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Biomedical subjects

K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

At least 145 records · Page 8Linked to original sources

[Serum levels of amino acid in patients with purple urine bag syndrome].

The plastic of urinary catheter drainage bags occasionally turns purple hours or days after catheterization and the color becomes increasingly intense the longer the same drainage system is left in place. This phenomenon was first reported in 1978 as "purple urine bag syndrome", and had been known to occur with bacterial infection of the urinary tract with chronic constipation. Chronic constipation is commonly associated with bacterial overgrowth in the bowel in which tryptophan has been converted to indol and yields the high levels of indigo (blue) and indirubin (red) in urinary bags of patients with bacterial infection of the urine, because indigo-producing bacteria have indoxyl phosphatase or sulfatase that can produce indigo and indirubin. We determined the serum levels of amino acids in patients with purple urine bag syndrome. The serum level of tryptophan and valine were significantly reduced in patients with purple urine bag syndrome. This result suggests that absorption of amino acids was affected by disturbances of colonic motility and intestinal bacterial overgrowth.

Aged↗

An ATP-sensitive potassium (KATP) channel opener, nicorandil, lowers the threshold for ischemic preconditioning in barbital-anesthetized dogs.

To determine whether the adenosine triphosphate (ATP)-sensitive potassium channel (KATP channel) opener, nicorandil, lowers the threshold for the infarct-reducing effect of preconditioning (PC), barbital-anesthetized dogs were subjected to 60-min occlusion (60'OC) of left anterior descending coronary artery (LAD) followed by 3-h reperfusion (3h-RP). At the end of the 3h-RP, heart was resected to measure infarct size. Infarct size was determined by triphenyltetrazolium chloride (TTC) staining, calculated gravimetrically and was expressed as a percent age of area at risk (AAR). Myocardial blood flow was measured by radioactive microspheres. Single 5-min LAD occlusion 10 min before 60'OC (5'PC group) markedly reduced infarct size, compared to the controls (11.8 +/- 3.7% versus 26.8 +/- 4.7%; P < 0.05). Neither 2.5-min PC (2.5'PC group), nor 2.5-min intracoronary infusion with 0.5 microgram/kg per min of nicorandil followed by a 10-min drug-free period (2.5'NC group), showed a cardioprotective effect (26.5 +/- 1.7% and 20.7 +/- 2.8%, respectively). However, when nicorandil was administered during the 2.5-min LAD occlusion period (2.5'PC + 2.5'NC group), infarct size was significantly reduced to an extent similar to that in 5'PC group (13.6 +/- 1.2%). There were no significant differences in hemodynamics, collateral circulation, or AAR between groups. These results suggest that nicorandil lowers the threshold for the infarct-reducing effect of PC in dogs by, at least in part, activation of myocardial KATP channels.

Animals↗

Assessment of plaque rupture by intravascular ultrasound.

To investigate the mechanism of plaque rupture, we carried out morphologic and quantitative assessments of ruptured plaque with a 30-MHz intravascular ultrasound catheter before coronary intervention. Plaque rupture, defined as an echolucent intraplaque area communicating with arterial lumen, was noted in all of 22 patients with coronary artery disease examined in the study. The plaque was eccentric in 16 patients (73%) and in 10 of these 16 patients there was a tear at the margin of the plaque (63%). Calcification was noted in only 6 patients (22%). Plaque area ranged from 8.7 to 44.1 mm2. The ruptured area ranged widely, from 1.0 to 14.0 mm2, and the percent ruptured area also ranged widely, from 3.9% to 50.9%. Fibrous cap was recognized in 20 patients. The thickness of the fibrous cap ranged from 0.1 to 0.6 mm (mean, 0.36 mm) and thinning of the fibrous cap was noted in 16 patients (80%). From these results, we conclude that intravascular ultrasound can provide detailed observations of plaque rupture consistent with pathologic studies. Accordingly, it is a suitable method for evaluation of plaque rupture in vivo. Plaque weakness, due to the presence of atheromatous core, thin fibrous cap, and no calcification, seems to be the major determinant of plaque rupture. In addition, the great variation in cap thickness and ruptured area suggests the role of other triggers, such as mechanical and hemodynamic stress, in plaque rupture.

