Masato Ohmura

Sphingosylphosphorylcholine induces cytosolic Ca2+ elevation in endothelial cells in situ and causes endothelium‐dependent relaxation through nitric oxide production in bovine coronary artery

Sphingosylphosphorylcholine (SPC) increased intracellular Ca2+ concentration ([Ca2+]i) and nitric oxide (NO) production in endothelial cells in situ on bovine aortic valves, and induced endothelium‐dependent relaxation of bovine coronary arteries precontracted with U‐46619. The SPC‐induced vasorelaxation was inhibited by N ω‐monomethyl‐L‐arginine, an inhibitor of both constitutive and inducible NO synthase (NOS), but not by 1‐(2‐trifluoromethylphenyl) imidazole, an inhibitor of inducible NOS (iNOS). Immunoblotting revealed that endothelial constitutive NOS, but not iNOS, was present in endothelial cells in situ on the bovine aortic valves. We propose that SPC activates [Ca2+]i levels and NO production of endothelial cells in situ, thereby causing an endothelium‐dependent vasorelaxation.

Assessment of right atrial mapping and P wave—triggered signal-average in patients with paroxysmal atrial fibrillation

Abstract To assess right atrial mapping and P wave—triggered signal-averaged electrocardiogram (ECG) in patients with paroxysmal atrial fibrillation (PAF), this study examined right atrial electrograms using atrial mapping and parameters by P wave—triggered signal-averaged ECG in 39 patients without sick sinus syndrome. Subjects were divided into those with PAF (n = 13; 60 ± 13 years old) and a control group (n = 26; 49 ± 19 years old). The total number of abnormal right atrial electrograms per patient was significantly greater in the PAF group (3.2 ± 1.9) than in the control group (1.1 ± 0.9; P P = .06). The filtered P wave duration was significantly longer in the PAF group than in the control group (144 ± 21 vs 125 ± 14 ms [ P P P 1.5 μV (2.2 ± 1.8 vs 1.3 ± 1.3 [ P

Double Ventricular Response by a Single Ventricular Extrastimulus to the Inner Loop of Reentry in a Patient Without Apparent Heart Disease

SHIMIZU, A., et al.: Double Ventricular Response by a Single Ventricular Extrastimulus to the Inner Loop of Reentry in a Patient Without Apparent Heart Disease. In a patient without apparent heart disease, a ventricular extrastimulus delivered from the left ventricular apex where the electrogram was recorded 30 ms after the onset of the QRS complex during VT advanced the second QRS complex, but not the first QRS complex. The morphology of the second QRS complex was the same as that of VT. The postpacing interval was the same as the cycle length of the VT. These findings indicated that the site of stimulation was at the inner loop of the reentry circuit of the VT. A ventricular extrastimulus with a shorter coupling interval advanced the first and second QRS complexes, indicating that the ventricle was activated by antidromic and orthodromic activation from the extrastimulus. Radiofrequency ablation at that site of stimulation terminated the VT and no further VT could be induced.

Potential signal mediators for CA2+ sensitization of smooth muscle contraction: Rho-associated kinase, atypical protein kinase C, and arachidonic acid

Abstract This chapter reviews interesting, potential mechanisms of G protein-coupled Ca 2+ sensitization, which include a RhoA and Rho-kinase signaling cascade, an AA-mediating pathway, some isoforms of PKCs (most likely aPKC, and an unidentified phosphatase-associated kinase. These possibilities are not mutually exclusive, may function in parallel, and even contribute to crosstalk.