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Biomedical subjects

T Sakamaki

Publications and source records attributed to T Sakamaki.

At least 73 records · Page 4Linked to original sources
PubMed1994

A cardiac myxoma with interleukin-6 production and cerebral metastasis.

The occurrence of cerebral metastasis from cardiac myxoma is extremely rare. We present a 70-year-old man who had atrial myxoma with two metastatic myxomas in his brain. Histopathologic examination revealed a benign myxoma. An elevated interleukin-6 (IL-6) concentration in the serum, and immunohistochemical staining of the primary myxoma by an anti-IL-6 monoclonal antibody confirmed interleukin production by the myxoma. The IL-6-positive myxoma cells were closely attached to the cerebral endothelial cells. This suggests that IL-6 production by the atrial myxoma may have been an important factor for intravascular metastasis or embolization.

Aged↗
PubMed1994

Effect of vasopressin V (OPC-21268) and V2 (OPC-31260) antagonists on renal hemodynamics and excretory function.

Our objective was to assess the effect of endogenous AVP on renal hemodynamics and excretory function. We measured mean arterial pressure (MAP), renal blood flow (RBF), glomerular filtration rate (GFR) and urine osmolality before and after the intravenous infusion of a V1 antagonist (OPC-21268), a V2 antagonist (OPC-31260) and their vehicle (saline) in anesthetized male Wistar rats. The infusion of the V2 antagonist increased the urine flow rate and reduced the urine osmolality significantly (p < 0.05). The infusion of saline and the V1 antagonist did not change the urine flow rate or the urine osmolality. The infusion of saline, the V1 antagonist and the V2 antagonist had no effect on MAP, RBF or GFR. These results suggest that endogenous AVP plays a critical role in the regulation of renal water reabsorption mediated through the V2 receptor.

Animals↗
PubMed1994

DNA typing of HLA class II genes; DRB1*0803 increases the susceptibility of Japanese to primary biliary cirrhosis.

The association between human leukocyte antigens and primary biliary cirrhosis is controversial, but major histocompatibility complex class II antigen DR8 was recently reported to be associated with increased susceptibility for primary biliary cirrhosis in some Caucasians and Japanese. Accordingly, we performed DNA typing of HLA class II genes in Japanese patients with primary biliary cirrhosis. The genotypes of HLA DRB1, DRB3-5, DQA and DQB were determined by polymerase chain reaction and subsequent hybridization with sequence specific oligonucleotides in 31 primary biliary cirrhosis patients and 215 racially matched local controls. DR8 was found in 24 of the 31 primary biliary cirrhosis patients and was highly concentrated in DRB1*0803. The gene frequency of DRB1*0803 was significantly increased in the patients (35.5% vs 7.4%, relative risk = 6.84, p < 0.0001). DQA1*0103 and DQB1*0601 were also increased in the primary biliary cirrhosis patients, in relation to linkage disequilibrium with DRB1*0803 on the same haplotype. In contrast, DQA1*0102 showed a significantly lower frequency in the primary biliary cirrhosis patients (p < 0.05). These data suggest that DRB1*0803 is one of the HLA class II genes related to an increased risk of primary biliary cirrhosis in Japanese individuals.

Adult↗
PubMed1994

HLA-DR alleles in patients with Sjögren's syndrome over-representing V beta 2 and V beta 13 genes in the labial salivary glands.

To identify genetic factors that play a role in the pathogenesis of patients with SS over-representing V beta 2 and V beta 13 genes in the lips, HLA-DR and -DQ alleles of 10 primary SS patients with predominant expression of V beta 2 and V beta 13 genes in the lips were analysed, using the polymerase chain reaction (PCR) and sequence specific oligonucleotide probes. The CDR3 amino acid sequences of cDNA clones encoding V beta 2 and V beta 13 genes were also determined by PCR. The results showed that the DRB4*0101 allele was significantly increased (80%) and that the frequency of DRB3 allele was decreased (0%) when compared to findings in healthy subjects (35.6 and 26%, respectively). Sequencing analyses demonstrated that 75% of V beta 2 cDNA clones and 87% of V beta 13 cDNA clones had a glutamine residue at position 106, in the CDR13 region. Moreover, the conserved sequences (Y*TLRNEQ) in the CDR3 of V beta 13-positive T cell were detected in two different clones (27%) from the two individual SS patients. These findings suggest that the decreased DRB3 and increased DRB4*0101 alleles may be associated with the antigens recognized by V beta 2- and V beta 13-positive T cells.