Coronary Artery Disease↗

Localized right ventricular structural abnormalities in patients with idiopathic ventricular fibrillation: magnetic resonance imaging study.

Lethal arrhythmias, including ventricular tachycardia and ventricular fibrillation, may occur in the absence of apparent morphological abnormalities. However, a recent study using magnetic resonance imaging (MRI) has suggested that localized, minor structural abnormalities of the right ventricle are responsible for right ventricular outflow tract ventricular tachycardia in a number of patients. We demonstrated regional wall thinning and systolic dyskinesia of the right ventricle by MRI in two patients with idiopathic ventricular fibrillation in whom other cardiac imaging modalities failed to show abnormalities. This finding implies that minor structural abnormalities do exist in patients with so-called idiopathic ventricular fibrillation.

Adult↗

A nitric oxide synthesis inhibitor decreased prostaglandin production in rat mesenteric vasculature.

Endothelial cells synthesize and release nitric oxide (NO) and prostacyclin (PGI2) which are involved in the regulation of vascular tone and blood pressure. Our objective was to evaluate the effects of inhibiting NO synthesis on vascular prostaglandin (PG) and cyclic nucleotide production, as well as the pressor response to norepinephrine (NE). Isolated mesenteric arterial beds were perfused with Krebs-Henseleit solution containing 100 microM NG-monomethyl-L-arginine (L-NMMA), 100 microM L-arginine (LA), or vehicle. After a 30 min equilibration 0.1, 0.5, 1, or 5 microM NE was infused into the superior mesenteric artery and the perfusion pressure was monitored. The basal perfusion pressure did not differ significantly between groups. The pressure-response curve was shifted to the right in the L-NMMA group vs. the LA and control groups. Perfusion was similarly performed with a Krebs-Henseleit solution containing 100 microM L-NMMA, LA, D-arginine, or vehicle. Perfusates were collected before and after NE infusion for the measurement of PGE2, 6-keto-PGF1 alpha, TxB2, cAMP, and cGMP. In the L-NMMA group the release of PGE2 and 6-keto-PGF1 alpha was decreased, and the release of cGMP was prevented. Production of cAMP did not differ between the four groups before NE infusion, and NE increased cAMP release in the L-NMMA group and controls. The results indicate that inhibition of NO synthesis by L-NMMA enhanced the pressor response to NE, possibly mediated by the decreased cGMP and PGI2 production in resistance vessels.

Animals↗

Prospective studies on left ventricular geometric patterns and exercise tolerance in unmedicated men with borderline and mild hypertension.

OBJECTIVE: This study was designed and conducted to assess the clinical significance of left ventricular geometric patterns and physical fitness in subjects with untreated borderline and mild hypertension. METHODS: Symptom-limited maximal treadmill stress testings and echocardiographic examinations were administered to 192 previously unmedicated men. Left ventricular geometric patterns were determined by the combined criteria of left ventricular mass index and relative wall thickness. Subjects whose left ventricular mass index was < 125 g/m2 were followed up for more than 3 years. RESULTS: Normalized treadmill time was lower and pressure rate products at peak exercise were higher in patients with concentric hypertrophy than in those with normal geometry. Of the 77 patients who revealed left ventricular mass index at baseline < 125 g/m2 and who were successfully followed without medication for more than 3 years, 18 demonstrated concentric hypertrophy at the final follow-up examination. During the follow-up period, these 18 patients had significant further augmentation of concentric geometric features, significant decreases in both cardiac output and normalized treadmill time, and significant increases in casual blood pressure and total peripheral resistance compared with those at baseline. CONCLUSION: Patients with concentric hypertrophy exhibited slightly but significantly impaired levels of physical fitness and cardiac work efficiency, and the progression of concentric hypertrophy demonstrated further impairments of these conditions. Therefore, not only lowering blood pressure, but also improving left ventricular hypertrophy, cardiovascular hemodynamics, and physical fitness might be required in patients with concentric hypertrophy.

