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Ryuko Matsuda

Publications and source records attributed to Ryuko Matsuda.

5 recordsLinked to original sources
PubMed2006

K201, a multi-channel blocker, inhibits clofilium-induced torsades de pointes and attenuates an increase in repolarization.

K201 (JTV519) is a 1,4-benzothiazepine derivative that exhibits a strong cardioprotective action and acts as a multiple-channel blocker, including as a K+ channel blocker. An experimental model of prolongation of the QT interval and torsades de pointes can be induced in rabbits by treatment with clofilium in the presence of the alpha1-adrenoreceptor agonist methoxamine. In this study we examined the effects of K201 with and without methoxamine on the QT and QTc intervals, and determined whether K201 inhibits clofilium-induced torsades de pointes in the presence of methoxamine (15 microg/kg/min) in rabbits (n=74). Administration of K201 (0, 40, 100, 200 and 400 microg/kg/min) with and without methoxamine prolonged the QT interval in a dose-dependent manner, and torsades de pointes did not occur in any animals. However, clofilium (50 microg/kg/min) with methoxamine induced torsades de pointes in all animals (6/6). Torsades de pointes occurred at rates of 100%, 67%, 40% and 0% at K201 concentrations of 0, 50, 200 and 400 microg/kg/min, respectively, in the clofilium-infused torsades de pointes model. Therefore, 400 microg/kg/min of K201 completely inhibited clofilium-induced torsades de pointes and attenuated the increase of repolarization caused by clofilium; the inhibitory effects of K201 may be related to its pharmacological properties as an alpha1-adrenoceptor blocker. Overall, our results show that K201 causes prolongation of the QT and QTc intervals, but does not induce torsades de pointes, with and without alpha1-adrenoceptor stimulation. Furthermore, K201 inhibits clofilium-induced torsades de pointes, despite QT prolongation, suggesting that QT prolongation alone is not a proarrhythmic signal.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2004

Effects of enhanced external counterpulsation on hemodynamics and its mechanism.

BACKGROUND: The hemodynamic effects of enhanced external counterpulsation (EECP) and its mechanism(s) were investigated in relation to neurohumoral factors in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-four patients with AMI were studied before, during and after EECP treatment for 60 min. Heart rate (HR), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were determined. In addition, circulating concentrations of neurohumoral factors were determined at each time point. HR did not change following EECP treatment. However, RAP and PCWP increased significantly and CI was significantly elevated during EECP and thereafter. Blood atrial natriuretic peptide (ANP) concentration was significantly increased 15 and 60 min after the start of EECP treatment, but brain natriuretic peptide (BNP) did not change. Renin, aldosterone and catecholamine concentrations also did not change. CONCLUSION: Treatment with EECP resulted in an increased preload because of increased venous return, and CI was increased thereafter. In patients with AMI, EECP increased blood ANP concentration, but not BNP, which suggests that an increase in ANP without an increase in BNP is an important mechanism for the effects of EECP treatment.

Aged↗
PubMed2003

Clinical significance of measurement of plasma annexin V concentration of patients in the emergency room.

Annexin V, a calcium-binding protein, is widely present in various organs and tissues. In the present study, plasma annexin V concentration was measured in 158 patients who were brought to the emergency room, including 25 patients suffering from acute myocardial infarction (AMI), 14 with cerebrovascular disease, 11 with trauma of the extremities, 11 with severe trauma associated with visceral damage, and 35 with witnessed cardiac arrest. Annexin V concentration in normal healthy individuals (n=110) was 1.9+/-0.7 ng/ml. Annexin V concentration in AMI and cardiac arrest patients was 11.0+/-4.9 and 15.3+/-7.9 ng/ml, respectively, being significantly higher than that in patients with cerebrovascular disease (5.4+/-2.7 ng/ml). The value in severe trauma patients was 15.9+/-9.4 ng/ml, being significantly higher than that in patients with trauma of the extremities (5.6+/-1.2 ng/ml). Annexin V concentrations in the cardiac arrest and AMI patients who survived more than 24 h after admission were lower than those in patients who died within 24 h after the onset of symptoms. Annexin V content in the lungs and myocardium in normal rats was extremely high in comparison to that in brain and skeletal muscle. These results suggest that the high levels of plasma annexin V in patients with AMI, cardiac arrest and severe trauma reflect the severity of damage of the myocardium and/or other visceral organs, and measurement of plasma annexin V concentration may help to assess the prognosis of patients brought to the emergency room.

Adolescent↗