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Biomedical subjects

S Kagiyama

Publications and source records attributed to S Kagiyama.

At least 37 records · Page 2Linked to original sources
PubMed1998

Enhanced depressor response to nitric oxide in the rostral ventrolateral medulla of spontaneously hypertensive rats.

Possible impairment of the L-arginine-nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting N(G)-nitro-L-arginine methyl ester (L-NAME), NOC 18 (an NO donor), or L-arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15+/-3 versus 10+/-2 mm Hg, respectively; n=8). In contrast, microinjection of L-arginine elicited significant (P<.05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of L-arginine: -29+/-2 versus -15+/-2 mm Hg, respectively; n=8, P<.01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY (-38+/-7 versus -22+/-3 mm Hg, respectively; n=8, P<.05). These results suggest that the L-arginine-NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.

Animals↗
PubMed1998

Single L-type calcium channels in smooth muscle cells from resistance arteries of spontaneously hypertensive rats.

The amplitude of the whole-cell L-type Ca2+ channel current recorded from vascular smooth muscle cells is reportedly greater in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto rats (WKY). However, no study has examined properties of single Ca2+ channels in arterial cells from these strains. To further test the hypothesis that activation of L-type Ca2+ channels in arterial smooth muscle cells would be enhanced in SHR, we recorded single Ca2+ channel currents in resistance mesenteric artery cells from SHR and WKY (8 to 9 weeks of age) using a cell-attached patch clamp technique. With 50 mmol/L Ba2+ in the recording pipette, the depolarizing pulse from a holding potential of -40 mV evoked the single L-type Ca2+ channel current. Opening of the single channels was more frequent in cells from SHR than from WKY. Single-channel conductance (20 pS) and open time (1 ms at 0 mV) did not differ in the two strains. The results suggest that an increased amplitude of the whole-cell current can be attributed to the enhanced opening of single Ca2+ channels in the arterial smooth muscle cells from SHR compared with WKY.

Animals↗
PubMed1998

Asymptomatic moyamoya disease associated with coronary and renal artery stenoses--a case report.

Moyamoya disease is an occlusive intracranial arteriopathy with abnormal cerebral vascular collateral networks. Although this disease is known to be associated with stenosis of extracranial arteries, such as the renal artery, a case associated with stenoses of the coronary and renal arteries has not been reported. We described here a 23-year-old man who had effort angina, renovascular hypertension, and asymptomatic moyamoya disease. Arterioangiography revealed bilateral occlusion of the intracranial carotid arteries and stenoses in the left coronary artery and the left renal artery.

Adult↗
PubMed1998

Central and peripheral mechanisms involved in hypertension induced by chronic inhibition of nitric oxide synthase in rats.

OBJECTIVE: To study the possible central and peripheral mechanisms involved in hypertension induced by chronic inhibition of nitric oxide synthase. METHODS: We evaluated neurohormonal and renal responses of Wistar rats to chronic oral administration of 20 and 100 mg/kg per day NG-nitro-L-arginine methyl ester (L-NAME). Effects of intracerebroventricular and intravenous injections of NO donors (NOC-18 and FK-409) and an angiotensin II type 1 receptor antagonist CV-11974, and intravenous injection of alpha-adrenergic receptor antagonist phentolamine after chronic treatment with 100 mg/kg per day L-NAME were also studied. RESULTS: The chronic treatment with L-NAME induced a sustained dose-dependent hypertension with a decrease in heart rate. Urinary levels of norepinephrine and epinephrine decreased with no changes in plasma catecholamine levels, renin activity, and vasopressin level. Serum nitrate/nitrite levels in the rats treated with the high dose of L-NAME decreased. The intracerebroventricular and intravenous injections of the NO donors reduced arterial pressure in L-NAME-treated rats to a significantly greater extent than they did that in control rats. The intravenous but not intracerebroventricular injection of CV-11974 produced a sustained decrease in arterial pressure of L-NAME-treated rats. The depressor responses to intravenous injection of phentolamine of L-NAME-treated and control rats were similar. CONCLUSIONS: Results indicate that L-NAME-induced hypertension is associated with a deficiency of nitric oxide, both peripherally and centrally. Circulating angiotensin II could contribute to the maintenance of hypertension via angiotensin II type 1 receptor while the sympathetic nervous system seems to be suppressed.