Adult↗

Inhibitory effect of an angiotensin II type 1 receptor antagonist on growth of vascular smooth muscle cells from spontaneously hypertensive rats.

To investigate the role of endogenous angiotensin II (Ang II) in the growth of vascular smooth muscle cells (VSMC), we examined the effect of the novel nonpeptide Ang II type 1 (AT1) receptor antagonist CV-11974 on basal and stimulated-growth of VSMC from normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). CV-11974 inhibited basal DNA synthesis by VSMC from SHR, but not from WKY, in the absence of serum. In the presence of 10% calf serum, DNA synthesis was significantly higher in VSMC from SHR than in cells from WKY, and the inhibitory effect of CV-11974 was attenuated. Ang II dose-dependently stimulated DNA synthesis by VSMC from both rat strains, and this effect was abolished by CV-11974. CV-11974 slightly but significantly suppressed proliferation of VSMC from both rat strains. CV-11974 competitively inhibited the specific binding of 125I-labeled Ang II to VSMC from both rat strains. The angiotensin-converting enzyme inhibitor (ACEI) delapril also reduced basal DNA synthesis by VSMC from SHR, but did not affect proliferation of VSMC from either rat strain. These findings suggest that VSMC from SHR may synthesize Ang II which promotes their basal growth in an autocrine/paracrine manner through the AT1 receptor, and that this system may be associated with the exaggerated growth of VSMC from SHR.

Angiotensin II↗

Prevention of cardiac hypertrophy by a sub-antihypertensive dose of the alpha 1-adrenergic antagonist bunazosin in Dahl salt-sensitive rats.

To assess the protective effect of an alpha 1-blocker on the development of cardiac hypertrophy, the selective alpha 1-receptor antagonist bunazosin (2 mg/kg/d, by oral gavage and in drinking water) was given to male Dahl salt-sensitive rats fed a 4% NaCl diet for 7 weeks. Control animals received water only by the same method. Treatment with bunazosin was started when the animals were 7 weeks of age. Blood pressure, pulse rates, and body weight were measured every week during the experiment. Urine was collected for 24 h on the final day of the experiment. All animals were killed by decapitation, blood was collected, and the heart was removed. In both the treated and control groups, time-dependent increase in blood pressure and body weight were observed, and there were no significant differences between the groups in blood pressure or body weight during the experiment. Pulse rate remained unchanged in both groups throughout the experiment. The left ventricular weight/body weight ratio and the left ventricular tissue DNA content were significantly lower in the rats receiving bunazosin than in the control rats. Plasma renin activity, plasma aldosterone, and plasma atrial natriuretic peptide did not differ significantly between the two groups. No significant differences in glomerular filtration rate, urine volume, sodium excretion, urinary metanephrine excretion, and urinary normetanephrine excretion were noted between the two groups. The results indicate that a sub-antihypertensive dose of bunazosin can inhibit the development of cardiac hypertrophy without suppression of the pressure load, suggesting an important role of alpha 1-adrenergic receptors in the pathogenesis of cardiac hypertrophy following the development of hypertension.

Adrenergic alpha-Antagonists↗

A nitric oxide synthesis inhibitor prevents the ACTH-stimulated production of aldosterone in rat adrenal gland.

The synthesis of nitric oxide (NO) has been demonstrated in the vascular endothelial cells and other tissues including in rat and bovine adrenal gland. To determine whether NO mediates aldosterone production in the adrenals, we evaluated the basal production of aldosterone, and the ACTH or angiotensin II (A II)-stimulated aldosterone in the presence of L-NG monomethyl arginine (L-NMMA) or L-arginine or L-NMMA + L-arginine in isolated rat adrenal capsular tissue by an ex vivo perfusion technique. ACTH increased the release of aldosterone by 40%. Such release of aldosterone was inhibited by L-NMMA, but not by a mixture of L-NMMA and L-arginine. A II stimulated aldosterone release by 40%. The increase in aldosterone release in response to A II was inhibited by L-NMMA or L-arginine. The increase in aldosterone release stimulated by A II was also inhibited by L-NMMA with L-arginine. L-glutamine did not inhibit the A II stimulated aldosterone release. In conclusion, the inhibition of NO synthesis prevented the release of aldosterone stimulated by ACTH, suggesting NO is required for the action of ACTH on aldosterone production.

