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

Z̆unić, Gordana; Romic, Predrag; Vučeljić, Marina; Jovanikic, Olivera

doi:10.2298/vsp0504273z

Cited by 14 publications

(8 citation statements)

References 26 publications

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“…These data are in accord with previous studies that plasma markers of oxidative stress are upregulated following blast exposure in human patients. 18,19,32 Taken together these results suggest increased oxidative stress in the retina acutely following blast exposure. Identification of the molecular mechanisms underlying such early oxidative stress and their potential contribution to observed chronic deficits could generate targets for early therapeutic intervention.…”

Section: Discussionmentioning

confidence: 64%

“…17 In addition, plasma concentrations of markers of oxidative stress are increased in blast-exposed patients and may have adverse systemic effects. 18,19 In spite of growing clinical evidence supporting blast-induced visual dysfunction, a paucity of controlled experimental data precludes a complete understanding of how blast injury has an impact on the structure and function of the retina and optic nerve. The purpose of this study was to characterize the potential retina and optic nerve deficits in a reproducible Copyright 2013 The Association for Research in Vision and Ophthalmology, Inc. www.iovs.org j ISSN: 1552-5783 rodent model of blast injury using both functional and structural analysis measurements.…”

Section: Discussionmentioning

confidence: 99%

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Retinal Ganglion Cell Damage in an Experimental Rodent Model of Blast-Mediated Traumatic Brain Injury

Mohan

Kecova

Hernandez-Merino

et al. 2013

Invest. Ophthalmol. Vis. Sci.

115

161

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Retinal Ganglion Cell Damage in an Experimental Rodent Model of Blast-Mediated Traumatic Brain Injury

Mohan

Kecova

Hernandez-Merino

et al. 2013

Invest. Ophthalmol. Vis. Sci.

115

161

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“…Primary blast injury to the lungs result in a series of pathophysiological changes culminating in hypoxaemia [34]. In addition, there are a range of cardiovascular [35 -37] and microcirculatory [38] disturbances which may further compromise nutritative tissue blood flow. There was therefore a concern that a combination of the low tissue blood flow state inherent in hypotensive resuscitation might be compounded by poor arterial oxygenation leading to an overwhelmingly inadequate tissue oxygen delivery.…”

Section: Physiology Of Resuscitation After Combined Primary Blast Injury and Haemorrhagementioning

confidence: 99%

Blast injury research models

Kirkman

Watts

Cooper

2011

Phil. Trans. R. Soc. B

106

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Blast injuries are an increasing problem in both military and civilian practice. Primary blast injury to the lungs (blast lung) is found in a clinically significant proportion of casualties from explosions even in an open environment, and in a high proportion of severely injured casualties following explosions in confined spaces. Blast casualties also commonly suffer secondary and tertiary blast injuries resulting in significant blood loss. The presence of hypoxaemia owing to blast lung complicates the process of fluid resuscitation. Consequently, prolonged hypotensive resuscitation was found to be incompatible with survival after combined blast lung and haemorrhage. This article describes studies addressing new forward resuscitation strategies involving a hybrid blood pressure profile (initially hypotensive followed later by normotensive resuscitation) and the use of supplemental oxygen to increase survival and reduce physiological deterioration during prolonged resuscitation. Surprisingly, hypertonic saline dextran was found to be inferior to normal saline after combined blast injury and haemorrhage. New strategies have therefore been developed to address the needs of blast-injured casualties and are likely to be particularly useful under circumstances of enforced delayed evacuation to surgical care.

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“…The etiology of the hypotension seen after BLI is complex. Previous studies suggest that it is due to the absence of peripheral vasoconstriction [ 13 , 15 , 16 ] caused by inhibition of the sympathetic vasoconstrictor tone [ 26 , 27 ] or release of potent vasodilator nitric oxide [ 28 , 29 ]. However, few studies have documented the details of the hemodynamic response, especially regarding cardiac contractions and SVR, to catecholamine administration after blast lung injury.…”

Section: Discussionmentioning

confidence: 99%

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

Miyawaki

Saitoh

Hagisawa

et al. 2015

ICMx

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BackgroundBlast lung injuries (BLI) caused by blast waves are extremely critical in the prehospital setting, and hypotension is thought to be the main cause of death in such cases. The present study aimed to elucidate the pathophysiology of severe BLI using laser-induced shock wave (LISW) and identify the initial treatment.MethodsThe current investigation comprised two parts. For the validation study, mice were randomly allocated to groups that received a single shot of 1.2, 1.3, or 1.4 J/cm2 LISW to both lungs. The survival rates, systolic blood pressure (sBP), heart rate (HR), peripheral oxyhemoglobin saturation (SpO2), and shock index were monitored for 60 min, and lung tissues were analyzed histopathologically. The study evaluated the effects of catecholamines as follows. Randomly assigned mice received 1.4 J/cm2 LISW followed by the immediate intraperitoneal administration of dobutamine, noradrenalin, or normal saline. The primary outcome was the survival rate. Additionally, sBP, HR, SpO2, and the shock index were measured before and 5 and 10 min after LISW, and the cardiac output, left ventricular ejection fraction, and systemic vascular resistance (SVR) were determined before and 1 min after LISW.ResultsThe triad of BLI (hypotension, bradycardia, and hypoxemia) was evident immediately after LISW. The survival rates worsened with increasing doses of LISW (100 % in 1.2 J/cm2 vs. 60 % in 1.3 J/cm2, 10 % in 1.4 J/cm2). The histopathological findings were compatible with those of human BLI. The survival rate in LISW high group (1.4 J/cm2) was highest in the group that received noradrenalin (100 %), with significantly elevated SVR values (from 565 to 1451 dyn s/min5). In contrast, the survival rates in the dobutamine and normal saline groups were 40 and 10 %, respectively, and the SVR values did not change significantly after LISW in either group.ConclusionsThe main cause of death during the initial phase of severe BLI is hypotension due to the absence of peripheral vasoconstriction. Therefore, the immediate administration of noradrenalin may be an effective treatment during the initial phase of severe BLI.

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

Cited by 14 publications

References 26 publications

Retinal Ganglion Cell Damage in an Experimental Rodent Model of Blast-Mediated Traumatic Brain Injury

Retinal Ganglion Cell Damage in an Experimental Rodent Model of Blast-Mediated Traumatic Brain Injury

Blast injury research models

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

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