Alleles↗
PubMed1994

Identification of the disease-related T cell epitope of ovalbumin and epitope-targeted T cell inactivation in egg allergy.

An ovalbumin (OVA)-specific T cell line (TCL) was established from a patient with hen egg allergy. The TCL was CD4+, expressed alpha beta T cell receptor, and recognized OVA presented by HLA-DR10. Based on the response of the TCL to synthetic OVA peptides, it was found that the TCL recognized OVA 323-339, which is a major T cell epitope presented by murine I-Ad. The TCL secreted high levels of IL-5, but undetectable amounts of IL-2, interferon-gamma, and IL-4 when stimulated with OVA or the OVA 323-339 peptide. Since IL-5 is an important growth and chemotactic factor for eosinophils, it is possible that these OVA 323-339-specific T cells can contribute to human egg allergy. To our knowledge, this is the first demonstration of food allergen-specific TCL establishment and identification of a T cell epitope possibly related to the allergic reaction to food antigens. An analog peptide of the OVA 323-339 which is known to strongly bind to I-Ad partially inhibited the response of the TCL to OVA 323-339 presented by HLA-DR10, raising the possibility of peptide-based immunotherapy of food allergy.

Amino Acid Sequence↗
PubMed1994

Exaggerated vascular response due to endothelial dysfunction and role of the renin-angiotensin system at early stage of renal hypertension in rats.

We investigated whether endothelial dysfunction might contribute to the exaggerated vasoconstriction that was induced by the administration of norepinephrine at the early stage of one-kidney, one-clip renal hypertension (1K1C) in rats. We also studied the role of the renin-angiotension system in this phenomenon. Male Wistar rats were killed 48 hours after the induction of renal artery stenosis or sham operation, and ring preparations of the thoracic aorta were obtained. The isometric contraction and relaxation of aortic strips produced by norepinephrine and acetylcholine, respectively, were recorded with a force-displacement transducer. The aorta of 1K1C rats showed a significantly (P < .05) exaggerated contractile response to norepinephrine as compared with that of control rats. Rubbing the endothelium and treatment with methylene blue or NG-monomethyl L-arginine acetate augmented the contractile responses to norepinephrine to a greater extent in control rats than in 1K1C rats; therefore, the responses of the groups did not differ significantly. In the second experiment, rats received 0.05% captopril, 0.02% enalapril, or 0.02% nicardipine in the drinking water for 1 day before and for 48 hours after the induction of renal artery stenosis or sham operation. The increased contractile responses of the aorta to norepinephrine in 1K1C rats were normalized to the level of the control rats by treatment with either captopril or enalapril but not with nicardipine. These results suggest that the endothelial dysfunction may contribute to the exaggerated norepinephrine-induced vasoconstriction observed in the 1K1C rats and that angiotensin I-converting enzyme inhibitors can restore the endothelial function.

Acetylcholine↗
PubMed1994

Use of a thermodilution renal vein catheter to measure renal blood flow in patients with essential hypertension.

Our objective was to investigate the changes in renal hemodynamics, and the role of these changes in the pathogenesis of essential hypertension. We used a thermodilution renal vein catheter and measured left renal blood flow in 21 patients with essential hypertension. Arterial pressure was monitored concurrently. Cardiac output was measured in 11 patients to calculate total peripheral vascular resistance. Systolic, diastolic, and mean arterial pressure were 187 +/- 7 mmHg, 97 +/- 5 mmHg and 127 +/- 5 mmHg, respectively. Left renal blood flow was 8.01 +/- 0.38 ml/s. Left renal vascular resistance, calculated as mean arterial pressure divided by left renal blood flow, was 16.4 +/- 0.8 mmHg ml-1s, and was positively correlated with systolic, diastolic and mean arterial pressures (p < 0.05). However, no significant correlation was observed between arterial pressure and left renal blood flow. Plasma renin activity in left renal venous blood, measured in 15 patients, was not significantly correlated with renal hemodynamics. Cardiac output and total peripheral vascular resistance were 81.4 +/- 6.0 l/min and 1.68 +/- 0.18 mmHg ml-1s, respectively. Total peripheral vascular resistance was not significantly correlated with either left renal blood flow or renal vascular resistance. The data suggest that a rise in renal vascular resistance may parallel the rise in blood pressure, but not that of total peripheral vascular resistance.

