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Volume 115 (2000)
- Issue 6 Pages 323-
- Issue 5 Pages 271-
- Issue 4 Pages 185-
- Issue 3 Pages 123-
- Issue 2 Pages 67-
- Issue 1 Pages 5-
Volume 115, Issue 5
Displaying 1-4 of 4 articles from this issue
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Mitsugu HACHISU, Yasuyuki ICHIMARU2000 Volume 115 Issue 5 Pages 271-279
Published: 2000
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSFluvoxamine (Depromel®), a selective serotonin reuptake inhibitor (SSRI), was launched in May 1999 in Japan with more than 10 years' delay from the marketing in Europe and the United States. Fluvoxamine has been approved in about 80 countries as the indication to “depression” since 1983. As the indication to obsessive-compulsive disorder (OCD), fluvoxamine was first approved in the United States in 1994 and then in about 30 countries. Efficacy of the drug on “depression and depressed state” was found to be comparable to traditional tricyclic antidepressants (TCAs) by the clinical studies in Japan. Indication to OCD was first approved for fluvoxamine in Japan. The antidepressant and the anti-OCD action are considered the result of the serotonin reuptake inhibition at the serotonergic neurons. Fluvoxamine has little affinity for muscarinic, adrenergicα1- and histamine Hl-receptors, which TCAs have. Therefore, fluvoxamine possesses less side effects such as dry mouse, disuria, dizziness, orthostatic hypotension and drowsiness, etc.; and it is useful for elderly patients and long-term treatments for depression and OCD.View full abstractDownload PDF (716K) -
Shunji NOMURA, Munehiro HASHIMOTO2000 Volume 115 Issue 5 Pages 280-286
Published: 2000
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSLatanoprost is a novel prostaglandin F2α (PGF2α) derivative. Topically applied latanoprost into the glaucomatous monkey eyes lowered intraocular pressure (IOP). Latanoprost, however, failed to produce the hypotensive effect in either rabbit or cat eyes. This species difference may be attributed to its high selectivity for the FP receptor and differences in prostaglandin receptor subtypes existed in the eye amongst these species. In ligand binding studies with bovine corpus luteum cell membranes, the Kd value for the FP receptor of latanoprost was the same as that for PGF2α, 2.8 nM. Latanoprost augmented uveoscleral outflow (Uv) in monkeys without affecting trabecular outflow or outflow facility like PGF2α. Although the precise mechanism of the increase in Uv is not fully understood, it is suggested that a decrease in extracellular matrix components in ciliary muscle may contribute to the increase in Uv. On the other hand, an increase in blood flow at the optic nerve head and neuroprotective action in addition to the IOP lowering effect may contribute to the efficacy of latanoprost in glaucoma therapy. Only tolerable conjunctival hyperemia was seen in rabbits. A phase III clinical trial revealed latanoprost (0.005%) once daily produced sustained reduction of IOP in ocular hypertension or primary open-angle glaucoma patients to a greater extent than timolol did. Furthermore, the effects of latanoprost on aqueous humor dynamics in normal human volunteers were similar to those in monkeys, indicating that latanoprost lowers IOP by the increase in Uv in humans.View full abstractDownload PDF (508K) -
Hiromu KAWASAKI, Satoshi KURODA, Yuichi MIMAKI2000 Volume 115 Issue 5 Pages 287-294
Published: 2000
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSInsulin as a vascular hormone, apart from its effect on intermediary metabolism, has been considered to play an important role in cardiovascular regulation and pathophysiology of cardiovascular diseases such as essential hypertension, congestive cardiac failure and atherosclerosis. Insulin induces pressor effects by mechanisms of increased sympathetic activity, renal sodium retention and proliferation of vascular smooth muscle cells. On the other hand, accumulating evidence indicates that insulin decreases vascular resistance and increases organ blood flow especially in skeletal muscle tissue, indicating that insulin is a vasodilator. Several mechanisms underlying insulin-induced vasodilation have been proposed. Insulin enhances calcium efflux from vascular smooth muscle cells by activating the plasma membrane Ca2+-ATPase and causes hyperpolarization by stimulating Na+, K+-ATPase and sodium/potassium pump. Insulin also stimulates nitric oxide (NO) synthase and increases release of NO from vascular endothelium to cause vasodilation. An increase in cyclic AMP levels is induced by insulin, via activation of insulin receptors, β-adrenoceptors and calcitonin gene-related peptide receptors. However, main cause of mechanisms mediating the vasodilation remain obscure. Hypertension is associated with insulin resistance and hyperinsulinemia. Insulin resistance may contribute to hypertension by sympathetic overactivity, endothelium dysfunction and decreased vasodilator action of insulin. Therefore, insulin must be considered a vasoactive peptide and more investigations are needed to better understand the full significance of the hemodynamic effect of insulin.View full abstractDownload PDF (602K) -
Toshinori HIDAKA, Takahito INOUE, Kazumi KOMORIYA, Yujiro HAYASHI, Nor ...2000 Volume 115 Issue 5 Pages 295-308
Published: 2000
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSAntiarrhythmic effects and cardiovascular effects of pilsicainide hydrochloride were compared with those of disopyramide in a canine model of coronary ligation-induced ventricular arrhythmias and anesthetized dogs. Pilsicainide (1.25, 2.5 and 5 mg/ kg) and disopyramide (2.5 and 5 mg/kg) decreased the arrhythmic ratio {(ventricular arrhythmias total heart rate)×100} dose-dependently. Pilsicainide at 2.5 and 5 mg/kg and disopyramide at 5 mg/kg suppressed ventricular arrhythmias more than 50%. The effective dose of pilsicainide was lower than that of disopyramide, but the effective plasma concentration of pilsicainide was between 3 and 8μg/ml, which was almost the same as that of disopyramide. In anesthetized dogs, both drugs decreased LV dP/dt max in almost the same concentration-dependent manner. PQ-interval was prolonged by pilsicainide, but not by disopyramide. QRS and QTc were prolonged by both drugs in a concentration-dependent manner. However, the prolongation of QTc by disopyramide was provoked at lower plasma concentrations than by pilsicainide. Because the excessive prolongation of QTc lead to the lethal arrhythmias such as torsades de pointes, pilsicainide may be useful as an injectable antiarrhythmic agent superior to disopyramide.View full abstractDownload PDF (787K)
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