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Effects of thoracic cavity seawater immersion on vascular endothelial cells following open chest injury in dogs

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
Issue:
2
DOI:
10.3760/cma.j.issn.1009-6906.2010.02.006
Key Word:
海水浸泡;急性肺损伤;血管内皮细胞;胸部开放伤;Seawater immersion;Acute lung injury;Vascular endothelial cell;Open chestinjury

Abstract: Objective To investigate effects of thoracic cavity seawater immersion on vascular endothelial cells following open chest injury in dogs. Methods Twelve healthy hybrid dogs were randomly divided into 2 groups: group A, animals with open chest injury; group B, animals with thoracic cavity seawater immersion following open chest injury. Arterial gas analysis, plasma osmotic pressure and serum electrolytes were measured at different time points. Blood samples were collected to measure circulating endothelial cells (CEC), von Willebrand Factor (vWF), TXB_2, PGF_(1a), and endothelin (ET). Results Arterial oxygen partial pressure (PaO_2) and oxygenation indices for the animals of group A and group B decreased markedly after injury, then recovered gradually, while arterial oxygen partial pressure (PaO_2) for the animals of group B decreased progressively and oxygenation indices (PaO_2/FiO_2) were lower than 300 at hour 6 following injury, conforming with the diagnostic standards of acute lung injury (ALI) and high elevations were noted in Na~+, K~+, and hyperosmotic pressure. CEC and the concentrations of vWF, TXB_2 and ET increased significantly for animals in group B at hour 4 and 6 after injury, when compared with those before injury (P < 0.05). TXB_2 and ET at hour 4 and 6 after injury for the animals of group B were significantly higher than those of the animals of group A(P <0.05). No statistical differences could be seen in PGF_(1a), when compared with that of group A (P >0.05). Conclusions Thoracic cavity seawater immersion after open chest injury could activate the release of many vaso-active substances, induce lesion of vascular endothelial ceils, which might be involved in acute lung injury.

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