Role of Vascular Endothelial Cells in Disseminated Intravascular Coagulation Induced by Seawater Immersion in a Rat Trauma Model

Zhang, Dajin; Qu, Jia; Xiong, Ming; Qiao, Yuanyuan; Wei, Dapeng; Liu, Fengjiao; Li, Dandan; Hu, Ming; Zhang, Jiashu; Wang, Fuyu; Zhao, Xiulan; Shi, Chenxi

doi:10.1155/2017/5147532

Cited by 4 publications

(6 citation statements)

References 48 publications

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“…vWF is a co-mediator for during platelet aggregation at injured vessel walls. The down-regulation of vWF expression implied that vWF was consumed during the process of platelet aggregation (D. Zhang et al 2017).…”

Section: Discussionmentioning

confidence: 99%

Repeat dose exposure of PM2.5 triggers the disseminated intravascular coagulation (DIC) in SD rats

Liang

Zhao

et al. 2019

Science of The Total Environment

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Epidemiological evidence suggests that fine particulate matter (PM 2.5 ) in air pollution promotes the formation of deep venous thrombosis. However, no evidence is available on the effects of PM 2.5 lead to disseminated intravascular coagulation (DIC). For the first time, this study explored the effects of PM 2.5 on DIC via coagulation disorders in vivo . SD rats received intratracheal instillation of PM 2.5 once every three days for one month. Doppler ultrasound showed that the pulmonary valve (PV) and aortic valve (AV) peak flow were decreased after exposure to PM 2.5 . Fibrin deposition and bleeding were observed in lung tissue and vascular endothelial injury was found after exposure to PM 2.5 . Expression of thrombomodulin (TM) in vessel was downregulated after PM 2.5 -treated, whereas the levels of proinflammatory factors and adhesion molecules (IL-6, IL-1β, CRP, ICAM-1 and VCAM-1) were markedly elevated after exposure to PM 2.5 . Tissue factor (TF) and the coagulation factor of FXa were increased, while vWF was significantly lowered induced by PM 2.5 . Thrombin-antithrombin complex (TAT) and fibrinolytic factor (t-PA) were elevated, while there was no significantly change in the expression of anticoagulant factors (TFPI and AT-III). To clarify the relationship between PM 2.5 and DIC, we examined the general diagnostic indices of DIC: PM 2.5 prolonged PT and increased the expression of D-dimer but decreased platelet count and fibrinogen. In addition, the gene levels of JAK1 and STAT3 showed an upward trend, whereas there was little effect on JAK2 expression. And inflammatory factors (IL-6, IL-1β and TNF) in blood vessels of were up-reglated in PM 2.5 -treated rats. In summary, our results found that PM 2.5 could induce inflammatory response, vascular endothelial injury and prothrombotic state, eventually resulted in DIC. It will provide new evidence for a link between PM 2.5 and cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Repeat dose exposure of PM2.5 triggers the disseminated intravascular coagulation (DIC) in SD rats

Liang

Zhao

et al. 2019

Science of The Total Environment

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“…Various kinds of animals have been tried as DIC models in experiments, but the model using rats is the most reported. The DIC rat model expresses the symptoms of DIC using endotoxin, trauma, sepsis, bacteria, scorpion venom, viper venom, and other substances [ 23 , 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

Attempt to Develop Rat Disseminated Intravascular Coagulation Model Using Yamakagashi (Rhabdophis tigrinus) Venom Injection

Yamamoto

Ito

Hifumi

2021

Toxins

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Disseminated intravascular coagulation, a severe clinical condition caused by an underlying disease, involves a markedly continuous and widespread activation of coagulation in the circulating blood and the formation of numerous microvascular thrombi. A snakebite, including that of the Yamakagashi (Rhabdophis tigrinus), demonstrates this clinical condition. Thus, an animal model using Yamakagashi venom was constructed. Yamakagashi venom was administered to rats, and its lethality and the changes in blood coagulation factors were detected after venom injection. When 300 μg venom was intramuscularly administered to 12-week-old rats, (1) they exhibited hematuria with plasma hemolysis and died within 48 h; (2) Thrombocytopenia in the blood was observed in the rats; (3) irreversible prolongation of prothrombin time in the plasma to the measurement limit occurred; (4) fibrinogen concentration in the plasma irreversibly decreased below the measurement limit; and (5) A transient increase in the plasma concentration of D-dimer was observed. In this model, a fixed amount of Rhabdophis tigrinus venom injection resulted in the clinical symptom similar to the human pathology with snakebite. The use of the rat model is very effective in validating the therapeutic effect of human disseminated intravascular coagulation condition due to snakebite.

