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

Abstract

Trauma complicated by seawater immersion is a complex pathophysiological process with higher mortality than trauma occurring on land. This study investigated the role of vascular endothelial cells (VECs) in trauma development in a seawater environment. An open abdominal injury rat model was used. The rat core temperatures in the seawater (SW, 22°C) group and normal sodium (NS, 22°C) group declined equivalently. No rats died within 12 hours in the control and NS groups. However, the median lethal time of the rats in the SW group was only 260 minutes. Among the 84 genes involved in rat VEC biology, the genes exhibiting the high expression changes (84.62%, 11/13) on a qPCR array were associated with thrombin activity. The plasma activated partial thromboplastin time and fibrinogen and vWF levels decreased, whereas the prothrombin time and TFPI levels increased, indicating intrinsic and extrinsic coagulation pathway activation and inhibition, respectively. The plasma plasminogen, FDP, and D-dimer levels were elevated after 2 hours, and those of uPA, tPA, and PAI-1 exhibited marked changes, indicating disseminated intravascular coagulation (DIC). Additionally, multiorgan haemorrhagia was observed. It indicated that seawater immersion during trauma may increase DIC, elevating mortality. VECs injury might play an essential role in this process.

Figure 1

Survival time of rats with an open abdominal injury in different environments. (a) An open abdominal injury animal model was established. Rats in the treatment group were vertically immersed into 22°C seawater (SW group) or normal saline (NS group). Rats in the control group were directly placed in a 22°C environment (control group). (b) The table displays the rectal temperatures of the test rats after 120 minutes of exposure. The rectal temperatures of the test animals were measured at different times. The rectal temperatures of the rats in both the NS group and SW group decreased rapidly but synchronously. (c) No rats in the NS group or control group died in 720 min. However, the average survival time of the rats in the SW group was 276 min, with a median lethal time of 260 minutes.

Figure 2

Relationships between functional VEC genes and coagulation cascades. (a) Roles of the functional VEC genes in the coagulation cascades. (b) Compared with the control group, the expression levels of 11 of 13 VEC genes in coagulation cascades in the SW group were increased by more than 2-fold, and 8 of 13 genes changed by more than 6-fold according to the Rat VEC Biology PCR Array. (c) Serum levels of coagulation-related factors in the test rats were assessed with a double-antibody sandwich ELISA. ^#P < 0.05; ^∗P < 0.01.

Figure 3

Coagulopathy of rats with an open abdominal injury complicated by seawater immersion. (a) Compared with the control group, the coagulation and DIC-related parameters in the plasma of the rats of the SW group were changed markedly, especially after 2 hours. ^#P < 0.05; ^∗P < 0.01. (b) A histological analysis revealed extensive haemorrhaging in multiple organs of the rats in the SW group, especially in the lung and intestine (HE 100x).