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Biomedical subjects

Shu Yamamoto

Publications and source records attributed to Shu Yamamoto.

5 recordsLinked to original sources

Anomalous origin of the right coronary artery from the pulmonary artery.

A case of anomalous origin of the right coronary artery from the pulmonary artery in a 73-year-old man is presented. The patient had been suffering from chronic heart failure with mitral and tricuspid regurgitation and atrial fibrillation for two years. Surgical repair was performed successfully, including ligation of the right coronary artery and coronary arterial bypass with a radial artery graft.

Aged↗

Mitral-aortic intervalvular pseudoaneurysm with ventricular septal defect.

A 35-year-old woman was found on echocardiography to have a pseudoaneurysm of the mitral-aortic intervalvular fibrosa, residual ventricular septal defect, and aortic regurgitation. She had undergone surgical closure of a ventricular septal defect at age 7 and was found to have residual shunt several years later. She had been followed nonsurgically and had symptoms of cardiac failure during her 2 pregnancies. The pseudoaneurysm and the septal defect were successfully repaired.

Aneurysm, False↗

Time-dependent regional myocardial denervation as a nonspecific response to transmyocardial laser revascularization.

BACKGROUND: It is known that denervation occurs in the regions of myocardium treated by laser transmyocardial revascularization (TMR). The purpose of this study was to determine when regional denervation occurs in the early postoperative period and whether or not it is specific to laser TMR when compared with TMR using ultrasonically activated energy. METHODS: Dogs with normal myocardium underwent either holmium:yttrium-aluminum-garnet laser TMR, TMR using an ultrasonic activated surgical blade, or a thoracotomy as sham operation. The responses of mean arterial pressure to topical application of bradykinin were examined at 3 time points: before, 1 hour after, and 2 weeks after surgery. The hearts were excised for Western blot and immunohistochemical analysis. RESULTS: The response of mean arterial pressure to bradykinin was similarly attenuated in both TMR groups 1 hour after treatment and decreased to almost none after 2 weeks compared with pretreatment values. By comparison, the sham group showed persistent responses at both time points. Tissue tyrosine hydroxylase content of the treated area decreased significantly compared with the non-treated area in both TMR groups. Immunohistochemistry using anti-Protein Gene Product 9.5 and anti-synaptophysin antibodies showed a significant decrease in the number of positive nerve fibers in both TMR treatment groups compared with the sham group. CONCLUSIONS: Transmyocardial revascularization caused partial alteration in myocardial innervation immediately after TMR. Tissue responses may continue to occur for the first 2 weeks after treatment. Tissue responses may also contribute to the development of denervation regardless of the energy source in non-ischemic canine myocardium.

Animals↗

Digital radiographic quantification of myocardial blood flow around a transmyocardial laser channel in rabbit hearts.

BACKGROUND: A mechanism underlying the benefits of transmyocardial laser revascularization (TMLR) has been presumed to be improvement in perfusion. We evaluated myocardial blood flow around a laser channel using digital radiography combined with a 3H-labeled desmethylimipramine ([3H]DMI) deposition. METHODS AND RESULTS: A laser channel was created in the left ventricular wall using a YAG-laser in 6 non-ischemic rabbit hearts. After 8 weeks, [3H]DMI(1.11 MBq) was injected into the left atrium and the TMLR-treated myocardium was sectioned. Another 6 hearts were examined as controls. We measured [3H]DMI density in arbitrary units with digital radiography in the channel remnant, the surrounding area and a remote area. Flow distribution was quantified by the coefficient of variation of flows (CV). The surrounding area had the highest density (p < 0.001) and the lowest CV (p < 0.001), and had higher density (p < 0.001) and lower CV (p < 0.001) than the controls. There was no transmural difference in the density in all domains. The CV increased with depth in the remote area, as well as in controls (p < 0.001), but there was no transmural difference in the surrounding area. CONCLUSIONS: The TMLR increases myocardial blood flow and decreases flow heterogeneity in the surrounding area. The disappearance of transmural difference in flow heterogeneity might indicate the remodeling of microcirculation to improve regional oxygen delivery.

Animals↗

Nicorandil ameliorates posttransplant dysfunction in cardiac allografts harvested from non-heart-beating donors.

OBJECTIVE: Warm ischemia is a major cause of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). We evaluated the cardioprotective effects of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on the early posttransplant left ventricular (LV) function of hearts harvested from asphyxiated canine NHBDs. METHODS: Hypoxic cardiac arrest was induced in 12 donor dogs. In 6, nicorandil was administered intravenously at 100 micrograms/kg + 25 micrograms/kg/min after respiratory arrest and hearts were preserved with nicorandil-supplemented cardioplegic solution (nicorandil group). The remaining 6 did not receive nicorandil at any time during the experiment (control group). Hearts were orthotopically transplanted after a mean myocardial ischemic time of 4 hours. RESULTS: All 12 recipients were weaned from cardiopulmonary bypass without inotropic support. In the control group, posttransplant cardiac indices and left ventricular end-systolic pressure (LVESP) decreased significantly, while LV max-dP/dt and Tau increased over pretransplant values. No differences were seen in parameters between pretransplant and posttransplant values in the nicorandil group. Posttransplant cardiac indices, LVESP, and LV max + dP/dt were higher in the nicorandil group than in controls, while posttransplant LV max-dP/dt in the nicorandil group was lower. CONCLUSIONS: Our results indicate that pretreatment with nicorandil during hypoxic perfusion before cardiac arrest and subsequent preservation with nicorandil-supplemented cardioplegia ameliorates early posttransplant LV dysfunction of hearts harvested from asphyxiated NHBDs.

Animals↗