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Biomedical subjects

Hisato Takagi

Publications and source records attributed to Hisato Takagi.

At least 37 records · Page 2Linked to original sources
PubMed2005

Sonoporation with doxorubicin enhances suppression of intimal hyperplasia in a vein graft model.

BACKGROUND: The purpose of the present study is to examine whether sonoporation with doxorubicin enhances suppression of intimal hyperplasia (IH) in a vein graft model. MATERIALS AND METHODS: After the administration of 1.5 mg/kg doxorubicin intravenously, the right external jugular vein of six rabbits was exposed at 2 W/cm2 and 1 MHz of ultrasound for 2 min (Sonoporation group). Tissue doxorubicin concentration was measured. In 48 rabbits, the right common carotid artery was ligated after performing a vein graft bypass. The animals were divided into the following four groups: the C0 group (surgical procedure only); the C0S (sonoporation without doxorubicin); the C1 (doxorubicin administration only); the C1S (sonoporation with doxorubicin). Twenty-four grafts were subjected to Elastic van Gieson staining for morphometric analysis 4 weeks after the operation; others were subjected to TdT-mediated X-dUTP nick end-labeling for detection of apoptic cells and to staining with a monoclonal antibody against the proliferating cell nuclear antigen for assessment of cell proliferation 1 week after. RESULTS: The tissue doxorubicin concentration was significantly higher in the Sonoporation group than in the Control group. Compared with the C0 group, IH was not suppressed in the C1 group but was significantly suppressed in the C1S group. Sonoporation with doxorubicin administration suppressed IH significantly (C1 group versusC1S group: P < 0.05). Cell apoptosis was induced and cell proliferation was suppressed significantly in the C1S group. CONCLUSIONS: Sonoporation with doxorubicin suppressed IH of the vein graft. Sonoporation may be effective in coronary or peripheral revascularization using vein grafts.

Anastomosis, Surgical↗
PubMed2005

Intercostal artery pseudoaneurysm due to stab wound.

Intercostal artery pseudoaneurysm is extremely rare, and only six cases have been reported in the English literature. We describe a case of intercostal artery pseudoaneurysm due to a stab wound, review the literature, and discuss therapeutic modalities. Intercostal artery pseudoaneurysm is at risk for early rupture, and diagnosis before rupture is mandatory. Although embolization is considered to be a feasible therapeutic method, we would emphasize the significance of the anatomic features of the intercostal arteries: multiple blood supplies into the pseudoaneurysm, such as the anterior and posterior intercostal arteries, and musculophrenic artery.

Adult↗
PubMed2005

Nontraumatic pseudoaneurysm of the proximal ulnar artery with eosinophilia.

Proximal ulnar artery aneurysms, including pseudoaneurysms, have not been described in the English literature. We report a nontraumatic pseudoaneurysm of the proximal ulnar artery with eosinophilia in a 54-year-old man. Radial, coronary, and hepatic artery aneurysms associated with eosinophilia in idiopathic hypereosinophilic syndrome or allergic granulomatous angiitis (Churg Strauss syndrome) have been reported. Although it is unclear in the present case whether eosinophilia was associated with the pseudoaneurysm of the ulnar artery, eosinophil infiltration into the aneurysmal wall may have influenced vascular injury as the cause of the pseudoaneurysm formation.

Anastomosis, Surgical↗
PubMed2005

Matrix metalloproteinases synthesized in autosomal dominant polycystic kidney disease play a role in development of a concurrent abdominal aortic aneurysm.

