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Biomedical subjects

H Matsuda

Publications and source records attributed to H Matsuda.

At least 361 records · Page 20Linked to original sources

Myocardial protection with endogenous overexpression of manganese superoxide dismutase.

BACKGROUND: Superoxide dismutase (SOD) is a potent candidate for myocardial protection against ischemia-reperfusion injury; however, its clinical significance by means of exogenous administration remains controversial. METHODS: To determine a role of endogenously overexpressed manganese SOD (Mn-SOD) in myocardial tolerance, rat hearts were transfected with Mn-SOD gene (group M) or no gene (group C) through intracoronary infusion of hemagglutinating virus of Japan (HVJ) liposome. Each group was divided into two subgroups to be subjected to ischemia-reperfusion using Langendorff apparatus with (subgroups M+ and C+) or without (M- and C-) administration of recombinant SOD. RESULTS: Mn-SOD overexpression was confirmed in M with ELISA, activity measurement, and immunohistochemistry. The highest recoveries of maximum and minimum dp/dt and the least creatine phosphokinase (CPK) leakage were observed in M+. These recoveries were higher in M- than in C- and C+. CONCLUSIONS: Thus, endogenous overexpression of Mn-SOD improved myocardial tolerance and its protective effect was enhanced by exogenous administration of SOD. These results suggest a possible strategy for myocardial protection with SOD: a combination of endogenous introduction through gene transfer with exogenous administration.

Animals↗

Surgical rescue for life-threatening hypoxemia caused by a mediastinal tumor.

We recently encountered a patient with a large anterior mediastinal tumor who developed severe hypoxemia during general anesthesia. This life-threatening hypoxemia was treated by extracorporeal membrane oxygenation using emergent percutaneous cardiopulmonary support followed by extirpation of the tumor. We found that total arteriovenous shunt resulting from compression by the mediastinal tumor caused this severe hypoxemia (total obstruction of left main bronchus and of the right pulmonary artery).

Adult↗

Selectin on activated platelets enhances neutrophil endothelial adherence in myocardial reperfusion injury.

OBJECTIVES: The glycoprotein P-selectin is an adhesion molecule that is rapidly expressed on the surface of platelets and endothelium during the inflammatory process. P-selectin on endothelium has been reported to play an important role in reperfusion injury. However, little is known regarding P-selectin on platelets in contributing to the pathophysiology of myocardial reperfusion injury. In this study, we hypothesized that P-selectin on platelets may enhance neutrophil endothelial adherence and this may play a role in neutrophil-mediated reperfusion injury. METHODS: Endothelial cells, cardiomyocytes, platelets and neutrophils were isolated from adult rats. Endothelial cells and cardiomyocytes were cultivated in a co-culture system. After exposure to hypoxia and reoxygenation, neutrophil adherence and migration were examined. RESULTS: After exposure to 6 h of hypoxia, endothelial cells co-incubated with platelets showed significantly greater neutrophil adherence (63.1 +/- 4.0%) and migration (78.2 +/- 6.7%) than endothelial cells alone (adhesion: 44.2 +/- 2.8%, migration: 57.9 +/- 4.9%). These increases were significantly inhibited (adhesion: 42.1 +/- 3.5%, migration: 65.5 +/- 3.8%) by an anti-P-selectin monoclonal antibody. Moreover, the superoxide-anion production was significantly elevated when activated platelets were added to neutrophils. This enhanced production was also inhibited by anti-P-selectin antibody. CONCLUSION: The presence of activated platelets enhanced neutrophil adhesion and migration process after hypoxia reoxygenation. This process may occur following platelet-neutrophil interactions via P-selectin and subsequent neutrophil activation.

Animals↗

Gene transfection of beta 2-adrenergic receptor into the normal rat heart enhances cardiac response to beta-adrenergic agonist.

