Keiko Takihara

Plasma endothelin levels during myocardial ischemia and reperfusion

Endothelin, an endothelium-derived vasoconstrictive peptide, has a strong potency of coronary artery constriction. However, the role of endogeneous endothelin under pathophysiological conditions has not yet been known. In this study, we examined plasma endothelin concentration in dogs with myocardial ischemia and reperfusion. Anesthetized open-chest dogs underwent either 45 minutes occlusion of the left anterior descending coronary artery followed by 3 hours reperfusion, or 4-10 hours of continuous occlusion. Plasma concentration of endothelin from the central vein was measured by the highly sensitive enzyme-immunoassay. Plasma endothelin concentration increased 2.2-fold with the peak level at 60 minutes after release of the ligated artery, but occlusion per se caused no remarkable change. These data suggest that reperfusion of the occluded artery might be needed to increase the plasma concentration of endothelin in case of myocardial infarction.

Calcium Overload-Induced Myocardial Damage Caused by Isoproterenol and by Adriamycin: Possible Role of Taurine in its Prevention

Calcium ion (Ca2+) is essential for excitation-contraction coupling and for maintenance of cell integrity in the myocardium. On the other hand, it is clear that cytosolic Ca2+ loading may be the first event leading to cell death in certain forms of myocytic injury, such as Ca2+ paradox and isoproterenol (ISO) toxicity. The Ca2+ overload injury is characterized by an exhaustion of tissue high-energy phosphate, massive release of enzymes and extensive ultrastructural damage, as well as excessive influx of Ca2+ into the myocardial cells.

Protective effect of taurine against isoprenaline-induced myocardial damage

SummaryThe effect of the sulfur amino acid, taurine, was examined on histological and biochemical changes induced by a toxic dose of isoprenaline in chick hearts. Isoprenaline treatment (80 or 240 mg/kg id twice daily for 4 days) caused a dose-dependent increase in heart weight and decrease in myocardial ATP. Isoprenaline administration (240 mg/kg id twice daily) produced necrotic changes in hearts, such as eosinophilic degeneration, myolysis, interstitial oedema, fibrosis, and inflammatory cell infiltration. Substantial accumulation of calcium was also observed. Taurine content of the heart was not significantly decreased. Parenteral administration of taurine (200 mg/day for 7 days) partially protected against these necrotic changes induced by isoprenaline. It is suggested that the protective effect of taurine against isoprenaline-induced myocardial injury might be due in part to the prevention of the massive overloading with calcium which is thought to cause myocardial cell necrosis.

TOCILIZUMAB AMELIORATES VASCULAR INFLAMMATION AND CLINICAL SYMPTOMS IN PATIENTS WITH TAKAYASU ARTERITIS REFRACTOTRY TO GLUCOCORTICOIDS

Treatment of refractory Takayasu arteritis (TA) remains a challenging clinical issue. Patients usually respond to glucocorticoid (GC) therapy, but often relapse on tapering of the GC dose. Additionally, GCs therapy is accompanied with a variety of adverse events. The aim of this study was to assess