Abdominal aortic aneurysm is well known to be associated with autosomal dominant polycystic kidney disease. Kidney tubules of autosomal dominant polycystic kidney disease synthesize and secrete high levels of matrix metalloproteinase 2, 3, and 9, especially matrix metalloproteinase 2, and serum matrix metalloproteinase 1 and plasma matrix metalloproteinase 9 concentrations in the disease are significantly higher than those in healthy controls. On the other hand, matrix metalloproteinases play a crucial role in the pathogenesis of abdominal aortic aneurysm. Inflammatory cell expression of matrix metalloproteinase 9 plays a critical role in an experimental model of aortic aneurysm disease. Macrophage-derived matrix metalloproteinase 9 and mesenchymal cell matrix metalloproteinase 2 are both required and work in concert to produce abdominal aortic aneurysm. The plasma matrix metalloproteinase 9 levels are significantly higher in the patients with abdominal aortic aneurysm than in the patients with aortoiliac occlusive disease or the healthy patients. Remarkably elevated matrix metalloproteinase 2 mRNA and protein levels in abdominal aortic aneurysm tissues as compared with normal and atherosclerotic aortic tissues are detected, and matrix metalloproteinase 2 proteolytic activity is several-fold higher in abdominal aortic aneurysms than in other pathological or normal states. Patients with abdominal aortic aneurysm elevate matrix metalloproteinase 2 levels in the vasculature remote from the aorta, supporting both the systemic nature of aneurysmal disease and a primary role of matrix metalloproteinase 2 in aneurysm formation. The authors propose a novel hypothesis that matrix metalloproteinases, synthesized and secreted by kidney tubules of autosomal dominant polycystic kidney disease, play a critical role in development of a concurrent abdominal aortic aneurysm.

Animals↗
PubMed2005

Homocysteinemia is a risk factor for aortic dissection.

There are significant associations between moderate increases in serum homocysteine and three cardiovascular diseases: ischemic heart disease, deep vein thrombosis and pulmonary embolism, and stroke. An association between the presence of abdominal aortic aneurysm and elevated homocysteine plasma levels has been indicated. Although chronic systemic hypertension is the most common factor predisposing the aorta to dissection, homocysteinemia has never been known as the risk for aortic dissection except for that with Marfan syndrome. Homocysteinemia is suggested to be the risk for aortic dissection in Marfan syndrome and spontaneous cervical artery dissection. Reduced fibrillin-1 deposition into the extracellular matrix is found not only in Marfan syndrome but also in isolated ascending aortic aneurysm and dissection. The reduced matrix deposition produces a mild form of weakness of elastic tissue, which predisposes to ascending aortic aneurysm and dissection in patients who do not have the Marfan syndrome. The defect in fibrillin-1 leads to: (1) formation of elastin that is abnormally aggregated and more easily degraded by matrix metalloproteinases than is normal elastin; (2) upregulation of the synthesis of matrix metalloproteinases; (3) progressive destruction of connective tissue by these enzymes; (4) development of thoracic aortic aneurysms. Homocysteine causes premature breakdown in the arterial elastic fibers by activation of the elastolytic activities. Irreversible homocysteinylation of long-lived proteins should lead to cumulative damage and progressive clinical manifestations, and fibrillin-1 is seen as the paradigm of extracellular connective tissue proteins that are specially susceptible to homocysteine (and presumably homocysteine thiolactone) attack. The authors hereupon propose a novel hypothesis that homocysteine plays an important role in development of aortic dissection and that homocysteinemia is one of the risk factors for aortic dissection.

Aortic Rupture↗
PubMed2005

Smoking promotes pathogenesis of aortic aneurysm through the 5-lipoxygenase pathway.

Smoking has been known as a risk factor for aortic aneurysm. 5-Lipoxygenase is the key enzyme in leukotriene biosynthesis and catalyzes initial steps in the conversion of arachidonic acid to these biologically active lipid mediators, which are known to exert proinflammatory effects in vivo. Smoking can induce 5-lipoxygenase expression in colon neoplasm, and may activate the 5-lipoxygenase pathway also in aortic tissue. 5-Lipoxygenase has a role in promoting the formation of aneurysms through potential plasma macrophage inflammatory protein-1alpha and -2 chemokine-dependent inflammatory circuits involving both myeloid and endothelial cells. Therefore, smoking may promote pathogenesis of aortic aneurysm through the 5-lipoxygenase pathway.

Animals↗