       Date:  2015-12-10
  4 in total

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