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Biomedical subjects

K Moriyama

Publications and source records attributed to K Moriyama.

At least 145 records · Page 8Linked to original sources
PubMed1992

Latent infection of SCID mice with herpes simplex virus 1 and lethal cutaneous lesions in pregnancy.

Some SCID mice survived primary infection with herpes simplex virus 1 without the development of peripheral lesions but established coculture-positive ganglionic latency when a low dose of a wild-type strain was inoculated intracutaneously. The latency was also evidenced by the development of the fatal zosteriform skin lesions and the isolation of the virus during pregnancy. We consider that the viral entry into neurons without successive replication, rather than the arrest of the lytic infection within the cells, is an important mechanism in the establishment of latency.

Animals↗
PubMed1992

Different biventricular remodelling of myosin and collagen in pulmonary hypertension.

1. To clarify the metabolism of contractile and non-contractile proteins of the ventricles during the development of right ventricular hypertrophy (RVH) and accompanying congestive heart failure (CHF) in response to a pressure overload, monocrotaline was injected subcutaneously into Sprague-Dawley (SD) rats. Myosin isoenzymes (MIE) were analysed by pyrophosphate gel electrophoresis under non-dissociating conditions. Acid-soluble collagens were analysed by an improved, noninterrupted sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE). Tissue collagen content was also measured after the estimation of hydroxyproline concentration in tissues. 2. Monocrotaline induced RVH, but not left ventricular hypertrophy, at 2 weeks after the injection of monocrotaline, with severe RVH with CHF present at 4 weeks. In the right ventricles (RV) treated with monocrotaline, MIE shifted significantly from V1 to V3 at 2 weeks. The shift of MIE was more pronounced at 4 weeks. The proportion of type III collagen increased significantly compared with controls at 2 weeks. At 4 weeks, the proportion of types III and V collagens increased significantly compared with controls. 3. In left ventricles (LV) treated with monocrotaline, a similar but less remarkable shift of MIE was observed without remodelling of collagen types at 2 and 4 weeks. The concentration of collagen in either the RV or LV treated with monocrotaline showed no significant changes at 2 and 4 weeks compared with controls. 4. These results demonstrate a remodelling of the contractile and non-contractile proteins during the development of RVH and accompanying CHF, and provide evidence for changes in protein metabolism of the counterpart of RV (i.e. the LV). These results may provide important insights into the pathophysiology of adaptive or non-adaptive cardiac hypertrophy in response to a pressure overload.

Animals↗
PubMed1992

Potentiation of twitch contraction in guinea pig ureter by sodium vanadate.

The effect of sodium vanadate on action potential and twitch contraction of guinea pig ureter was studied and compared with that of ouabain, elevated K+, low temperature, and a Ca agonist (BAY K 8644), which can be expected to exert certain comparative effects. Sodium vanadate markedly potentiated twitch contraction. Potentiation by vanadate was associated with marked prolongation of relaxation time. Sodium vanadate caused only slight depolarization of the membrane but marked changes in action potential. The duration of action potential was prolonged and the number of oscillatory spike potentials increased. These effects were different from those of other treatments. It is concluded that prolongation of action potential and the increase in the number of spikes are the main cause of potentiation of twitch contraction by sodium vanadate. In addition, inhibition of Ca pump activity of the smooth muscle membrane system by vanadate might also be involved in potentiation of twitch contraction.

Action Potentials↗
PubMed1992

Biochemical and structural remodeling of collagen in the right ventricular hypertrophy induced by monocrotaline.

