Literature DB >> 21909001

Hemoconcentration caused by microvascular dysfunction after blast injuries to the chest and abdomen of rabbits.

Bo Zhang1, Aimin Wang, Wei Hu, Liangchao Zhang, Yan Xiong, Jing Chen, Jianmin Wang.   

Abstract

BACKGROUND: One of the important causes of death after blast injuries is reduced blood volume, which typically results from hemorrhage but may also result from nonhemorrhagic causes. Hemoconcentration is one such alternate cause of reduced blood volume, but its mechanism is unclear. Because blood is condensed after chest-abdomen blast injuries in rabbits, a series of experiments was conducted to clarify this phenomenon.
METHODS: Chest-abdomen blast injuries from different distances (10 cm, 15 cm, 20 cm, and 30 cm) were induced in male rabbits. ¹²⁵I-albumin was injected into the blood, and its concentration in different organs was tested at various times after the blast injury. The residual radioactivity in different organs and the pre- and postinjury hematocrit was also tested. Histologic evaluations were conducted to detect the injuries to the different organs.
RESULTS: After injury, ¹²⁵I-albumin leaked out of the vessels into organs such as the lungs, liver, and kidneys. The volume of leakage was highly correlated with the distance from the blast. At a distance of 10 cm, the rate of leakage was the highest. The hematocrit was higher for 30 minutes and 3 hours after the injury; 6 hours after the injury, the hematocrit began to return to normal levels. The residual radioactivity of ¹²⁵I-albumin was increased in the heart, brain, lungs, and kidneys, especially at a distance of 10 cm. Histologic evaluation results showed that the cells, microvessels, and organelles of the microvessel endothelial cells in the vital organs, such as the kidneys, were damaged.
CONCLUSION: The preliminary results indicate that microvessels in the lungs and kidneys are the key targets of blast injuries. The damage to the microvessels leads to leakage of albumin, which is one of the important reasons for hemoconcentration in the absence of active bleeding after a blast injury. Treatment should be initiated in victims of blast injuries who are severely wounded as soon as possible after the explosion during the earliest stages of the injury to avoid the occurrence of shock or other severe complications.

Entities:  

Mesh:

Year:  2011        PMID: 21909001     DOI: 10.1097/TA.0b013e318224595f

Source DB:  PubMed          Journal:  J Trauma        ISSN: 0022-5282


  3 in total

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Authors:  Brandon P Lucke-Wold; Ryan C Turner; Aric Flint Logsdon; Charles L Rosen; Rabia Qaiser
Journal:  J Surg Emerg Med       Date:  2017-01-10

2.  Semimechanistic Modeling of the Effects of Blast Overpressure Exposure on Cefazolin Pharmacokinetics in Mice.

Authors:  Daniel J Selig; Geoffrey C Chin; Alexander G Bobrov; Jesse P DeLuca; Derese Getnet; Jeffrey R Livezey; Joseph B Long; Venkatasivasai S Sajja; Brett E Swierczewski; Stuart D Tyner; Vlado Antonic
Journal:  J Pharmacol Exp Ther       Date:  2021-08-25       Impact factor: 4.030

3.  Mechanisms of hearing loss after blast injury to the ear.

Authors:  Sung-Il Cho; Simon S Gao; Anping Xia; Rosalie Wang; Felipe T Salles; Patrick D Raphael; Homer Abaya; Jacqueline Wachtel; Jongmin Baek; David Jacobs; Matthew N Rasband; John S Oghalai
Journal:  PLoS One       Date:  2013-07-01       Impact factor: 3.240

  3 in total

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