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OBJECTIVE: To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury. METHODS: The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL, 3.0 mg/mL, 5.0 mg/mL) for 24 h, then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h. The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes, respectively. The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot, respectively. RESULTS: Compared to the negative group, pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury (P<0.05). The expression of Bcl-2 in tocilizumab treated group were higher than NC group (P<0.05), while the Bax expression were lower (P<0.05). CONCLUSIONS: Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury. Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.

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OBJECTIVE: Mitral valve disease tends to be treated with anterolateral minithoracotomy (ALMT) rather than median sternotomy (MS), as ALMT uses progressively smaller incisions to promote better cosmetic outcomes. This meta-analysis quantifies the effects of ALMT on surgical parameters and post-operative outcomes compared with MS. METHODS: One randomized controlled study and four case-control studies, published in English from January 1996 to January 2013, were identified and evaluated. RESULTS: ALMT showed a significantly longer cardiopulmonary bypass time (P=0.001) and aortic cross-clamp time (P=0.05) compared with MS. However, the benefits of ALMT were evident as demonstrated by a shorter length of hospital stay (P<0.00001). According to operative complications, the onset of new arrhythmias following ALMT decreased significantly as compared with MS (P=0.05); however, the incidence of peri-operative mortality (P=0.62), re-operation for bleeding (P=0.37), neurologic events (P=0.77), myocardial infarction (P=0.84), gastrointestinal complications (P=0.89), and renal insufficiency (P=0.67) were similar to these of MS. Long-term follow-up data were also examined, and revealed equivalent survival and freedom from mitral valve events. CONCLUSIONS: Current clinical data suggest that ALMT is a safe and effective alternative to the conventional approach and is associated with better short-term outcomes and a trend towards longer survival.

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OBJECTIVE: To establish an extracorporeal circulation (ECC) rat model, and evaluate the inflammatory response and organ injury induced in the model. METHODS: SD rats were anesthetized and cannulated from right common carotid artery to left femoral vein to establish the bypass of extracorporeal circulation. Then the rats were randomly divided into ECC group and sham group. The rats in ECC group were subjected to extracorporeal circulation for 2 hours and then rest for 2 hours, while the rats in sham group were only observed for 4 hours without extracorporeal circulation. After that, blood routine examination, blood gas analysis, the measurement of pro-inflammatory factors in bronchoalveolar lavage fluid and lung tissue were performed to evaluate the lung injury induced by ECC. Circulating endothelial cells were also calculated by flow cytometry to assess the vascular endothelial injury. RESULTS: At 2 hours after ECC, red blood cell counts in both groups kept normal, while leukocyte and neutrophil counts, plasmatic tumor necrosis factor-a level and neutrophil elastase level, circulating endothelial cells in the rats of ECC group were significantly higher than those in sham group. Tumor necrosis factor-alpha in bronchoalveolar lavage fluid and water content in lung of the ECC rats were also significantly higher, while the oxygenation index was significantly lower. Neutrophil infiltration was also observed in lung tissues with increased thickness of alveolar membrane in ECC group. CONCLUSION: The ECC model established from right common carotid artery to left femoral vein in our study can successfully induce systemic inflammatory response, and acute lung injury associated with inflammation.

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Transesophageal echocardiogram (TEE) guided perventricular cardiac intervention has gained popularity in recent years. We present a special case of perventricular closure conducted for a traumatic apical muscular ventricular septal defect (mVSD) under the guidance of three-dimensional (3D) TEE with an Amplatzer mVSD occluder and further discuss the important role of 3D TEE in perventricular cardiac intervention.