We investigated biochemical and structural changes in collagen in ventricles in right ventricular hypertrophy (RVH) induced by monocrotaline injection in Sprague-Dawley rats. Rats injected with monocrotaline showed significant RVH after 2 weeks compared with the vehicle-treated rats (controls). After 4 weeks, the monocrotaline-treated rats showed severe RVH with heart failure. After 2 weeks, the proportion of type III collagen in the right ventricles (RV) of the monocrotaline-treated rats increased significantly compared with controls, with a concomitant decrease in type I collagen. After 4 weeks, there was a significant increase in the proportion of type III and type V collagens in the RV. In the left ventricles (LV), the proportion of collagen types was similar in the monocrotaline-treated and control rats at 2 and 4 weeks. There was no significant difference in collagen concentration (% collagen in dry defatted tissue) between the monocrotaline-treated rats and controls at either 2 or 4 weeks in the LV and RV. Scanning electron microscopy revealed that the collagen fibrillar sheaths around the myocytes in the endomysium of the RV had thickened and formed a dense network in the monocrotaline-treated rats. In the perimysium, tendon-like collagen fibers increased and became thicker than those in the RV of controls. Giant coiled perimysial fibers were also observed in the monocrotaline-treated RV. These structural changes were more pronounced after 4 weeks of monocrotaline-treatment: Loss of myocytes was evident and was accompanied by replacement fibrosis, where dense collagen fibers aggregated parallel to the long axes of the myocytes. Our results show that biochemical and structural remodeling of collagen occurred in the RV but not in the LV during the development of RVH and heart failure, providing important clues to the pathogenesis and pathophysiology of RVH and cardiac failure in response to pressure overload.

Animals↗
PubMed1992

Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats.

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.

Animals↗
PubMed1992

Collagen in dilated cardiomyopathy--scanning electron microscopic and immunohistochemical observations.

The ultrastructural characteristics of collagen and the localization of collagen types were studied in formalin-fixed autopsied human hearts from patients who died in an advanced stage of dilated cardiomyopathy (DCM). The three-dimensional architecture of collagen fibers was studied by scanning electron microscopy by using the cell-maceration method. The localization of collagen type I-VI was demonstrated immunohistochemically using monoclonal antibodies specific to each collagen following the treatment of specimens with trypsin. In the hearts obtained from control subjects without heart disease, there were no significant differences in the ultrastructure and localization of collagens between the fresh and the formalin-fixed hearts. Therefore, formalin-fixation did not affect the ultrastructure of collagen or the immunoreactivity. In DCM, a dense endomysial weave network consisting of fine fibrils was associated predominantly with collagen type I and III, associated moderately with type VI collagen, but less associated with type IV collagen. Perimysial collagen bundles and collagen strands increased both in number and thickness. The outstanding finding was the presence of giant coiled perimysial fibers measuring about 20-30 microns in diameter. The prominent increase in perimysial fibrosis was closely associated with the accumulation of both type I and type III collagen, and associated moderately with type VI collagen. Interestingly, type V collagen increased in the intracellular matrix of the myocardium in DCM. Type II collagen was not present in either normal or diseased hearts. These structural and immunohistochemical characteristics of collagen may provide insights important to assessing the pathogenesis of the cardiac lesion of DCM.

Adult↗
PubMed1992

The gap between mitral leaflets as a cause of mitral regurgitation: relationship to mitral valve prolapse.

The gap between the tips of the anterior and posterior mitral leaflets was studied to assess the significance of this gap in the diagnosis of mitral valve prolapse. The subjects were 39 patients in whom the gap was seen and the mitral valve did not exceed the mitral annular line in systole on two-dimensional echocardiography. Forty eight healthy subjects, in whom phonocardiography disclosed no abnormalities, served as controls. The site of the gap as well as the site and severity of mitral regurgitation were assessed with two-dimensional echocardiography and Doppler flow imaging. The incidence of mitral regurgitation was 82%, which was comparable to that in the controls (67%). The site of the gap was consistent with that of regurgitation. The gap was also seen in a low percentage of healthy subjects, but clinically significant mitral regurgitation did not accompany the gap in healthy subjects including the gap-carrying controls. On the other hand, many of the gap-carrying patients showed clinically significant mitral regurgitation. Also the fact that a gap between the tip of the anterior and posterior mitral leaflets was found to be frequently accompanied by phonocardiographical features corresponding to mitral valve prolapse indicates that the presence of a gap is a significant finding.

