Scope of Wounds

Crabtree, Thomas G.

doi:10.5435/00124635-200600001-00017

Cited by 6 publications

(3 citation statements)

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“…This was first observed in the 1960s when animals receiving aminoglycosides appeared to be more susceptible to noise-induced hearing loss [11] and confirmed by subsequent studies [12], [13], [14], [15]. The same ototoxic mechanism is likely responsible for the increased deafness risk in pre-term infants from neonatal intensive care units [16], [17] and in wounded soldiers [18], [19], [20], [21], [22]. Multiple cochlear events may be responsible for sound-and-drug induced synergy.…”

Section: Introductionmentioning

confidence: 78%

“…However, this is not always possible, e.g., prior exposure to blasts and explosions followed by wound treatment with aminoglycosides in war zones [18], [19], [20], [21], [22]; or chronic exposure to moderate sound levels and aminoglycosides by pre-term infants in intensive care units [16]. Therefore, it is critical to understand how sound exposure can enhance the unwanted ototoxic side-effects of the clinically-indispensable aminoglycosides.…”

Section: Discussionmentioning

confidence: 99%

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Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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BackgroundExposure to intense sound or high doses of aminoglycoside antibiotics can increase hearing thresholds, induce cochlear dysfunction, disrupt hair cell morphology and promote hair cell death, leading to permanent hearing loss. When the two insults are combined, synergistic ototoxicity occurs, exacerbating cochlear vulnerability to sound exposure. The underlying mechanism of this synergism remains unknown. In this study, we tested the hypothesis that sound exposure enhances the intra-cochlear trafficking of aminoglycosides, such as gentamicin, leading to increased hair cell uptake of aminoglycosides and subsequent ototoxicity.MethodsJuvenile C57Bl/6 mice were exposed to moderate or intense sound levels, while fluorescently-conjugated or native gentamicin was administered concurrently or following sound exposure. Drug uptake was then examined in cochlear tissues by confocal microscopy.ResultsProlonged sound exposure that induced temporary threshold shifts increased gentamicin uptake by cochlear hair cells, and increased gentamicin permeation across the strial blood-labyrinth barrier. Enhanced intra-cochlear trafficking and hair cell uptake of gentamicin also occurred when prolonged sound, and subsequent aminoglycoside exposure were temporally separated, confirming previous observations. Acute, concurrent sound exposure did not increase cochlear uptake of aminoglycosides.ConclusionsProlonged, moderate sound exposures enhanced intra-cochlear aminoglycoside trafficking into the stria vascularis and hair cells. Changes in strial and/or hair cell physiology and integrity due to acoustic overstimulation could increase hair cell uptake of gentamicin, and may represent one mechanism of synergistic ototoxicity.

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Section: Introductionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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“…8 An open tibia fracture caused by a blast mechanism would seem to be the least tolerant of local rotational coverage with the highest wound complications as a result of a large and evolving zone of injury. 9 We hypothesized that the open Type III B and III C tibia fractures from Operation Iraqi Freedom and Operation Enduring Freedom would have a higher complication rate when treated with rotational versus free soft tissue coverage. Between March 2003 and September 2007, 193 patients with 213 Gustilo and Anderson Type III open diaphyseal tibia fractures were treated at our three institutions.…”

Section: Introductionmentioning

confidence: 99%