Adolescent↗
PubMed1994

A new device for indirect blood pressure measurement in rabbits.

We evaluated the reliability of a new device for indirect measurement of systolic blood pressure in normal and hypertensive New Zealand White rabbits. This device consisted of an ear unit composed of an air chamber and sensitive photoelectric sensors, and was connected to an apparatus used for the tail-cuff method. Systolic blood pressure was determined by simultaneous recordings of pulse volume oscillations of the central ear artery and the chamber pressure. The blood pressure in 8 normal rabbits was 116 +/- 7/78 +/- 6 mmHg (mean +/- SEM) by direct measurement and 100 +/- 6 mmHg by indirect measurement. In a one-kidney, one-clip hypertensive model, the new device showed that blood pressure increased from 100 +/- 7 to 158 +/- 7 mmHg over 4 weeks. After nicardipine was injected, blood pressure fell from 191 +/- 10/114 +/- 10 to 117 +/- 7/72 +/- 8 mmHg as measured by the direct method, and from 158 +/- 7 to 92 +/- 6 mmHg as measured by the new device. A strong correlation (r = 0.91, p < 0.01) was observed between direct and indirect measurements. Our findings indicate that this device provides rapid, easy and reliable measurement of blood pressure in rabbits.

Animals↗
PubMed1994

Aldosterone response to adrenocorticotrophin and furosemide in primary aldosteronism after prolonged spironolactone treatment.

We evaluated the effects of prolonged spironolactone treatment on aldosterone secretion in patients with primary aldosteronism. The patients were hospitalized and underwent a furosemide test with or without dexamethasone, as well as an adrenocorticotrophin (ACTH) test. In untreated patients, neither plasma renin activity (PRA) nor plasma aldosterone showed a response in the furosemide test. In patients receiving spironolactone, furosemide increased significantly both the PRA and the plasma aldosterone concentration (from 2.6 +/- 0.8 to 7.0 +/- 2.0 micrograms.l-1.h-1 (p < 0.05) and from 345.6 +/- 55.8 to 492.7 +/- 76.8 ng/l (p < 0.05), mean +/- SEM, respectively). Dexamethasone administration had no effect on the results of the furosemide test (p > 0.1). However, dexamethasone tended to decrease the basal plasma aldosterone concentration in the untreated patients, but not in the patients receiving spironolactone. In the ACTH test, the plasma aldosterone concentration increased significantly in the untreated patients (from 549.0 +/- 69.8 to 1169.3 +/- 165.5 ng/l, p < 0.01), but there was no significant aldosterone response in the spironolactone-treated patients (from 885.5 +/- 204.9 to 1260.3 +/- 289.2 ng/l, p > 0.1). We conclude that aldosterone secretion is mainly dependent on ACTH in the untreated patients with primary aldosteronism and is more strongly regulated by the renin-angiotensin system during spironolactone treatment.

Adrenocorticotropic Hormone↗
PubMed1994

Effect of NG-monomethyl-L-arginine on regional vascular resistance in rats.

This study investigated the effects of intravenous injection of the specific inhibitor of nitric oxide (NO) formation, NG-monomethyl-L-arginine (L-NMMA), on mean arterial pressure and regional vascular resistance in rats (n = 7). Regional vascular resistances of brain, heart, left kidney, intestine (jejunum), left testis and right testis were measured using radiolabelled microspheres before and after injection of 12.5 mg/kg of L-NMMA. Injection of L-NMMA raised mean arterial pressure significantly (p < 0.05) from 119 +/- 4 (mean +/- SEM) mmHg to 139 +/- 7 mmHg, accompanied by a significant (p < 0.05) decrease in both heart rate and cardiac index and an increase in total peripheral resistance. Regional vascular resistances in brain, heart, kidney and intestine increased significantly (p < 0.05) with L-NMMA, but no change was observed in the testes. The results indicate that the resistance of vascular beds is affected by NO synthesis, while the extent of regulation may differ among the various vascular beds.

