Apoptotic mechanisms in rabbits with blast-induced acute lung injury

Abstract Purpose: To investigate the apoptotic mechanisms in rabbits with blast-induced acute lung injury (ALI). Methods: A total of 40 rabbits were randomly divided into a blank control group (A, n=10) and an experimental group (EXP, n=30). Explosion-induced chest-ALI models were prepared and sampled at different time points (4, 12, and 24h after modeling, T1-T3) to test the lung dry weight/wet weight ratio (W/D) and arterial oxygen pressure (PaO2), apoptosis of lung tissue by the TUNEL assay, and Caspase-3, Bax, and Bcl-2 levels by immunohistochemical analysis. Furthermore, lung tissue was sampled to observe pathological morphology by microscopy. Results: Under a light microscope, Group EXP exhibited obvious edema in the pulmonary interstitial substance and alveoli, a large number of red blood cells, inflammatory cells, and serous exudation in the alveolar cavity, as well as thickening of the pulmonary interstitial fluid. Compared to Group A, the W/D ratio was significantly increased in Group EXP (P<0.01), while PaO2 was significantly reduced (P<0.01). The apoptosis index was significantly increased (P<0.01), and caspase-3 and Bax/Bcl-2 levels were increased (P<0.01). Conclusion: Apoptosis plays an important role in the occurrence and development of acute lung injury in rabbits by participating in lung injury and promoting the progression of ALI.

Risk factors for coagulopathy after Stanford type A acute aortic dissection repair / 中国胸心血管外科临床杂志

@#Objective    To identify the risk factors for coagulopathy after Stanford type A acute aortic dissection (AAD) repair to offer evidence for improvement of patients' prognosis. Methods    We retrospectively analyzed the clinical data of 95 patients undergoing Stanford type A AAD repair in Beijing Anzhen Hospital between January 2013 and December 2014. Patients with thromboelastography-coagulation index (TEG-CI) ≤–3 after surgery were allocated to a coagulopathy group (n=17, average age 48.70 years), whereas patients with TEG-CI >–3 after surgery were allocated to a control group (n=78, average age 46.80 years). Multivariate analysis was used to identify risk factors for coagulopathy after surgery. Results    Seventeen patients suffered from coagulopathy after surgery. Patients in the coagulopathy group had larger amount of fluid drainage than that in the control group (P=0.008). Risk factors for postoperative coagulopathy were activated partial thromboplastin time (APTT) at the end of surgery ( OR=0.011, 95% confidence interval 0.001 to 0.021, P=0.035), fibrinogen degradation products (FDP) at the end of surgery (OR=0.004, 95% confidence interval 0.001 to 0.007, P=0.022) and platelet count (×109/L) at the end of surgery (OR=–0.002, 95% confidence interval –0.003 to 0.000, P=0.049). The lower risk of postoperative coagulopathy was related to the platelet count at the end of surgery up to 137.00 × 109/L. Conclusion    Postoperative coagulopathy could be related to the clinical and experimental variables. In a   representative sample of Chinese adults undergoing Stanford type A AAD surgery, APTT, FDP and platelet count at the end of surgery are independent risk factors associated with postoperative coagulopathy. Adding haemostatic, such as fibrinogen and prothrombinase complex, is good for improving the recovery of coagulation function to reduce bleeding and postoperative blood transfusion, as well as adding platelet, plasma and other coagulation factors after AAD surgery.