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Shigeru Masuda

Publications and source records attributed to Shigeru Masuda.

4 recordsLinked to original sources
PubMed2005

An X-Ray diffraction study on mouse cardiac cross-bridge function in vivo: effects of adrenergic {beta}-stimulation.

To investigate how beta-stimulation affects the contractility of cardiac muscle, x-ray diffraction from cardiac muscle in the left ventricular free wall of a mouse heart was recorded in vivo. To our knowledge, this is the first x-ray diffraction study on a heart in a living body. After the R wave in electrocardiograms, the ratio of the intensities of the equatorial (1,0) and (1,1) reflections decreased for approximately 50 ms from a diastolic value of 2.1 to a minimum of 0.8, and then recovered. The spacing of the (1,0) lattice planes increased for approximately 90 ms from a diastolic value of 37.2 nm to a maximum of 39.1 nm, and then returned to the diastolic level, corresponding to approximately 10% stretch of sarcomere. Stimulation of beta-adrenergic receptor by dobutamine (20 microg/kg/min) accelerated both the decrease in the intensity ratio, which reached a smaller systolic value, and the increase in the lattice spacing. However, the intensity ratio and spacing at the end-diastole were unchanged. The recovery of the lattice spacing during relaxation was also accelerated. The mass transfer to the thin filaments at systole in a beta-stimulated heart was close to the peak value in twitch of frog skeletal muscle at 4 degrees C, showing that the majority of cross-bridges have been recruited with few in reserve.

Actins↗
PubMed2005

Superantigen-induced multiple organ dysfunction in a toxin-concentration-controlled and sequential parameter-monitored swine sepsis model.

OBJECTIVE: In order to examine the biological activity of low-dose and continuously infused superantigen, and to establish a superantigen-induced multiple organ dysfunction animal model, several pathophysiological parameters were sequentially monitored in a toxin-concentration-controlled pig model. METHODS: Anesthetized, mechanically ventilated and Swan-Ganz thermodilution catheter-inserted pigs were treated with toxic shock syndrome toxin-1 (TSST-1) by infusion at 2 microg/kg/h for 5 h. Monitoring was performed for both the infusion period and a subsequent 1-h post-infusion period. RESULTS: The serum concentration of TSST-1 was controlled so as to elevate it to a level over 1000 pg/mL within 1 h of initiation of infusion, and then gradually increased further and reached a plateau of about 2500 pg/mL at 4h after initiation. The animals showed a significant increase in cardiac output, the intrapulmonary arteriovenous shunt ratio, and infiltration of white blood cells into the lung. Although the observed increase in pulmonary vascular resistance was not statistically significant, it did correlate with the reduction in white blood cell counts. CONCLUSION: The superantigen TSST-1 plays an important role in the pathogenesis of Gram-positive bacterial sepsis by inducing multiple organ dysfunction. Thus, this model provides the first tool to allow the simultaneous examination of the serum toxin levels and other organ parameters in a time-course manner.

Animals↗
PubMed2005

Dual ECE/NEP inhibition on cardiac and neurohumoral function during the transition from hypertrophy to heart failure in rats.

CGS 26303 is a vasopeptidase inhibitor that simultaneously inhibits endothelin-converting enzyme (ECE) and neutral endopeptidase (NEP). We compared the effects of chronic treatment with CGS 26303 to the selective inhibition of angiotensin-converting enzyme (ACE) and NEP during the transition from left ventricular hypertrophy (LVH) to congestive heart failure (CHF) in hypertensive rats. LV geometry and function were assessed in Dahl salt-sensitive rats placed on a high-salt diet from age 6 weeks (hypertensive rats) and in control rats fed a low-salt diet. The hypertensive rats were randomized into groups that received no treatment or were treated with an ACE inhibitor (temocapril), an ECE/NEP inhibitor (CGS 26303), or a NEP inhibitor (CGS 24592) from the LVH stage (11 weeks) to the CHF stage (17 weeks). All treatments decreased the systolic blood pressure equally and significantly improved LV fractional shortening. Both temocapril and CGS 26303 ameliorated LV perivascular fibrosis, reduced mRNA levels of types I and III collagen, and decreased the heart weight/body weight ratio. CHF rats had increased plasma ET-1 levels compared with control rats. Only CGS 26303 reduced ET-1 to normal levels. ET-1 levels were found to correlate with heart/body weight, right ventricle/body weight and perivascular fibrosis ratios. During the transition to CHF, CGS 26303 produces effects that are comparable to temocapril and superior to CGS 24592. The beneficial effects of CGS 26303 are likely caused in part by the greater reduction of plasma ET-1. Dual ECE/NEP inhibitor may provide a new strategy for the treatment of human heart failure.

Angiotensin-Converting Enzyme Inhibitors↗