| In the battlefield environment in cold regions, hypothermia and trauma are two unavoidable practical problems, when a soldier is wounded, traumatic hemorrhagic shock(Traumatic Hemorrhagic Shock THS) occurs frequently, accounting for 50% of soldiers who were killed in battle. Severe trauma leads to tissue injury which cause the body the blood coagulation dysfunction as the main clinical manifestations of the clinical symptoms, known for Acute Traumatic Coagulation Disease(ATC), also known as Microvascular Bleeding,its incidence accounts for 25% of the trauma patients. In the past ATCs are concentrated in the cause of selectively targeting intravascular coagulation(DIC), recent studies have found that the early stage of platelet inhibition is a major risk factor for tissue trauma and hemorrhagic shock. Although coagulation dysfunction ? acidosis and hypothermia are the three risk factors for severe trauma.Low temperature in clinical application is more extensive, mainly to protect and reduce the demand for oxygen. Recent studies have shown that low temperature plays a role in the activation of platelets and the effect of hypothermia on platelets are still not clear in traumatic hemorrhagic shock. We know that blood loss is one of the main causes of death after trauma, but the most life-threatening is Acute Aortic Dissection(AAD).AAD is a disease with a high mortality rate, patients with ascending aortic dissection(Stanford A) require immediate surgery to avoid sudden cardiac death and cardiac death. Aortic dissection is divided into acute and chronic phase. In the acute period, consumption of platelets and clotting factors, meanwhile thrombosis and disseminated intravascular coagulation(DIC) are similar in the false lumen. AAD is often accompanied by systemic inflammatory response, which is caused by acute aortic injury. Manabu's report confirms that the severity of AAD has a direct relationship with inflammation in 2010. The mean platelet volume in patients with high response inflammation was small however it was higher in patients with low reactive inflammation. So far, we are still not clear about the relationship between the severity of AAD patients and the platelet.Objective 1. Effect of hypothermia on platelet activation in the model of traumatic hemorrhagic shock in pigs. 2. To clarify the effect of AAD on the platelet activation.Method 1. Ten healthy adult Bama miniature pigs, establishing traumatic hemorrhagic shock model: The blood capacity(30ml/kg) according to the calculation in the 15 min uniform release, body temperature is maintained between 38.5?and 39.5?,maintain and observe for 1h and then into the freezer temperature to 34?and 30 ? of 1h, measure the ADP receptor inhibition rate,Calculated SI?T?HR?MAP and other related physiological indexes. 2. This experiment was divided into two groups, a group of AAD patients(n=147), another group of healthy health care workers in the control group(n=30). 230 patients with AAD were admitted to a hospital from Feb. 2013 to Feb. 2016. The following patients will be excluded from our experiment: onset more than 48h(n=20), severe valvular dysfunction(n=20), recidivity AAD(n=12), malignant tumor and renal failure(n=11), coagulation disorders, liver disease, oral anticoagulation or antiplatelet therapy(n=20). Blood samples were collected at admission and the axillary temperature was recorded. Platelet count, MPV, and PDW were used to evaluate the activation of platelets. Serum C reactive protein levels were used to assess the severity of inflammation. Analysis of the severity of AAD by CT. The calculation formula of VTI is FL divided by BSA.Result 1. At the time of T1, the inhibition rate of ADP rece Ptor was significantly higher than that of T0(91.83±5.63 vs.83.69±3.68, P<0.001),And there is a certain correlation with the shock index(P<0.001,R=0.8343), and the inhibition rate of ADP at T2 was decreased significantly(84.64±4.14 vs91.83±5.63, P<0.001). At T3 time point, the inhibition rate of ADP receptor was significantly lower than that of T2(77.62±4.80 vs.84.64±4.14, P<0.001). 2. The platelet count in the AAD group was significantly lower than that in the normal group(156.35±34.12×109/L vs.221.56±28.79×109, P<0.001). PDW in AAD group was significantly higher than that in normal group(22.13±1.96 fl vs.15.69±1.97 fl,P<0.001). The level of C reactive Protein in the AAD group was significantly higher than that in the normal group(32.98±8.76mg/L vs.7.45±1.16mg/L, P<0.001). VTI and platelet count has a significant negative correlation(r =-0.665, P<0.001) and C-reactive protein(CRP) and platelet count exist significant negative correlation(r =- 0.632, P<0.001). Between VTI and CRP was significantly positive correlation(r = 0.678, P<0.001). Between VTI and PDW was significantly positive correlation(r = 0.598, P<0.001). There is a positive correlation between CRP and PDW.(r= 0.568, P<0.001).Conclusion 1. Hypothermia plays a promoting role in the activation of platelets in traumatic hemorrhagic shock. In traumatic hemorrhagic shock model of pigs, shock can significantly increase the inhibition rate of ADP receptor and bleeding. hypothermia significantly decreased the ADP receptor inhibition rate and accelerated the rate of blood coagulation. Therefore, and the recognition of ADP plays an important role in the activation of platelets induced by hypothermia. 2. AAD to promote platelet activation. Platelet activation and inflammation in patients with AAD appear to be closely related to the degree of injury, maybe it was caused by a tear in the aortic wall. Eliminating the false lumen is the objective of traditional surgery. Inhibition of platelet activation is a therapeutic target for the prevention of systemic inflammation in patients with AAD... |
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