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Biomedical subjects

N Sano

Publications and source records attributed to N Sano.

At least 145 records · Page 8Linked to original sources
PubMed1987

The baroreflex-mediated changes in plasma norepinephrine and heart rate in patients with essential hypertension.

Baroreflex sensitivity was evaluated in 19 patients with essential hypertension (EH), 8 patients with borderline hypertension (BH) and 12 age-matched normal controls (N), by measuring the reflex-mediated changes in plasma norepinephrine (NE) and heart rate (RR interval) while a phenylephrine hydrochloride or a sodium nitroprusside solution was infused in graded doses for a total of 24 minutes. Changes in RR interval and plasma NE showed a significant linear correlation to those in mean arterial pressure (MAP) in every subject studied. The slopes of RR/MAP and %NE/MAP tended to be reduced in EH and BH patients during both pressor and depressor stimulations. There was a significant (p less than 0.01) inverse correlation between the basal MAP levels and RR/MAP or %NE/MAP except for %NE/MAP during pressor stimulation. Fifteen minutes after the pressor stimulation was stopped, MAP and RR interval in each group tended to be greater than their baselines. Plasma NE remained significantly (p less than 0.01) depressed in N and BH subjects while those in EH returned to their baselines. When pressor stimulations were repeated twice at intervals of 15 minutes in hypertensive subjects, the second response curves of MAP-RR interval tended to shift slightly to the right while the slopes of the second response curves of plasma NE were significantly (p less than 0.05) reduced compared with the first ones. These findings indicate that an inability of the baroreflex to produce a sustained suppression of sympathetic nerve activity associated with an efficient ability to reset at the higher pressure levels in EH patients results in a continued tendency for blood pressure to rise and contributes to the development of hypertension.

Adult↗
PubMed1987

Tumorigenicity test of 1,3- and 1,8-dinitropyrene in BALB/c mice.

1,3-Dinitropyrene (DNP) and 1,8-DNP (CAS: 42397-65-9) are very potent mutagens and induce a frameshift-type mutation in the Salmonella test system. Each compound was tested for tumorigenicity in BALB/c mice by sc inoculation of 0.05 mg of the compound once a week for 20 weeks. Tumors developed at the site of injection of 1,8-DNP in 6 of 15 mice up to 60 weeks after the first injection. The incidence of tumors was statistically significant at a P-value of less than .05 but not of less than .01. Therefore, the carcinogenicity of 1,8-DNP in BALB/c mice was concluded to be weaker than that of benzo[a]pyrene [(BP) CAS: 50-32-8], which induced a 100% tumor incidence when it was injected at the same dose as that of 1,8-DNP. No tumors occurred at the injection site in mice given 1,3-DNP. Most of the tumors induced by 1,8-DNP and BP showed histologic features characteristic of malignant fibrous histiocytoma.

Animals↗
PubMed1987

Carcinogenicity of bucetin in (C57BL/6 X C3H)F1 mice.

The carcinogenicity of bucetin [(3-hydroxy-p-butyrophenetidide) CAS: 1083-57-4], an antipyretic analgesic drug, was examined in 300 (C57BL/6 X C3H)F1 mice. Groups of 50 mice of each sex were treated with 1.5 or 0.75% bucetin in their basal diet for 76 weeks and then fed a basal diet for 8 weeks. Control groups were given a basal diet for 84 weeks. In 10 of 46 (22%) male mice given the high dose of bucetin and in 6 of 45 (13%) given the low dose, renal cell tumors were induced. Dysplastic lesions of the proximal tubules were frequently seen in the males given bucetin in a dose-related fashion. Neither tumorous nor preneoplastic lesions developed in the kidneys of bucetin-treated female mice and control animals. Papilloma of the urinary bladder in 1 male mouse and papillary or nodular hyperplasia in 9 mice of both sexes were observed in groups given the high dose of bucetin.

Aminophenols↗
PubMed1986

[Plasma dopamine concentrations in various types of hypertension].