Acute Disease↗
PubMed1997

Cardiovascular effects of nitric oxide in the rostral ventrolateral medulla of rats.

To investigate the cardiovascular role of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), NOC 18, an NO donor, was microinjected into the RVLM of rats. NOC 18 significantly decreased mean arterial pressure (MAP). Pre-treatment with an NO trapper, carboxy-PTIO, abolished the NOC 18-induced decrease in MAP. Microinjection of L-NAME, an NO synthase inhibitor, increased MAP. L-Arginine reduced MAP and inhibited the pressor response induced by L-NAME. Results suggest that NO acts on the RVLM neurons and plays an important role in cardiovascular regulation.

Animals↗
PubMed1997

Pressor and sympathetic responses to excitatory amino acids are not augmented in the ventrolateral medulla of Dahl salt-sensitive rats.

We assessed the pressor and sympathetic responses to microinjection of excitatory amino acids (EAA) into the rostral ventrolateral medulla (RVLM) to see whether the response would be augmented in salt-induced hypertension. Seven-week-old Dahl-Iwai salt-sensitive rats were fed either a high- (8%, n = 10) or a low- (0.3%, n = 12) salt diet for 3 weeks. Then, L-glutamate (2 nmol), N-methyl-D-aspartate (NMDA; ionotropic EAA receptor agonist, 20 pmol) or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD; metabotropic EAA receptor agonist, 1 nmol] was microinjected into the RVLM of urethane-anesthetized, artifically ventilated rats. The rats fed a high-salt diet showed a significantly (P < 0.001) higher mean arterial pressure (123 +/- 3 mmHg) than those fed a low-salt diet (99 +/- 2 mmHg). We found similar increases in mean arterial pressure and splanchnic sympathetic nerve activity elicited by microinjection of L-glutamate into the RVLM in the high- (33 +/- 2 mmHg and 52 +/- 10%) and low- (35 +/- 3 mmHg and 46 +/- 8%) salt groups. Similarly, pressor and sympathoexcitatory responses to either NMDA or (1S,3R)-ACPD did not differ between the groups. Microinjections of the lower doses of L-glutamate, NMDA and (1S,3R)-ACPD also showed comparable pressor responses between the groups. These results indicate that salt-induced hypertension in Dahl salt-sensitive rats is not associated with enhanced responsiveness of the RVLM to EAA. This is in contrast with our previous findings that pressor and sympathetic responses to EAA are enhanced in spontaneously hypertensive rats.

Analysis of Variance↗
PubMed1997

Percutaneous transluminal angioplasty attenuates day-night difference in ambulatory blood pressure in renovascular hypertension.

To evaluate whether the circadian rhythm of blood pressure (BP) was altered in renovascular hypertension (RVH), ambulatory BP was monitored using a noninvasive recorder in nine patients with RVH attributable to fibromuscular dysplasia before and after percutaneous transluminal angioplasty (PCTA). The circadian rhythm of BP was assessed by the day-night difference in BP and by the single cosinor method. The day-night difference in BP before PCTA was significantly greater than in age- and sex-matched normotensive subjects (n = 9, P < .01) and patients with essential hypertension (n = 9, P < .05). PCTA decreased significantly the 24-h BP as well as plasma renin activity (P < .01). In the chronogram, the BP reduction after PCTA was evident especially during the day. Accordingly, the day-night difference in BP decreased significantly after PCTA (P < .01). In the cosinor analysis, the mesor and the percent amplitude of BP decreased significantly after PCTA (P < .01). In summary, circadian rhythm of BP was preserved or rather exaggerated in RVH. The stimulated renin angiotensin system in RVH possibly contributes to the altered circadian rhythm of BP primarily by elevating the daytime BP.