Adolescent↗
PubMed1992

Systolic and diastolic left ventricular dysfunction in middle-aged asymptomatic non-insulin-dependent diabetics.

Radionuclide ventriculographic studies were performed at rest and during exercise in 15 middle-aged asymptomatic patients with non-insulin-dependent diabetes mellitus (NIDDM) whose mean age was 58.7 +/- 10.5 years (mean +/- SD), and in 10 age- and sex-matched normal control subjects. The patients had neither clinical evidence of cardiovascular diseases nor obvious perfusion defects during maximal exercise testing with thallium-201 myocardial scintigraphy. The average left ventricular ejection fraction (LVEF) at rest was 69.1 +/- 5.3% in the diabetic patients and 65.6 +/- 4.2% in the control subjects, and during exercise, the average LVEFs were 68.3 +/- 6.9% and 72.1 +/- 5.0%, respectively. The changes in LVEF during exercise were -0.7 +/- 7.6% in the diabetic group and +6.5 +/- 2.6% in the control group (p < 0.01). However, the filling fraction during the first third of diastole at rest was significantly less in the diabetic group than in the control group (p < 0.05), the time to peak filling rate (TPF) was longer, and the TPF/R-R, normalized by the R-R interval and expressed as a percentage, was greater in the NIDDM patients than in the control subjects. There was close correlation between the abnormal response of LVEF to exercise and the reduced early diastolic filling in the diabetic patients. We concluded that 1) not only the response of LVEF to exercise but also the early left ventricular diastolic filling at rest are impaired in middle-aged asymptomatic NIDDM patients, and 2) some common factors could cause dysfunction of both the systolic and diastolic left ventricles in NIDDM patients, possibly latent global myocardial ischemia or metabolic myocardial disturbances.

Adult↗
PubMed1992

Metabolic aspects of endothelial cells cultured from rat aortae.

We measured the lactate production, oxygen uptake and ATP in aortic endothelial cells cultured from young Wistar female rats. For these experiments, thoracic aortae were removed from the animals, minced into small pieces and transferred onto culture plates, to which a growth factor was added. When the endothelial cells had proliferated, the original pieces were removed from the culture and the remaining cells were subcultured until the 3rd passage. Regarding the growth curves of the 3rd passage, a logarithmic growth phase (Pg) was found from the 2nd to the 7th days and a stationary phase (Ps) followed thereafter. The ATP levels in the Pg and Ps were unchanged. Rates of lactate production and oxygen uptake were higher in the Pg than in the Ps. Only in the Ps was an interrelationship between these estimations found, suggesting that the confluent state exhibits metabolic cooperation between the cells in culture.

Adenosine Triphosphate↗
PubMed1991

Superior vena cava flow and tricuspid anular motion after cardioversion of atrial fibrillation, and role of right atrial relaxation on systolic venous return.

To determine whether atrial relaxation or systolic descent of the tricuspid anulus is the predominant factor determining systolic venous return, 22 patients with atrial fibrillation were studied. Venous return (i.e., superior vena cava (SVC) flow) was measured using pulsed Doppler echocardiography. Systolic descent of the tricuspid anulus (i.e., total excursion of tricuspid anulus during systole) was also measured using echocardiography. Serial examinations were performed before and after cardioversion of atrial fibrillation in 15 patients. In 11 patients, both the total excursion of the tricuspid anulus and SVC flow were examined in relation to the ratio of the preceding to the pre-preceding RR interval (R2/R1). Systolic forward flow of SVC increased as the ratio of late diastolic to total excursion of the tricuspid anulus (i.e., right atrial systolic function) increased. It correlated significantly with the ratio of late diastolic to total excursion of the tricuspid anulus but not with total excursion. Total excursion of the tricuspid anulus correlated significantly with R2/R1, but systolic forward flow of SVC did not. These results indicate that atrial relaxation rather than systolic descent of the tricuspid anulus was the predominant factor determining systolic forward flow in the SVC.

Atrial Fibrillation↗
PubMed1991

Angina pectoris due to possible vasospasm of small coronary arteries.