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BACKGROUND: Inflammation and coagulation are two intimately cross-linked defense mechanisms of most, if not all organisms to injuries. During cardiopulmonary bypass (CPB), these two processes are activated and interact with each other through several common pathways, which may result in subsequent organ dysfunction. In the present study, we hypothesized that the addition of nitric oxide, prostaglandin E1 (PGE1), and aprotinin to the systemic circulation, hereby referred to as blood hibernation, would attenuate the inflammation and coagulation induced by CPB. METHODS: Thirty adult mongrel dogs were equally divided into five groups, anesthetized and placed on hypothermic CPB (32 degrees C). Each group received respectively the following treatments: (1) inhalation of 40 ppm nitric oxide; (2) intravenous infusion of 20 ng x kg(-1) x min(-1) of PGE1; (3) 80,000 kallikrein inhibitor units (KIU)/kg of aprotinin; (4) the combination of all three agents (blood hibernation group); and (5) no treatment (control group) during CPB. Activation of leukocyte, platelet, endothelial cell, and formation of thrombin were assessed after CPB. RESULTS: As compared with the other four groups, leukocyte counts were higher, while plasma elastase, interleukin-8, CD11b mRNA expression, myeloperoxidase activities and lung tissue leukocyte counts were lower in the blood hibernation group (P < 0.05 versus other four groups after CPB). Plasma prothrombin fragment (PTF)1+2, and platelet activation factors were lower, while platelet counts were higher in the blood hibernation group (P < 0.05 versus other four groups at 6 and 12 hours after CPB). Electron microscopy showed endothelial pseudopods protrusion, with cell adherence in all four groups except the blood hibernation group where endothelial cells remained intact. CONCLUSION: Blood hibernation, effected by the addition of nitric oxide, PGE1 and aprotinin to the circulating blood during extra-corporeal circulation, was observed to attenuate the inflammation and coagulation induced by cardiopulmonary bypass, most likely by inhibiting the important common intermediates between the two cross-linked processes.

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OBJECTIVE: To investigate if increase of adhesion function and capability to destroy and decrease of phagocytosis of neutrophils occur after cardiopulmonary bypass (CPB). METHODS: 12 mongrel dogs were randomly divided into two equal groups: CPB group, weaned from CPB after 100 min of CPB; and sham group standing for 100 min without CPB. All dogs were observed for another 4 hrs. Blood samples were collected from the femoral vein before heparinization and by the end of experiment to measure the white blood cell count and classification, and expression of CD11b and CD18. Tissue samples of the right and left lungs were collected before heparinization and by the end of experiment. The expression of CD11b/CD18 in neutrophils, myeloperoxidase (MPO) activities in lung tissue, and pulmonary function were determined to access the adhesion function of neutrophils and the injuries to tissues. The phagocytotic activities, the release of MPO and the generation of oxygen free radical induced by IL-8 were surveyed to access the immune function of neutrophils. RESULTS: The fluorescence level of CD11b of the neutrophils in the CPB group was (2675 +/- 479) and the fluorescence level of CD18 of the neutrophils was (1574 +/- 262), both significantly higher than those before heparinization and those of the sham group (all P < 0.05). Four hours after CPB, the MPO activity of lung tissue of the CPB group was (55.02 +/- 21.04 U/100 g wet tissue), significantly higher than those before heparinization and that of the sham group (both P < 0.05); the ratios of PaO2/FiO2 of the CPB group was (319 +/- 79), significantly lower than those before heparinization and that of the sham group (both P < 0.05). Transmission electron microscopic examination revealed tentacle protrusion on the neutrophil in the CPB group, while the neutrophils were intact in the sham group. Contrary to the increase of adhere function, the numbers of neutrophil with phagocytic function of the CPB group was 35% +/- 11%, significantly lower than that of the sham group (74% +/- 9%, P < 0.01) the number of bacteria phagocytized by neutrophils per ml blood of the CPB group was (1484 +/- 238 ), significantly lower than that of the sham group (3106 +/- 714). There were no differences in the accumulated points of MPO in neutrophils, release of MPO, and generation of oxygen free radical between these 2 groups. CONCLUSION: CPB causes neutrophil function disorder, including increase of adhesion function and reduction of phagocytic function.

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