BACKGROUND: Beta-adrenergic receptor system has a major role in cardiac contraction. If the receptor can be increased by gene transfection by means of intracoronary infusion of beta 2-adrenergic receptor to the hearts in which the receptor is down-regulated, this maneuver may improve the cardiac function and may be applied as one therapeutic approach during cardiopulmonary bypass or percutaneous cardiopulmonary support. METHODS AND RESULTS: The beta 2-adrenergic receptor complementary DNA was transfected in vivo to the normal rat heart by intracoronary infusion by means of a hemagglutinating virus of Japan liposome method, and the transfected heart was transplanted into the abdomen of another rat. Four days after transfection, the sarcolemma of the cardiomyocytes was well labeled by immunohistochemical labeling. Expression of beta-adrenergic receptor in the heart was approximately 4 times greater than that in control hearts (134 +/- 42 vs 33 +/- 4 fmol/mg protein) according to a ligand binding assay. The cardiac response of the transfected heart to isoproterenol was shown to be enhanced in a Langendorff perfusion system: after isoproterenol, developed pressure and maximal derivative of the left ventricle were greater than in the control heart (200 +/- 12 vs 174 +/- 6 mm Hg and 4110 +/- 130 vs 3491 +/- 255 mm Hg/sec), and the minimal derivative of the left ventricle was markedly smaller (-3040 +/- 267 vs -2528 +/- 131 mm Hg/sec). CONCLUSIONS: These results indicate that expression of beta 2-adrenergic receptor was approximately 4 times greater than in normal rat hearts by gene transfection using a hemagglutinating virus of Japan liposome method, and the transfected hearts demonstrated marked enhancements in cardiac response to beta-agonist, suggesting that transfer of this gene by intracoronary infusion has potential as a novel approach to enhance cardiac function.

Adrenergic beta-Agonists↗

Results of surgical treatment of thymomas with special reference to the involved organs.

OBJECTIVE: The purpose of this study is to clarify the significance of the particular involved organ as a prognostic factor and its relation to other previously reported factors. METHODS: The prognoses of 194 consecutive patients with thymoma who had undergone complete or subtotal resection were reviewed retrospectively. Survival was evaluated as actuarial freedom from tumor death. Analysis of prognostic factors was performed by the Kaplan-Meier method with the log rank test and Cox's proportional hazards model. RESULTS: The Masaoka staging system and involvement of the great vessels were the independent prognostic factors in the entire study group; age, sex, histologic subtype, completeness of resection, association of myasthenia gravis, or involvement of other organs were not factors. The 10-year and 20-year survivals were 99% and 90% in stage I, 94% and 90% in stage II, 88% and 56% in stage III, 30% and 15% in stage IVa, 0% and 0% in stage IVb, 93% and 83% in the absence of involvement of the great vessels, and 54% and 20% in the presence of it. Involvement of the great vessels was also the single independent prognostic factor in the patients with stage III disease although completeness of resection or involvement of other organs were not. The 10-year and 20-year survivals in patients with stage III disease were 97% and 75% in the absence of involvement of the great vessels, and 70% and 29% in the presence of it. CONCLUSION: Although the Masaoka staging system is a valuable prognostic factor, the category of stage III is heterogeneous and consists of 2 groups with distinct prognoses depending on involvement of the great vessels.

Adolescent↗

Roles of capsaicin-sensitive sensory nerves, endogenous nitric oxide, sulfhydryls, and prostaglandins in gastroprotection by momordin Ic, an oleanolic acid oligoglycoside, on ethanol-induced gastric mucosal lesions in rats.

The roles of capsaicin-sensitive sensory nerves (CPSN), endogenous nitric oxide (NO), sulfhydryls (SHs), prostaglandins (PGs) in the gastroprotection by momordin Ic, an oleanolic acid oligoglycoside isolated from the fruit of Kochia scoparia (L.) SCHRAD., on ethanol-induced gastric mucosal lesions were investigated in rats. Momordin Ic (10 mg/kg, p.o.) potentially inhibited ethanol-induced gastric mucosal lesions. The effect of momordin Ic was markedly attenuated by the pretreatment with capsaicin (125 mg/kg in total, s.c., an ablater of CPSN), N(G)-nitro-L-arginine methyl ester (L-NAME, 70 mg/kg, i.p., an inhibitor of NO synthase), N-ethylmaleimide (NEM, 10 mg/kg, s.c., a blocker of SHs), or indomethacin (10 mg/kg, s.c., an inhibitor of PGs biosynthesis). The attenuation of L-NAME was abolished by L-arginine (300 mg/kg, i.v., a substrate of NO synthase), but not by D-arginine (300 mg/kg, i.v., the enatiomer of L-arginine). The effect of the combination of capsaicin with indomethacin, NEM, or L-NAME was not more potent than that of capsaicin alone. The combination of indomethacin and NEM, indomethacin and L-NAME, or indomethacin and NEM and L-NAME increased the attenuation of each alone. These results suggest that CPSN play an important role in the gastroprotection by momordin Ic on ethanol-induced gastric mucosal lesions, and endogenous PGs, NO, and SHs interactively participate, in rats.

Animals↗