Adolescent↗
PubMed1990

Genetic polymorphisms of gene conversion within the duplicated human alpha-globin loci.

Of the 645 Japanese subjects studied, we have identified 10 individuals heterozygous for a chromosome with the triplicated alpha-globin loci. The frequency of the triple alpha-loci was 0.008 in this population, while that of the single alpha-locus, i.e., alpha-thalassemia 2 gene, might be lower than 0.0008. Analysis of haplotypes using particular RsaI site polymorphism in the alpha-globin gene complex strongly suggests that the triple alpha loci may have had multiple origins in this population.

Gene Conversion↗
PubMed1990

[Acute lymphocytic leukemia with Philadelphia chromosome and rearrangements of bcr gene and deletion of 5' side and of TCR-delta gene].

A 58-year old man was admitted because of general malaise in April 1987. Physical examination revealed systemic lymphadenopathy and hepatosplenomegaly. The white blood cell count was 252, 900/microliters with 82% of blasts. Bone marrow aspiration contained 93.8% lymphoblasts, which were positive for TdT and negative for peroxidase reaction. Immunologic marker studies showed OKT 11 positive and CALLA negative. Cytogenetic analysis revealed a clone with 46, XY, t (9; 22) (q34; q11), del(5) (q15) in 12 of the 13 metaphases. Ph1 positive T-acute lymphoblastic leukemia was considered. After AdVP and following AdVEMP (induction) chemotherapy, complete remission was obtained in August 1987. Cytogenetic study at the remission stage showed complete disappearance of Ph1 positive clone. Treatment with BH-AC DMP protocol at the time of recurrence in November 1987, brought no improvement and he died of respiratory failure. Chromosome study at recurrence showed an additional complex abnormal karyotype (double Ph1, +2, 5q-, -10, -13, -17). DNA analysis revealed rearrangements of bcr gene with deletion of 5' side and of TCR delta gene, without any rearrangements in other immunoglobulin genes. From cytogenetic, immunophenotypic and genetic analysis the patient was diagnosed as having acute lymphocytic leukemia (FAB L1) with Philadelphia chromosome and rearrangements of bcr gene with deletion of 5' side and of TCR delta gene.

Animals↗
PubMed1990

Congenital hypoplasia of the dorsal pancreas: with special reference to duodenal papillary dysfunction.

We report a case of dorsal pancreatic hypoplasia complicated with atresia of the vagina, type-A chronic atrophic gastritis, duodenal papillary dysfunction, and insulin-requiring diabetes mellitus, in a 32-yr-old woman. The laboratory data showed elevated hepatobiliary enzymes. Endoscopic retrograde cholangiopancreatography (ERCP) revealed a slightly dilated common bile duct and a short major pancreatic duct connected with a minor pancreatic duct. Ultrasonography and computerized tomography could not identify any pancreatic tissue in the region of the body or tail of the pancreas. The pancreatic tissue weight calculated by the serial thin slice of computerized tomography was 43.1 g, approximately 45% of the standard Japanese adult pancreas. Reevaluated pancreatic exocrine function based on this weight showed a hypersecretory state. The pancreatic ductal pressure was slightly increased, and the motility of the sphincter of Oddi (SO) was abnormal when measured with a 4Fr. microtransducer inserted through a duodenoscope. These findings suggest that dysfunction of the sphincter of Oddi may play some role in the pathophysiology in the hypoplasia of the dorsal pancreas and pancreaticobiliary diseases associated with it.

Adult↗
PubMed1989

Reflex regulation of the sphincter of Oddi by intrapancreatic ductal pressure in the Japanese monkey.