The concentrations of unconjugated plasma dopamine (PDA) were studied in patients with various types of hypertension. Catecholamines were extracted from plasma specimens (1.0-3.0 ml) through an Amberlite CG50 (Li+-form) microcolumn and eluted by a magnesium sulfate - ethanol solution. The elute was then desalinated and deproteinized by the ethanol-treated precipitation procedure and dried in a vacuum oven at 25 degrees C. A fraction of catecholamines was assayed with the modified procedures of the COMT-mediated radio-enzymatic method. This assay system was sensitive enough to permit an accurate measurement of PDA as low as 6.0 pg per ml of plasma without any detectable contamination of the conjugated dopamine. The resting levels of PDA were 10.1 +/- 1.0 pg/ml (mean +/- SEM), 9.5 +/- 1.0 and 13.7 +/- 0.6 in patients with borderline hypertension (BH, n = 25), essential hypertension (EH, n = 22) and renovascular hypertension (RVH, n = 8), respectively. The values in EH patients were significantly smaller than those in age-matched normal controls (13.0 +/- 1.4, n = 14, p less than 0.05). Remarkably increased PDA values were observed in patients with pheochromocytoma (76.5 +/- 25.4, n = 9, p less than 0.01). Significantly raised PDA values were also found in patients with primary aldosteronism (PA, 27.8 +/- 9.0, n = 6, p less than 0.05), while their plasma norepinephrine levels (PNE, 169 +/- 39 pg/ml) tended to be lower than those of normal controls (206 +/- 20), showing an apparent dissociation between the values of PDA and PNE. Upright posture for 15 minutes induced a significant rise in PDA (p less than 0.05) in all subjects except PA patients. The postural changes of PDA, however, were invariably smaller than those of PNE (p less than 0.05). The resting values of PDA in normal, BH and EH patients showed a significant negative correlation with their mean arterial pressures (r = -0.301, n = 61, p less than 0.05) and a positive correlation with those of PNE (r = 0.381, p less than 0.01). There was no correlation between PDA and age in any group studied. These findings indicate that PDA might not be only a precursor fraction of neurotransmitters released from the sympathetic nervous system but could also represent a physiological function of the dopaminergic regulatory system. The varied but distinctive features of PDA status in various types of hypertension suggest the possibility that the peripheral dopaminergic mechanisms play an inherent role in the pathogenesis of hypertension.

Adult↗
PubMed1986

AMP deaminase activity of skeletal muscle in neuromuscular disorders in childhood. Histochemical and biochemical studies.

We studied the histochemical staining and biochemical activity of AMP deaminase in biopsied muscle in Becker-type muscular dystrophy (BMD), Fukuyama-type congenital muscular dystrophy (FCMD), Duchenne-type muscular dystrophy (DMD), Werdnig-Hoffmann disease (WH) in order to elucidate the change of AMP deaminase activity in muscle with neuromuscular disorders in childhood. The intensity of AMP deaminase staining did not decrease in BMD with mild pathologic change, but in DMD, FCMD and WH it decreased in parallel with the severity of the pathologic change. The biochemical activity of AMP deaminase did not decrease in muscle with mild pathologic change in patients with DMD and tended to decrease according to the progress of the disease. The activity of AMP deaminase in muscle of patients with FCMD and WH which showed severe pathologic change was remarkably low. It was demonstrated that the decrease in the activity of AMP deaminase was related to the intensity of pathologic change rather than diagnosis of a neuromuscular disorder.

AMP Deaminase↗
PubMed1986

Dinitro derivatives of pyrene and fluoranthene in diesel emission particulates and their tumorigenicity in mice and rats.

