Neutrophils Mediate Pulmonary Artery Thrombosis In Situ.

Pulmonary embolism is a life-threatening condition, which can result in respiratory insufficiency and death. Blood clots occluding branches of the pulmonary artery (PA) are traditionally considered to originate from thrombi in deep veins (usually in legs). However, growing evidence suggests that occlusion of the vessels in the lungs can develop without preceding deep vein thrombosis (DVT). In this work, we used an inferior vena cava (IVC) complete ligation model of DVT in Wistar rats to explore the possibility and mechanisms of PA thrombosis under the conditions where all routes of thrombotic mass migration from peripheral veins are blocked. We demonstrate that rats both with normal and reduced neutrophil counts developed thrombi in the IVC, although, neutropenia caused a substantial decrease in thrombus size and a shift from fresh fibrin toward mature fibrin and connective tissue inside the thrombus. Massive fibrin deposition was found in the PA branches in the majority of DVT rats with normal neutrophil counts, but in none of the neutropenic animals. Neutrophil ablation also abolished macroscopic signs of lung damage. Altogether, the results demonstrate that thrombi in the lung vasculature can form in situ by mechanisms that require local neutrophil recruitment taking place in the DVT setting.

Effect of sleeve gastrectomy, Roux-en-Y gastric bypass, and ileal transposition on myocardial ischaemia-reperfusion injury in non-obese non-diabetic rats.

Bariatric surgery (BS) improves outcomes in patients with myocardial infarction (MI). Here we tested the hypothesis that BS-mediated reduction in fatal MI could be attributed to its infarct-limiting effect. Wistar rats were randomized into five groups: control (CON), sham (SHAM), Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and ileotransposition (IT). Ten weeks later, animals were subjected to 30-min myocardial ischemia plus 120-min reperfusion. Infarct size (IS) and no-reflow area were determined histochemically. Fasting plasma levels of glucagon-like peptide-1 (GLP-1), leptin, ghrelin, and insulin were measured using ELISA. Compared with SHAM, RYGB and SG reduced IS by 22% (p = 0.011) and 10% (p = 0.027), and no-reflow by 38% (p = 0.01) and 32% (p = 0.004), respectively. IT failed to reduce IS and no-reflow. GLP-1 level was increased in the SG and RYGB groups compared with CON. In both the SG and RYGB, leptin level was decreased compared with CON and SHAM. In the SG group, ghrelin level was lower than that in the CON and SHAM. Insulin levels were not different between groups. In conclusion, RYGB and SG increased myocardial tolerance to ischemia-reperfusion injury of non-obese, non-diabetic rats, and their infarct-limiting effect is associated with decreased leptin and ghrelin levels and increased GLP-1 level.