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Volume 103 (1994)
- Issue 6 Pages 245-
- Issue 5 Pages 193-
- Issue 4 Pages 141-
- Issue 3 Pages 83-
- Issue 2 Pages 43-
- Issue 1 Pages 1-
Volume 103, Issue 3
Displaying 1-5 of 5 articles from this issue
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Toshiaki TAMAKI, Youichi ABE1994 Volume 103 Issue 3 Pages 83-89
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSGlomerular circulation is mainly regulated by two resistance arterioles, the afferent arteriole and the efferent arteriole. Many experimental findings show that each arteriole has a different sensitivity to various kinds of physiological stimuli and some vasoactive substances. Moreover, there is a regional heterogeneity of the glomerular microcirculation. Thus, many researchers have been challenged to develop direct studies that focus on the control of the renal microcirculation. The recent development of innovative in vivo and in vitro preparations provide the opportunity to directly study the renal microcirculation. In this article, we introduce the methods for isolation, cannulation and in vitro study of a single renal arteriole. The isolated renal microvessel technique permits direct in vitro assessment of single arteriolar responses in defined segments to vasoactive substances without the neurohumoral and parenchymal tissue environment. Intracelluar ion concentration and functional change of the renal microvessel can be evaluated simultaneously using both this technique and fluorescent ion indicators. Accumulation of data that directly assesses the renal microcirculation may clarify mechanisms for the regulation of renal hemodynamics.View full abstractDownload PDF (13901K) -
Satoshi YODONAWA, Motohiro KUROSAWA1994 Volume 103 Issue 3 Pages 91-99
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSProstaglandin F2α (PGF2α) has been suggested to play a role in the pathogenesis of bronchial asthma. In this study, the effects of intravenous administration of 13, 14-dihydro-15-keto-PGF2α, a stable metabolite of PGF2α, on bronchial smooth muscle in guinea pigs were investigated by measuring dynamic respiratory resistance using a formula that excludes the effects of differences in airway wall thickness. With this formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness. Administration of 13, 14-dihydro-15-keto-PGF2α did not induce airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was significantly enhanced by the administration of 13, 14-dihydro-15-keto-PGF2α. Moreover, TXA2 antagonists, ONO-NT-126 and ONO-8809, inhibited the effect of 13, 14-dihydro-15-keto-PGF2α administration. These results suggest that 13, 14-dihydro-15-keto-PGF2α can be important mediators affecting bronchial hyperresponsiveness, and TXA2 may play a part in the 13, 14-dihydro-15-keto-PGF2α-induced bronchial hyperresponsiveness.View full abstractDownload PDF (13930K) -
Makoto OHURA, Toyoki MORI, Kozo WATANABE, Katsumi IKEZONO, Natsuki NAK ...1994 Volume 103 Issue 3 Pages 101-109
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSPranidipine (OPC-13340) is a novel, potent and long-acting 1, 4-dihydropyridine derivative Ca-antagonist being developed for clinical use as an antihypertensive and antianginal drug. Pranidipine at concentrations of 10-9 ?? 10-6 M suppressed the contraction induced by serotonin (10-8 ?? 10-5 M) or histamine (10-8 ?? 10-4 M) in isolated porcine coronary arteries in a non-competitive and concentration-dependent manner. The potency of this effect of pranidipine was almost similar to that of nifedipine. In anesthetized open-chest pigs with coronary artery occlusion, pranidipine at a dose of 10 μg/kg, i.v. lowered blood pressure and increased heart rate, peak dP/dt and % segment shortening of the non-ischemic zone before occlusion. Pranidipine inhibited the ST elevation of the electrocardiogram and the increase in left ventricular end-diastolic pressure during ischemia. These results suggest that pranidipine might relieve symptoms via inhibition of coronary spasm and reduce myocardial ischemia due to reduction of both preload (left ventricular end-diastolic pressure) and afterload (blood pressure).View full abstractDownload PDF (15643K) -
Masayuki UCHIDA, Hiroki HAMURA, Satoshi TAKAGI, Yuji NOGUCHI, Hiroko S ...1994 Volume 103 Issue 3 Pages 111-120
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSGastric lesion was induced by the oral administration of acidified aspirin in rats with hepatic cirrhosis produced by N-nitrosodiethylamine (NDA) or carbon tetrachloride (CCl4). Gastric lesion by acidified aspirin was aggravated in NDA-induced cirrhosis, but not in CCl4-cirrhotic rats. To clarify this difference in the susceptibility of the gastric mucosa, gastric mucosal blood flow and gastric emptying were measured by the hydrogen gas clearance method and beads method, respectively. Gastric mucosal blood flow was lower and gastric emptying was significantly delayed in NDA-induced cirrhotic rats as compared with the controls, but not in CCl4-induced cirrhotic rats. Gastric mucosal blood flow in NDA-induced cirrhotic rats was significantly decreased by the oral administration of acidified aspirin as compared with the controls. Aldioxa dose-dependently inhibited the gastric lesion formation by acidified aspirin and inhibited the decrease of gastric mucosal blood flow in NDA-induced cirrhotic rats. These results suggest that aggravation of gastric lesion induced by acidified aspirin in NDA-induced cirrhotic rats would be due to the decrease of gastric mucosal blood flow and delay of gastric emptying. In addition, aldioxa showed a protective effect against gastric lesions induced by acidified aspirin in NDA-induced cirrhotic rats, suggesting that this compound would have an inhibitory effect on gastric lesions that are accompanied by hepatic cirrhosis.View full abstractDownload PDF (28459K) -
Ikuhisa YAKUO, Katsumi ISHII, Yasuhiro SETO, Kiyomi IMANO, Kunihiko TA ...1994 Volume 103 Issue 3 Pages 121-135
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe anti-allergic activity of ebastine, a novel antihistamine, was assessed in comparison with several antihistamines. 1)Orally administered ebastine dose-dependently inhibited 7-day homologous passive cutaneous anaphylaxis (PCA), experimental allergic rhinitis and experimental asthma in guinea pigs or rats (ED50-values were 2.17, 0.29 and 0.35 mg/kg, respectively); and its anti-allergic activity was more potent than those of terfenadine and mequitazine. Moreover, its PCA-inhibitory activity was still observed 24 hr after the administration. 2)Orally administered ebastine also inhibited histamine-induced skin reaction in rats (ED50: 1.10 mg/kg). 3)In isolated guinea pig trachea, ebastine had no effect on histamine-induced contraction, but carebastine, a main metabolite of ebastine, inhibited this contraction (IC50: 0.12 μM). 4)Carebastine (30-100 μM) supressed the histamine release from rat peritoneal mast cells and human basophils. 5)Ebastine at a high oral dose showed slight inhibition of the specific binding of 3H-mepyramine to the histamine H1-receptor in rat brain. This binding-inhibitory activity of ebastine was little more potent than that of terfenadine, but much less potent than those of mequitazine and ketotifen. These results indicated that ebastine has potent and long acting anti-allergic activity with few side effects based on the antihistaminic activity in the central nervous system. Furthermore, it was suggested that these effects of ebastine are due to the action of a main metabolite, carebastine.View full abstractDownload PDF (25412K)
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