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“…We built a hypothermia-rewarming rats model based on our previous study [17]. A total of 50 SD male rats implanted with a temperature recorder were randomly assigned to three groups: Normal control group (C group, n=10), hypothermia group(H group, n=10) and a hypothermia followed by rewarming group (R group, n=30).The R group included three time-point subgroups: 2, 6 and 12h (R2, R6 and R12, respectively).There were 10 rats in each subgroup.…”

Section: Animal Preparation and Hypothermia-rewarming Modelmentioning

confidence: 99%

“…At present, treatment measures for hypothermia primarily include rewarming, reversing acidosis and treating any dysregulated coagulation [16,17]. Among these, rewarming is the most important treatment measure for hypothermia patients [18].…”

Section: Introductionmentioning

confidence: 99%

“…In the present study, an improved hypothermia-rewarming model for Sprague-Dawley (SD) rats was established based on a hypothermia model established in our previous study [17,21]. A focus was placed on exploring the changes in the physiological state, structure and the pro le of in ammatory cytokines in the intestinal tissue under hypothermic and rewarming conditions.…”

Section: Introductionmentioning

confidence: 99%

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Rewarming rats at 37˚C rescues hypothermia with significant changes in IL-1β levels in the intestinal tissue and blood

Xiong

et al. 2021

Preprint

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Background Hypothermia secondary to accidental exposure is becoming increasingly prevalent in the general population; however, the mechanisms and early treatments of hypothermia require additional study. Methods A hypothermia-rewarming SD rat model was established by immersing rats in 15˚C seawater for 5h and then rewarming at 37˚C for 2, 6 and 12 h. The rats were randomly divided into a normal control group (group C), hypothermia group (group H) and rewarming group (group R). The changes in the levels of inflammatory factors and pathophysiology of the intestinal tissues of rats were assessed. The blood was collected in test tubes, and the levels of cytokines in the separated plasma were detected using ELISA. The intestinal tissue was ground and lysed, and protein expression profiles of 67 inflammatory factors were measured using a protein chip. These samples were further subjected to reverse transcription-quantitative (RT-q)PCR analysis and tissue section staining. Results The temperature of the abdomen and the physiological state of the rats was significantly altered during immersion in the hypothermic seawater, and returned to normal after rewarming. The protein chip showed that inflammatory factors, including IL-1β, IL-10 and IL-6, were differentially expressed in the intestine. Using ELISA, it was shown that IL-1β, IL-6 and IL-10 levels were also upregulated in the plasma. Comparing the ratios of IL-1β to IL-6 and IL-1β to IL-10, IL-1β was found to be significantly more upregulated compared with IL-10 and IL-6 in the intestine during hypothermia. The immunohistochemical staining of IL-1β showed that IL-1βexpression first increased then decreased during the rewarming period, and similar results were obtained based on RT-qPCR analysis. Conclusion Rewarming at 37˚C may be a suitable method for early treatment of hypothermia, and IL-1β may serve as a potential biomarker for assessing the severity of hypothermia.

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Role of Vascular Endothelial Cells in Disseminated Intravascular Coagulation Induced by Seawater Immersion in a Rat Trauma Model

Cited by 4 publications

References 48 publications

Repeat dose exposure of PM2.5 triggers the disseminated intravascular coagulation (DIC) in SD rats

Repeat dose exposure of PM2.5 triggers the disseminated intravascular coagulation (DIC) in SD rats

Attempt to Develop Rat Disseminated Intravascular Coagulation Model Using Yamakagashi (Rhabdophis tigrinus) Venom Injection

Rewarming rats at 37˚C rescues hypothermia with significant changes in IL-1β levels in the intestinal tissue and blood

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