Japanese monkey has a common ampullary channel. By a continuous injection of sterile saline (1 mL/min) into the pancreatic main duct, the pancreatic main ductal pressure increased from 8.4 +/- 1.0 (mean +/- SD) to a plateau level (16-25 mmHg) in 5 Japanese monkeys. The frequency and amplitude of the slow wave in electromyography of the sphincter of Oddi (SO) were significantly decreased from 14 to 2/min and 0.06 to 0.04 mV (p less than 0.01), and the frequency of the spike component significantly decreased from 53 to 14/min (p less than 0.05). As soon as infusion of saline ceased, the electromyography recovered to the original level. The mean value of the minimum loading pressure affecting myoelectrical activities of the SO was 19.8 +/- 3.0 mmHg. When the pancreatic duct was obstructed at the head, there was no significant change in the SO myoelectrographic activities in spite of increased pancreatic ductal pressure by infusion. These findings suggest that a homeostatic mechanism of pancreatic ductal pressure exists when the activity of the SO is regulated by the distending pressure in the pancreatic ductal system. This reflex regulation seemed to be mediated by the distension of the ampullary duct itself.

Ampulla of Vater↗
PubMed1988

Pressure of papillary sphincter zone and pancreatic main duct in patients with alcoholic and idiopathic chronic pancreatitis.

To determine the significance of manometric pressure of the pancreatic duct in patients with alcoholic and idiopathic chronic pancreatitis, we used a microtransducer inserted through a duodenoscope to measure pressures in the papillary sphincter zone and pancreatic main duct in 20 control subjects and 31 patients with chronic pancreatitis without papillary stenosis including 10 cases of alcoholic chronic pancreatitis (ALCP) and 21 cases of idiopathic chronic pancreatitis (ICP). The pancreatic main ductal pressure was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg) or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP and ICP. There was no significant difference between control subjects and ICP in the motility of the sphincter of Oddi. In ICP there were no correlationships between pancreatic ductal pressure and the motility of papillary sphincter zone. In ALCP, the frequency of the papillary sphincter waves was significantly higher than in normal subjects and there was a correlation between the pancreatic ductal pressure and the motility of the papillary sphincter zone. These data suggest that increased pancreatic ductal pressure in ALCP may be in part due to papillary dysfunction, but not in ICP.

Alcoholism↗
PubMed1988

Pressure of papillary sphincter zone and pancreatic main duct in patients with chronic pancreatitis in the early stage.

We measured pressures of the papillary sphincter zone and pancreatic main duct endoscopically in 20 control subjects and in 38 patients with chronic pancreatitis without papillary stenosis, including 19 cases believed to be in the early stages of chronic pancreatitis. There was no significant difference between control subjects and patients with chronic pancreatitis without papillary stenosis in the motility of the sphincter of Oddi. The pancreatic main ductal pressure was significantly higher in the patients in the early stage of chronic pancreatitis (35.7 +/- 9.1 mm Hg (mean +/- SD) in patients suspected of having chronic pancreatitis and 44.9 +/- 20.4 mm Hg in minimal-change chronic pancreatitis) than in the controls (16.2 +/- 8.7 mm Hg). The viscosity of pure pancreatic juice of patients with chronic pancreatitis (5.0 centi-Poise (cP] in the basal secretory phase was significantly higher than that of the controls (1.32 cP). These data suggest that endoscopic measurement of pancreatic ductal pressure is useful for diagnosis of the early stages of chronic pancreatitis.

Adult↗
PubMed1988

Motility of the sphincter of Oddi and pancreatic main ductal pressure in patients with alcoholic, gallstone-associated, and idiopathic chronic pancreatitis.

We endoscopically measured pressures of the pancreatic duct (PP) and the sphincter of Oddi (SO) in patients with alcoholic (ALCP, n = 10), gallstone-associated (GSCP, n = 7), and idiopathic chronic pancreatitis (ICP, n = 21), and in 20 controls. The PP was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg), GSCP (33.6 +/- 16.2 mm Hg), or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP, GSCP, and ICP. There was no significant difference between control subjects and ICP in the motility of SO. In ICP, there was no correlation between the PP and the motility of SO. In ALCP and GSCP, the frequencies of the papillary sphincter waves were significantly higher than in normal subjects, and there were correlations between the PP and the motility of SO. These data suggest that increased pancreatic ductal pressure in GSCP with papillitis or ALCP may be due in part to papillary dysfunction, but not in ICP.

Alcoholism↗