Recently, the presence of vasospasm in small coronary arteries is speculated in animals and humans. A 40-year-old female patient complained of chest pain at rest. Left ventriculogram showed normal wall motions. Left and right coronary arteries were also normal. After methylergometrine maleate was selectively administered to a right coronary artery, she complained of chest pain, and ST-segment elevation was detected in leads II, III, and aVF of ECG. Right coronary arteriography was performed immediately, but no coronary stenosis was found. The next day, methylergometrine maleate was again administered intravenously and the patient complained of chest pain, but no ischemic changes were observed in ECG. Thallium-201 myocardial scintigraphy followed immediately. Apical perfusion defect was detected in stress image. In the delayed image, it showed complete redistribution. Three days later, catheterization and scintigraphy were performed at the same time. When methylergometrine maleate was administered to the left coronary artery, she complained of chest pain within a few minutes of the injection; however, ECG remained unchanged. 201Tl myocardial scintigraphy was performed immediately. In the stress image, it showed apical perfusion defect as shown in the intravenous methylergometrine maleate injection study. It also showed complete redistribution in the delayed image. Apical perfusion defect can be attributed to myocardial ischemia of left coronary artery, which are too small to be detected by conventional coronary arteriography. Vasospasm in small coronary arteries may be involved in this phenomenon.

Adult↗
PubMed1991

The detection of myocardial ischemia by thallium-201 myocardial scintigraphy in patients with multiple coronary arterioventricular connections.

The question of whether myocardial ischemia could be induced in 5 patients with multiple coronary arterioventricular connections by thallium-201 (201Tl) exercise stress myocardial scintigraphy was investigated. Both ST-T changes on ECG and transient myocardial perfusion defects in myocardial scintigrams were observed in 2 patients (40%). In previous reports, all multiple coronary arterioventricular connections, which were shown in angiograms, have been regarded as either Thebesian veins or embryonic sinusoids. However, it is unlikely that Thebesian veins cause myocardial ischemia judging from anatomy. If the vessels cause myocardial ischemia, they should be regarded as multiple coronary arterioventricular fistula. Angiography itself cannot differentiate multiple coronary arterioventricular fistula from Thebesian veins or remnants of embryonic sinusoids. Exercise stress myocardial scintigraphy has a high potential to detect myocardial ischemia due to intracoronary steal. Exercise stress myocardial scintigraphy was used to demonstrate myocardial ischemia in multiple coronary arterioventricular connections. It is concluded that exercise stress myocardial scintigraphy is a reliable test to differentiate multiple coronary arterioventricular fistula from Thebesian veins or remnants of embryonic sinusoids in clinical practice.

Aged↗
PubMed1991

Xenopus M phase MAP kinase: isolation of its cDNA and activation by MPF.

MAP kinase is activated and phosphorylated during M phase of the Xenopus oocyte cell cycle, and induces the interphase-M phase transition of microtubule dynamics in vitro. We have carried out molecular cloning of Xenopus M phase MAP kinase and report its entire amino acid sequence. There is no marked change in the MAP kinase mRNA level during the cell cycle. Moreover, studies with an anti-MAP kinase antiserum indicate that MAP kinase activity may be regulated posttranslationally, most likely by phosphorylation. We show that MAP kinase can be activated by microinjection of MPF into immature oocytes or by adding MPF to cell-free extracts of interphase eggs. These results suggest that MAP kinase functions as an intermediate between MPF and the interphase-M phase transition of microtubule organization.

Amino Acid Sequence↗
PubMed1991

The relaxation and Ca-pump inhibition in mesenteric artery of normotensive and stroke-prone spontaneously hypertensive rats.

