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Biomedical subjects

M Asano

Publications and source records attributed to M Asano.

641 records · Page 36Linked to original sources
PubMedDate not supplied

Tumor vessels and contrast enhancement of hepatocellular carcinoma demonstrated by percutaneous transhepatic portography. Report of a case.

A patient with an Edmondson type I-II hepatocellular carcinoma had, at celiac angiography, a poor arterial supply but a rich portal supply as observed at percutaneous transhepatic portography, an observation not previously reported in this disease. The importance of demonstrating the vascular supply of the tumor previous to planned intravascular treatment is obvious.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

Suppression of ascites formation and re-accumulation associated with human ovarian cancer by an anti-VPF monoclonal antibody in vivo.

Ascites formation is often observed in ovarian cancer patients. Vascular permeability factor (VPF) may induce ascites formation. We established an animal model of ascites formation and re-accumulation by i.p. transplantation of a human ovarian adenocarcinoma cell line, NOS2, into nude mice. The formation of ascites was observed after 10 days of tumor inoculation and continued for up to 4 weeks. In the ascitic fluid, biologically active VPF was detected. The repeated i.p. administration of an immunoneutralizing monoclonal antibody (MAb) to VPF, MV833, significantly inhibited the formation of ascites throughout the experiments. Re-accumulation of ascites occurred quickly in control mice after aspiration of ascites and these mice died within 20 days. MV833 again inhibited the re-accumulation of ascites and significantly prolonged the life span of mice without any side effect. These results indicate that VPF plays an important role in the accumulation of ascites induced by ovarian cancer and an anti-VPF MAb is a new specific drug to suppress the formation and re-accumulation of ascites. This MAb may contribute to ameliorating quality of life of cancer patients as well as prolong their survival.

Animals↗
PubMedDate not supplied

Effects of a human urinary kininogenase (SK-827) on cerebral microcirculation after glass bead-induced cerebral embolism in rabbits.

The pharmacological effects of a human urinary kininogenase (SK-827) on the cerebral microcirculation were studied intravital-microscopically in a rabbit with cerebral microvessel injury induced by glass bead injection into an internal carotid artery. Intravenous administration of SK-827 dilated pial arteries of the brain and increased cerebral hemoglobin content (IHb). SK-827 tended to dilate smaller arterioles more markedly than larger arterioles, and larger arterioles than small arteries. SK-827 appeared to have a vasodilating effects qualitatively different from those of nicardipine and CDP-choline. Findings obtained by concurrent hematological and biochemical examinations also suggested its beneficial effects on the function of platelets and erythrocytes.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Calcium entry blocking, beta 1-adrenoceptor blocking and hypotensive effects of YM-16151-4.

The calcium entry blocking, beta 1-adrenoceptor blocking and hypotensive effects of YM-16151-4 were studied in pithed rats and in conscious normotensive rats. In pithed rats, intravenous injection of YM-16151-4 inhibited a YC-170-induced pressor response and an isoproterenol-induced positive chronotropic response with DR10 values of 4.20 and 0.31 mg/kg, respectively. Similarly, a single oral dose of YM-16151-4 inhibited YC-170 and isoproterenol-induced responses with DR10 values of 109.94 and 9.14 mg/kg, respectively. On the other hand, both intravenous and single oral doses of YM-16151-4 produced a dose-dependent hypotensive effect with no increase in heart rate in conscious normotensive rats. The onset of this effect was slow but long-lasting. During repeated oral administration of YM-16151-4 (30 mg/kg) for 5 days, the hypotensive effect of the compound did not change, indicating that this effect did not increase and tolerance did not develop. The time course of the calcium entry blocking activity of YM-16151-4 was very similar to that of its beta 1-adrenoceptor blocking activity, suggesting that the activities of calcium antagonism and beta 1-adrenoceptor blockade of the compound were almost constant at any time after oral dosing. We conclude that YM-16151-4 combines calcium entry and beta 1-adrenoceptor blocking activities in vivo, and produces a hypotensive effect without an increase in heart rate.

Administration, Oral↗
PubMedDate not supplied

Is atrial natriuretic polypeptide a cause of pathophysiology in total artificial heart animals?

