| Seawater is a distinct injurious agent for trauma victim because sea water has special characterization such as hyperosmosis, hypersaline and hypothermia. The course of a trauma might develop differently when the injury is complicated by sea water immersion. Jiyao Yu et al, experts of sea war injury, have carried out studies on pathophysiological characteristics of various common trauma accompany with seawater immersion, and have put forward the early treatment principle. However, there was few reports focus on the molecular mechanism of human body's physiological function injury induced by seawater immersion. To realize scientific treatment of trauma victim, molecular mechanism of injury by seawater immersion is an important topic in medical support at sea.Endothelium cell is a kind of tissue cell widely existed in human body, with special clinical significance in maintenance blood flow state, regulating vascular tone and material exchange in body, preventing the platelet aggregation and thrombosis. The recent studies showed that vascular endothelium is not only the protective layer situated between the blood circulation and tissues, and also possesses metabolic as well as endocrine functions. Therefore, vascular endothelium injury has a tight link in many diseases development.The present study is to investigate the effects of sea water immersion on the functional in vascular endothelial cells, and to observe the relative changes in blood coagulation and angiogenesis. In order to reveal the molecular mechanism of pathologic progression of injury with sea water immersion.To establish open abdominal injured rat model and experimental conditions survival of the rats with open abdominal injury when immersed to 10℃,15℃,22℃,26℃or 33℃normal saline or seawater were observed. After the injury both with or without immersion, the expression levels of the functional genes in vascular endothelial cells of small intestinal mesentery were analyzed by real-time quantitative PCR-array. According to the qPCR-array results, coagulation index in blood of the rats with open abdominal injury were examined after immersed in sea water for various hours. Migrations of ECV304 cells and on blood vessel formation of transplantable tumors of nude mice were observed to study angiogenesis changes induced by seawater immersion.The main results are as follows:1. In the same temperature, the survival time of groups with open abdominal injury and seawater immersion were markedly shortened than groups with open abdominal injury alone and groups with normal saline immersion. When suffered with seawater immersion, survival time of rats with open abdominal injury was longer in 15℃and 22℃environment exposure than 10℃,26℃and 33℃. These results indicated that seawater immersion is one of the primary lethal factors in open abdominal injured rats. Not only extreme cold environment (10℃) exposure but also relative high temperature (such as 33℃close to normal body temperature) exposure may increase the mortality of rats with open abdominal injury and seawater immersion. Effect of temperature to injure with sea water is complicated.2. Compared with that of the rats in simple open abdominal injury group, the expression levels were markedly changed in 65 of a total of 84 functional genes (77.38%) in the vascular endothelial cells from small intestinal mesentery of the rats in open abdominal injury + sea water immersion group, including 52 genes (61.90%) up-regulated and 13 genes (15.48%) down-regulated. The array results showed that, in the expression levels of functional genes of vascular endothelial cells, the expression level of chemokine (C-X-C motif) ligand 2 was elevated by 29.82 folds, and that of L-selectin declined by 46.59 folds, respectively. And the expression levels of genes concerning thrombin activity and angiogenesis changed most significant. These results indicated that the seawater immersion maybe injury the functional in vascular endothelial cells.3. Comparing to rats with open abdominal injury alone, the parameters of blood coagulation in the rats with open abdominal injury and sea water immersion were quite different. Prothrombin time of rats with open abdominal and sea water immersion was longer, showed that activated intrinsic pathway of coagulation; and partial thromboplastin time was shorter, showed that inhibited extrinsic coagulation pathway. And plasma fibrinogen was lower, further showed that activated coagulation system in early period of seawater immersion. Levels of plasminogen and D-dimer in plasma were elevated after seawater immersion for two hours, indicate that in late period of immersion, the injury rats were trend to suffering with disseminated intravascular coagulation.4. By the cells scratch wound experiment, introducing normal morphology of ECV304 cells in seawater immersion was changed and migration ability of cells was depressed. ECV304 cells scratch recovery on seawater immersion was delayed with the time. Indicating that seawater immersion may depress the migration ability of vascular endothelial cell. By observe vessels surrounding EC0156 cell transplantation tumor of nude mice, that the vessels surrounding tumor in seawater were significantly less than in normal saline, and the tumor in seawater grew slowdown. Seawater inhibiting angiogenesis. Seawater immersion may injury the structure of vascular endothelial, and leads to vascular endothelial dysfunction.In conclusion, seawater immersion can causes extensively changes in the expression levels of functional genes of vascular endothelial cells, causing endothelial damage. Thus it may cause coagulation function disorder and angiogenesis inhibition. The illustration of the molecular mechanism that vascular endothelial injury influencing trauma progression by seawater immersion would contribute to know charictarization of trauma with seawater immersion, and provide theoretical basis for reasonable clinical treatments.
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