Animals↗
PubMed1994

Release of nitric oxide in response to acetylcholine is unaltered in spontaneously hypertensive rats.

OBJECTIVE: Although a decreased responsiveness to acetylcholine, an endothelium-dependent vasodilator, has been reported in arteries isolated from spontaneously hypertensive rats (SHR), the precise role of nitric oxide (NO) in the in vivo regulation of blood pressure is not clear. We investigated the effects of acetylcholine and of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, on mean arterial pressure and the production of NO metabolites (nitrate and nitrite) in SHR and in Wistar-Kyoto (WKY) rats, their normotensive control strain. DESIGN: We determined serum levels of nitrate and nitrite before and after the intravenous injection of 40 micrograms/kg acetylcholine following the administration of L-NAME (30 mg/kg) or its vehicle in adult SHR and WKY rats. RESULTS: Acetylcholine administration significantly reduced mean arterial pressure in both SHR and WKY rats, accompanied by a significant rise in serum nitrate and nitrite. Administration of L-NAME significantly increased the mean arterial pressure in SHR and in WKY rats. L-NAME inhibited the hypotension induced by acetylcholine and the rise in serum nitrate and nitrite both in SHR and in WKY rats. CONCLUSION: The release of NO stimulated by acetylcholine was unaltered in SHR, supporting previous in vitro results.

Acetylcholine↗
PubMed1993

A de novo deletion in the C1 inhibitor gene in a case of sporadic hereditary angioneurotic edema.

A sporadic case of hereditary angioneurotic edema (HANE) is reported here. The patient was a 15-year-old girl who for 4 years had suffered recurrent episodes of urticaria-like erythema, followed by vomiting with abdominal pain. She was diagnosed as having Sjögren syndrome by results of sialography and serological studies, and moreover, it was also observed that the C1 inhibitor (C1-INH) activity in her plasma was very low during these episodes of urticarial erythema. Diagnosis of acquired angioneurotic edema (AANE) was excluded because the patient's plasma had no inhibitory effect on the C1-INH activity of normal individuals. Although neither of her parents had a history of HANE, we were able to show that the patient had HANE by Southern blot analysis using C1-INH cDNA as a probe. One of the patient's C1-INH gene alleles was revealed to have at least a 17-kb-length deletion including exons 5-8. Neither her parents nor her healthy brother showed any abnormalities on Southern blot analysis. The parent-child relationship in this family was confirmed by an HLA-typing study of all family members.

Adolescent↗
PubMed1993

[The effects of intrarenal infusion of recombinant human erythropoietin on renal hemodynamics and renal function in anesthesized rabbits].

To determine whether recombinant human erythropoietin (rHuEPO) has direct effect on mean arterial pressure or renal function, rHuEPO was infused intrarenally at a rate of 100 U min-1 for 30 min in anesthetized rabbits without renal failure. Intrarenal infusion of rHuEPO resulted in no change in mean arterial pressure, renal blood flow, or renal vascular resistance as compared with vehicle control. rHuEPO also produced no significant change in glomerular filtration rate, filtration fraction, or arterial hematocrit. However, urine volume, urinary excretion of sodium and potassium, and fractional sodium excretion were significantly reduced by intrarenal infusion of rHuEPO. These observations demonstrate that rHuEPO has no direct effects on mean arterial pressure or renal hemodynamics, whereas rHuEPO stimulates net tubular sodium reabsorption possibly by direct tubular action, and reduces urine volume and urinary excretion of sodium and potassium in anesthetized rabbits without renal failure.

Anesthesia, Intravenous↗
PubMed1992

[The mechanism of glucose intolerance in patients with Graves' disease].