The purpose of this study was to clarify whether plasma ANP levels (p-ANP) are abnormal in TAH animals, and if ANP plays an important role in circulatory failure in TAH animals. In five TAH goats that survived for 51-171 days, changes in hemodynamic parameters, plasma levels of renin, angiotensin I and II, aldosterone (p-RAA), and p-ANP were measured, and correlations between p-ANP and other parameters were studied, and histologic study of ANP and assay of the ANP content in atrial tissue was undertaken. Generally, p-ANP of TAH goats fell temporarily after surgery but then recovered to preoperative levels. Histopathologic studies of atrial tissue and ANP granules proved almost normal, although the coronary blood supply was occluded for more than 170 days; the ANP content in the atrium did not show significant changes after 51 days of TAH pumping. In one case prominent correlations between p-ANP and p-RAA were observed, and in another case significant correlation between p-ANP and arterial pressure was observed. However, these correlations were not observed in every case. In TAH goats the plasma ANP level did not increase in spite of high atrial pressures. Plasma ANP levels in TAH animals are almost normal. In TAH animals no role in the pathogenesis of hemodynamic abnormalities is played by abnormality of plasma ANP levels. However, TAH animals may display an abnormality in sensitivity to the p-ANP.

Aldosterone↗
PubMedDate not supplied

Pharmacological properties of YM-15430-1, a 1,4-dihydropyridine derivative with beta 1-adrenoceptor-blocking activity.

The pharmacological properties of YM-15430-1 and its stereoisomers (YM-15430-2, YM-15430-3 and YM-15430-4) were evaluated in in vitro experiments. In the rabbit isolated aorta, all compounds antagonized the CaCl2-induced contraction with a negative logarithm of the dissociation constant in calcium antagonism of 8.51, 7.13, 8.68 and 7.16, respectively. In the rat isolated right atrium, YM-15430-1 produced a competitive antagonism of the isoprenaline-induced tachycardia with a pA2 value of 7.59. YM-15430-2, YM-15430-3 and YM-15430-4 also antagonized the isoprenaline-induced tachycardia, with pA2 values of 7.91, 7.09 and 6.24, respectively. Because it was the most active of the 4 stereoisomers, YM-15430-1 was particularly studied. YM-15430-1 showed an about 100-fold greater selectivity for beta 1- than for beta 2-adrenoceptors, and had no intrinsic sympathomimetic activity. These results suggest that YM-15430-1 is a hybrid compound which combines calcium entry-blocking and selective beta 1-adrenoceptor-blocking activities in one molecule.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Cardiovascular effects of YM-16151-1 and its optical isomers: a novel calcium entry blocking and beta 1-adrenoceptor blocking agent.

The pharmacological activities of YM-16151-1, a combined calcium entry blocking and beta 1-adrenoceptor blocking agent, and its optical isomers were investigated on the cardiovascular system of dogs anesthetized with pentobarbital. YM-16151-1 (0.1-1 mg/kg, i.v.) dose-dependently increased coronary arterial blood flow and decreased mean blood pressure, total peripheral resistance, heart rate and dp/dtmax with almost no effect on cardiac output. S-(-)- and R-(+)-isomers (0.1-1 mg/kg, i.v.) resembled YM-16151-1 in increasing coronary arterial blood flow and decreasing mean blood pressure and total peripheral resistance and were almost equipotent with YM-16151-1 in these effects. However, these optical isomers differed from YM-16151-1 in the changes in heart rate, dp/dtmax and cardiac output. The rank order of potency for these cardiac effects was S-(-)-YM-16151-1 > YM-16151-1 > R-(+)-YM-16151-1. In vagotomized dogs, YM-16151-1 inhibited the isoproterenol (0.2 microgram/kg, i.v.)-induced tachycardia with an ED50 value of 0.11 mg/kg, i.v. S-(-)- and R-(+)-isomers also inhibited the isoproterenol-induced tachycardia with ED50 values of 0.039 and 0.39 mg/kg, i.v., respectively. Thus, the difference in cardiac effects obtained from the anesthetized dog study among these compounds may be caused by the potency difference of their beta 1-adrenoceptor blocking activities. In addition, R-(+)-isomer, possessing a less potent beta 1-adrenoceptor blocking activity than S-(-)-isomer, only produced a dose-dependent tachycardia at the hypotensive doses in conscious dogs. The present results demonstrate that YM-16151-1 behaves as a hybrid compound combining calcium entry blocking and beta 1-adrenoceptor blocking activities, and also demonstrate that YM-16151-1 is a racemic mixture with equal proportions of the two optical isomers, and, as such, the overall activity may be due to the sum of the activities of the individual optical isomers.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Effects of a human urinary kininogenase (SK-827) on cerebral and cutaneous microcirculation in rabbits.

Pharmacological effects of a human urinary kininogenase (SK-827) on the cerebral and cutaneous microcirculation were studied in anesthetized normal rabbits. Intravenous administration of SK-827 had no effect on the diameter of pial arterioles or the hemoglobin content (IHb) of the brain. On the other hand, SK-827 increased IHb of the skin, dose-dependently and dilated cutaneous arterioles transiently with increased capillary red blood cell velocity. These findings suggest that the pharmacological effects of SK-827 on the microcirculation of the brain and the skin differ from each other due to the activity of the autoregulatory mechanism.

Animals↗