Adrenal Glands↗

Long-term reproducibility and usefulness of daytime recording of noninvasive 24-hour ambulatory blood pressure monitoring in borderline hypertension: a two-year follow-up study.

We investigated the long-term reproducibility of noninvasive 24-hour ambulatory blood pressure monitoring (ABPM) compared with casual blood pressure measurements in 54 individuals (47 +/- 11 years) with borderline hypertension. ABPM and casual blood pressure measurements were obtained 3 times over 2 year period. ABPM data were analyzed to determine the average 24-hour blood pressure (24-BP), the average blood pressure during the waking hours (Day-BP), and the average blood pressure from the time the subject went to bed until he awoke (Night-BP). ABPM measurements were similar for Year 1, 2, and 3 (24-BP: Year 1; 130 +/- 10/79 +/- 6 mmHg; Year 2; 130 +/- 10/79 +/- 7 mmHg; and Year 3; 130 +/- 10/78 +/- 7 mmHg). Bland-Altman analysis and standard deviation of the difference also indicated the reproducibility of 24-BP was better than casual pressure. The 24-BP was significantly correlated with both Day-BP and Night-BP for each year. Day-BP showed the stronger correlation. Our results suggest that Day-BP provides reproducible estimation in subjects with borderline hypertension.

Adult↗

Elevation of plasma thrombomodulin level in primary glomerulonephritis with heavy proteinuria.

Thrombomodulin (TM) is a thrombin receptor found on endothelial cells. TM acts as a cofactor for the thrombin-catabolized activation of protein C and protects these cells from the formation of thrombi. We hypothesized that the soluble form of TM which reflects the damage of the endothelial cells and that simultaneously, soluble TM will be affected by renal excretion because a significant positive correlation has been found between soluble TM and serum creatinine (sCr) in the renal failure state. However, there have been no reports on the relationship between plasma TM and clinical parameters except for sCr in primary glomerulonephritis (PGN). Plasma TM (pTM) and urinary TM (uTM) were measured in 107 patients with PGN using a one-step sandwich enzyme immunoassay. These values were assessed together with other laboratory and histological findings. We were able to divide all subjects into two groups: an sCr-dependent group whose sCr level was over 1.2 mg/dl and an sCr-independent group whose sCr level was under 1.2 mg/dl. In the sCr-independent group, patients who suffered from nephrotic syndrome (NS) had a much higher pTM level than patients who did not suffer from NS. Histological findings and other parameters were not correlated with pTM or uTM. Therefore, the two patients who suffered from NS with very high pTM levels and normal sCr level at the time of admission exhibited a decrease in their pTM value as their condition improved. We concluded that in our patients, pTM was affected not only by renal excretion of TM, but also by renal damage with heavy proteinuria and may have been associated with an ongoing disease process in PGN.

Adolescent↗

[Microsatellite polymorphism of muscle glycogen synthase gene and non-insulin dependent diabetes mellitus].

It has been reported recently that A2 allele of muscle glycogen synthase gene determined by Xba I RFLP (restriction fragment length polymorphism) is related to the frequency of NIDDM in Finland. Using PCR-RFLP analysis, we detected no A2 allele in Japanese patients with NIDDM and control. We found a new microsatellite of CA repeat in the human muscle glycogen synthase gene, and the polymorphism of the repeat number was detected by the polymerase chain reaction. Six different alleles were observed, indicating the highly polymorphic nature of this marker. We analyzed the repeat numbers and the genotypes in diabetics and control. The allele frequencies were not significantly different between NIDDM and control. However, the allele frequencies in the patients without high total cholesterolemia was significantly different from those of control. These findings suggest that the muscle glycogen synthase gene or neighboring genes are related to one of the disease genes of diabetes mellitus without high total cholesterolemia.

Adolescent↗