To investigate the mechanism of glucose intolerance in patients with Graves' disease, a 2-hour oral glucose tolerance test and euglycemic glucose clamp study using Biostator were performed in patients with Graves' disease and control subjects. 80 per cent of the patients showed impaired glucose tolerance. Insulinogenic index in the patients with borderline or diabetic glucose response was lower than that in subjects with normal glucose response. Insulinogenic index was inversely correlated with sigma PG during the test. Despite normal basal plasma glucose concentrations, basal plasma insulin levels in the patients with Graves' disease were higher than in the controls. Using the euglycemic glucose clamp technique, the glucose utilization rate (M value), the metabolic clearance rate of glucose (MCRG) and the insulin sensitivity index (M/I x 100) in the patients with Graves' disease were lower than in the controls. After treatment with antithyroid drug in 3 patients, glucose tolerance completely normalized, and there was a significant increase in the M value and the MCRG and a significant decrease in the metabolic clearance rate of insulin (MCRI) compared to the values before treatment. In the patients with Graves' disease, basal serum glucagon levels were higher than in the controls, and glucagon suppression during insulin infusion was found to be decreased. From these data, it is concluded that the decrease in glucose tolerance in patients with Graves' disease can be explained by 1) the impairment of early insulin release response to rapid intestinal glucose absorption, 2) increased insulin metabolic clearance and 3) hyperglucagonemia.

Adult↗
PubMed1992

[Difference of acute ketone body metabolism between insulin-dependent diabetic and non-insulin-dependent diabetic individuals].

The difference in the acute metabolic change in ketone bodies between patients with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) was investigated in this study. The subjects employed were 7 patients with IDDM losing residual insulin secretion and 7 patients with NIDDM matched to the former patients for age, body mass index, duration of diabetes, daily insulin dosage, fasting plasma glucose and HbA1c. Blood samples were drawn at 3A.M. and 7A.M. on the same day, and plasma glucose, acetoacetic acid (AcAc), 3-beta-hydroxybutylic acid (3-OHBA), free fatty acid (FFA), glycerol, cortisol and growth hormone (GH) concentrations were determined. Plasma total ketone bodies (AcAc and 3-OHBA), 3-OHBA and FFA concentrations at 7A.M. were significantly higher in the patients with IDDM than in those with NIDDM (p < 0.05), while there were no significant differences in any other parameters at 3A.M. between the patients with IDDM and those with NIDDM. The ratios of 7A.M. value/3A.M. value of total ketone bodies, AcAc and 3-OHBA concentrations were also more significantly elevated in the patients with IDDM than in those with NIDDM. It was observed that the ratio of 3-OHBA was more than 2.0 in all of the patients with IDDM and less than 2.0 in all of the patients with NIDDM, the difference being significant with p < 0.001.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Role of norepinephrine in the lack of reflex tachycardia after angiotensin converting enzyme inhibitor treatment.

Angiotensin converting enzyme inhibitors decrease blood pressure without causing reflex tachycardia in hypertensives, but do not always do so in normotensives. To investigate this phenomenon, hemodynamic changes in normotensive rabbits receiving a subpressor dose of norepinephrine were studied following captopril or diltiazem treatment. We also investigated the effect of captopril on baroreceptor reflex in relation to norepinephrine infusion; the baroreflex sensitivity was determined by the relationship between mean arterial pressure and pulse interval receiving graded doses of phenylephrine. Captopril infusion decreased mean arterial pressure and pulse interval from 84 +/- 4 to 74 +/- 5 mmHg and 244 +/- 7.4 to 216 +/- 7.6 msec, respectively. In contrast, in rabbits receiving a norepinephrine infusion captopril lowered mean arterial pressure to the same extent (92 +/- 5 to 76 +/- 3 mmHg, p less than 0.05) without producing reflex tachycardia. When diltiazem was administered, reflex tachycardia occurred in rabbits both with and without a norepinephrine infusion. There was no difference in the baroreflex sensitivity between rabbits receiving norepinephrine with and without captopril treatment. However, the baroreflex curve showed a slight shift to lower pressures after norepinephrine infusion in the rabbits receiving captopril. These results suggest that elevating circulating norepinephrine might be involved in preventing reflex tachycardia after captopril.

Animals↗