Background and Purpose-We recently found that chronic estrogen depletion enhances leukocyte adhesion in pial venules in the female rat, while estrogen repletion decreases it. Estrogen-associated repression of inflammation may be due to upregulation of the endothelial isoform of nitric oxide synthase (eNOS) and concomitant downregulation of the endogenous inhibitor of eNOS, caveolin-1 (CAV-1). In this study we examined the effects of estrogen-independent eNOS upregulation (via simvastatin) and/or CAV-1 downregulation (antisense) on pial venular leukocyte adhesion in ovariectomized (OVX) rats. Methods-Intact and OVX rats were prepared with closed cranial windows. Adherent rhodamine 6G-labeled leukocytes were viewed by intravital microscopy. To demonstrate the importance of pial venular eNOS in the resistance to leukocyte adhesion, intact female rats were treated with a nonselective (N G -nitro-L-arginine) or a neuronal NOSselective (7-nitroindazole) inhibitor. In OVX females, leukocyte adhesion was compared in the following groups: (1) untreated; (2) treated with simvastatin; (3) treated with simvastatin plus CAV-1 antisense; (4) treated with simvastatin plus CAV-1 missense; (5) treated with CAV-1 antisense; and (6) treated with CAV-1 missense. Results-In intact females, pial venular leukocyte adhesion was increased when total NOS activity, but not neuronal NOS activity alone, was blocked. In OVX rats, basal leukocyte adhesion, measured as the percentage of venular area occupied by adherent leukocytes, was attenuated (by Ϸ60%) only in the presence of combined simvastatin plus CAV-1 antisense treatment. Conclusions-Present findings demonstrate that eNOS-derived NO plays an important role in limiting cerebral venular leukocyte adhesion in female rats. These data also suggest that simvastatin-induced upregulation of eNOS expression in OVX rats will not restore eNOS function, as measured by decreased leukocyte adhesion, unless CAV-1 levels are reduced as well. Key Words: cell adhesion Ⅲ cerebral circulation Ⅲ estrogens Ⅲ nitric oxide Ⅲ simvastatin Ⅲ rats W e previously reported that estrogen depletion increases, while estrogen replacement decreases, leukocyte adhesion in the cerebral circulation of female rats during resting conditions and after transient forebrain ischemia. 1,2 This effect may be due, at least in part, to the capacity of estrogen to upregulate endothelial nitric oxide synthase (eNOS) expression and increase NO generation in endothelial cells. 3,4 NO produced in the endothelium is well known for its antiadhesive properties. 5,6 Recently, in a preliminary study, we attempted to decrease leukocyte adhesion in ovariectomized (OVX) female rats via an estrogen-independent upregulation of brain eNOS expression. Thus, experiments using chronic treatment of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin were performed. Simvastatin has been shown to stabilize eNOS mRNA in rodents, resulting in a cholesterol-independent increased expression of eNOS protein. 7,8 Surprisingly, despite i...

We report the percutaneous closure of a complex traumatic ventricular septal defect resulting from a stab wound to the anterior chest. The patient presented with heart failure 3 months after the initial trauma. Evaluation revealed a new large ventricular septal defect with diminished cardiac function. Closure was accomplished with a combination of an Amplatzer muscular ventricular septal defect occluder and two Amplatzer vascular plugs.

Transcatheter treatment of Sano conduit obstruction can be performed safely and results in immediate improvement in oxygenation, thereby allowing substantial delay of the cavo-pulmonary shunt.

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Background. Anatomic repair for congenitally corrected transposition of the great arteries with ventricular septal defect (VSD) and pulmonic stenosis has been accomplished with atrial switch and Rastelli. Aortic translocation offers a direct left ventricular outflow without an extraanatomic right ventricular-to-pulmonary conduit, which may lead to decreased reoperations. We reviewed our entire experience performing Senning with aortic translocation (SAT).Methods. From 2007 to 2017, 8 patients (mean age, 14.1 months; size, 8.86 kg) underwent SAT. Associated anomalies included situs inversus (n [ 2), dextrocardia (n [ 6), multiple muscular VSDs (n [ 2), abnormal or straddling atrioventricular valve chords (n [ 5), and branch pulmonary artery stenosis (n [ 3). Four of 8 had previous systemic arterial shunts. Mean cardiopulmonary bypass was 487 minutes, and mean cardiac ischemic time was 307 minutes. Additional procedures included repair