Anomalous subaortic left brachiocephalic vein (ASLBV) is a rare systemic venous anomaly. We review our experience with patients associated with ASLBV who underwent cardiac surgery at three institutions. From 1989 to 2009, the medical records of surgically treated patients with ASLBV were analyzed; the incidence of ASLBV, clinical characteristics, and associated anatomical findings were assessed. Fifteen patients had ASLBV. All ASLBVs coursed left lateral to the aortic arch, passed under the ascending aorta anterior to the central pulmonary artery, and joined the right brachiocephalic vein. Fourteen patients had congenital heart disease (CHD), and the remaining patient did not have cardiac anomalies. Its incidence was 0.57% (14 of 2,449) in patients with CHD and only 0.02% (1 of 4,805) in patients without CHD. In patients with CHD, 73.3% (11 of 15) of the patients had conotruncal cardiac anomalies such as tetralogy of Fallot, ventricular septal defect with pulmonary atresia, truncus arteriosus, and interruption of the aortic arch. Eight patients had aortic arch anomalies, including right aortic arch and cervical aortic arch. The deletion of chromosomal 22q11.2 was confirmed in two patients, and one patient was diagnosed with DiGeorge syndrome. ASLBV was clinically silent even without any surgical intervention. ASLBV is a very rare anomaly and is highly associated with conotruncal cardiac anomalies and aortic arch anomalies, including right aortic arch and cervical aortic arch. Preoperative diagnosis is important when any surgical interventions are intended, especially, in patients with conotruncal cardiac anomalies.

Sivelestat sodium suppressed the production of PMN elastase and IL-8, resulting in improved respiratory function in patients with ALI caused by CPB.

These results demonstrated that TAT-BH4 attenuates myocardial ischemia/reperfusion injury through preventing myocardial apoptosis. Thus, TAT-BH4 may be a novel therapeutic agent for myocardial protection in cardiac surgery.

BackgroundLiver dysfunction and cirrhosis affect vasculature in several organ systems and cause impairment of organ functions, thereby increasing morbidity and mortality. Establishment of a mouse model of hepatopulmonary syndrome (HPS) would provide greater insights into the genetic basis of the disease. Our objectives were to establish a mouse model of lung injury after common bile duct ligation (CBDL) and to investigate pulmonary pathogenesis for application in future therapeutic approaches.MethodsEight-week-old Balb/c mice were subjected to CBDL. Immunohistochemical analyses and real-time quantitative reverse transcriptional polymerase chain reaction were performed on pulmonary tissues. The presence of HPS markers was detected by western blot and microarray analyses.ResultsWe observed extensive proliferation of CD31-positive pulmonary vascular endothelial cells at 2 weeks after CBDL and identified 10 upregulated and 9 down-regulated proteins that were associated with angiogenesis. TNF-α and MMP-9 were highly expressed at 3 weeks after CBDL and were less expressed in the lungs of the control group.ConclusionsWe constructed a mouse lung injury model by using CBDL. Contrary to our expectation, lung pathology in our mouse model exhibited differences from that of rat models, and the mechanisms responsible for these differences are unknown. This phenomenon may be explained by contrasting processes related to TNF induction of angiogenic signaling pathways in the inflammatory phase. Thus, we suggest that our mouse model can be applied to pulmonary pathological analyses in the inflammatory phase, i.e., to systemic inflammatory response syndrome, acute lung injury, and multiple organ dysfunction syndrome.

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