A number of mutagens/carcinogens in diesel emission particulates are produced and distributed into the atmosphere. On the basis of the results of chemical analysis, it was found that most of the mutagenicity in diesel particulate extracts is due to super-mutagens such as 1,3-, 1,6- and 1,8-DNP, and 3,7- and 3,9-DNF. 3,7- and 3,9-DNF are new mutagens which were isolated in this study and they induced a frameshift type mutation in the Salmonella microsome test. Each derivative of DNP and DNF was detected at a concentration of 0.01 to 0.03 ppm in the particulates while the diesel engine was used under the condition of idling. 1,6- and 1,8-DNP were tumorigenic at the injection site in BALB/c male mice when a total of 2 and 1 mg, respectively, of the compounds was given subcutaneously. The incidences for tumors by 60 weeks were at a ratio of 50 and 30%, respectively, for 1,6- and 1,8-DNP-treated mice. 4-NQO and BaP, as positive control, induced tumors at the injection site in BALB/c mice when a total of 2 and 1 mg, respectively, of the compound was given. The incidences of tumors were observed at a high ratio of 90 and 93.4%, respectively, for 4-NQO- and BaP-treated mice. Histologically the tumors were diagnosed as malignant fibrous histiocytomas in all the tumors which developed. No tumors occurred at the injection site in mice given injections of 1,3-DNP. Tumorigenicity tests of 3,7- and 3,9-DNF are now being attempted using F344/DuCrj male rats. This animal experiment is now in progress. In the 3,9-DNF-treated rats (a total of 1 mg per rat), subcutaneous tumors developed in 8 of 11 rats up to 150 days after injection, and a part of a tumor resected from a rat showed the typical features of rhabdomyosarcoma.

Animals↗
PubMed1985

Effects of dietary potassium on the hemodynamics and plasma norepinephrine kinetics in patients with essential hypertension.

The effects of dietary potassium on the hemodynamics and plasma norepinephrine (NE) kinetics were studied in 10 patients with borderline hypertension. Potassium supplement (96 mEq daily for 5-7 days) induced a significant (p less than 0.05) fall in blood pressure and a slight decrease in cardiac output. Both urine volume and urinary sodium excretion increased significantly (p less than 0.05) for a first few days following the potassium supplement. The baseline values of the half-time of the rapid NE removal from plasma was significantly delayed in the hypertensive patients (1.05 +/- 0.06 min, p less than 0.05) when compared with those (0.88 +/- 0.04) in normal controls. Potassium supplement induced a significant rise in both plasma NE levels and NE outflow rate (p less than 0.01) in the hypertensive patients, while their half-times were significantly shortened (0.89 +/- 0.07 min, p less than 0.01). The pressor responsiveness to exogenously infused NE tended to diminish during the potassium supplement. These findings indicate that a high potassium intake might accelerate the slowed neuronal NE uptake in the hypertensive patients, while a potassium-induced fall in blood pressure might exert a baroreflex stimulation of NE release. As a net result, an increased NE outflow into the circulation has been confirmed. It is likely that a natriuresis-induced volume contraction might be a predominant factor responsible for the early reduction of blood pressure during the high potassium intake.

Adult↗
PubMed1981

[Effects of dilazep on cerebral blood flow under normal conditions and recirculation impairment after cerebral ischemia (author's transl)].

Regional cerebral blood flow (r-CBF) in anesthetized dogs was measured by the H2 clearance method. Cerebral ischemia was induced by permanent ligation of bilateral vertebral arteries (VA) and a 10 min occlusion of bilateral common carotid arteries (CCA). Under normal conditions, dilazep (100 and 300 micrograms/kg i.v.) increased r-CBF dose-dependently without affecting arterial PO2, PCO2 and pH. r-CBF was reduced by 40% during cerebral ischemia. Relative r-CBF rates, as compared with pre-ischemic rates, were 85%, 80%, 77% and 75% at 30, 60, 90 and 120 min after cerebral ischemia, respectively, indicating development of recirculation impairment. Dilazep (100 and 300 micrograms/kg i.v. 30 min before CCA occlusion) did not affect r-CBF reduction during the state of cerebral ischemia, whereas it prevented re-circulation impairment after cerebral ischemia. Papaverine (300 micrograms/kg i.v. 30 min before CCA occlusion) exerted similar effects. These results suggest that dilazep is a potentially effective drug for treating cerebrovascular disorders.

Animals↗