The influences of low temperature and vanadate, both of which have been known to inhibit the Ca-pump activity of membranous systems of smooth muscle cells, on the relaxation of mesenteric artery of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were studied. Relaxation was induced by the removal of extracellular Ca in high-K-depolarized preparations, so that the involvement of receptor kinetics and changes in membrane potential could be excluded. Relaxation was significantly slower in the preparation from SHRSP than in that from SHRSP. Low temperature prolonged relaxation in preparations from both SHRSP and WKY. No difference in the effect of low temperature was observed between the preparations, which showed Q10 values between 2.8 and 3.5 for 50 and 80% relaxation time. Sodium vanadate also prolonged the time course of relaxation in both preparations. No difference in the effect of sodium vanadate was observed between the preparations from WKY and SHRSP. These results suggest that Ca-pump activity is involved in the relaxation of K-depolarized smooth muscle of mesenteric arteries from both WKY and SHRSP. However, the difference in the pump activity may not contribute greatly to the difference in the relaxation of K-depolarized preparations by the removal of extracellular Ca.

Animals↗
PubMed1991

Age-related increase in the uptake of acetylated low density lipoprotein into cultured endothelial cells from rat aorta.

A simple and reliable method for the separation of endothelial cells from the thoracic aorta of rats was established in the present study. The cultured endothelial cells separated by this improved explantation method showed typical characteristics of endothelial cells, morphology of cobblestone monolayer, immunoreactivity against antibodies to Von Willebrand's factor and angiotensin I converting enzyme, and the ability to uptake acetylated low density lipoprotein (LDL) labeled with 1,1'-dioctadecyl-1-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate (DiI-Ac-LDL). The purity of the cultured endothelial cells separated by this method was over 98%, and the cells were maintained in culture for 3-4 months. Age-related changes of the uptake of DiI-Ac-LDL into the endothelial cells were then estimated by using the cultured endothelial cells separated from the aortas of young (4-8 weeks old) and old (95-100 weeks old) rats. When fluorescent DiI-Ac-LDL-labeled endothelial cells were sorted and analyzed by a cell sorter, the fluorescence intensity of the cultured cells from old rats was stronger than that of the cells from young rats. Therefore, the present results show that the uptake of the acetylated LDL into the endothelial cells increases with rat aging, and suggest the age-related increase in the acetyl LDL receptor in the endothelial cells of the rat aorta.

Acetylation↗
PubMed1991

Effects of growth factors on mucosal scar fibroblasts in culture--a possible role of growth factors in scar formation.

Various growth factors are known to play important roles in wound healing, especially in an early inflammatory phase. However, their roles in subsequent scar formation phase are relatively unexplored. The aim of this study is to investigate the mechanisms of regulation in scar formation by these factors. Scar fibroblasts (SF) were obtained from immature scar tissue made at rat hard palate 1 month after excision and normal fibroblasts (NF) were obtained from the palatal mucosa of untreated control animals. SF showed a longer doubling time, and increased level of protein synthesis when compared to NF. Platelet-derived growth factor (PDGF) and epidermal growth factor (EGF) stimulated [3H]-thymidine uptake less effectively in SF than in NF. In both cells, transforming growth factor-beta 1 (TGF-beta 1) inhibited EGF-induced stimulation of [3H]-thymidine uptake, but had no effects when it was added alone. TGF-beta 1 increased collagen synthesis more effectively in SF than in NF. These data indicate that the growth factors may play key roles in regulating proliferation and metabolic activity of fibroblasts during scar formation.

Animals↗
PubMed1991

Changes in contractile and noncontractile protein metabolisms in both ventricles in monocrotaline-treated rats.

To clarify the metabolism of contractile and noncontractile proteins of both ventricles (BVs) during the development of right ventricular hypertrophy (RVH) induced by pressure overload, monocrotaline (M) was injected subcutaneously into Sprague-Dawley (SD) rats. Myosin isoenzymes (MIEs) were analyzed by pyrophosphate gel electrophoresis. Acid-soluble collagens were analyzed using improved noninterrupted sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Tissue collagen concentrations were also measured. M induced RVH, but not left ventricular hypertrophy, at 2 weeks, and severe RVH at 4 weeks. In right ventricles (RVs) of M-treated rats, MIE significantly shifted from V1 to V3, and the proportions of type III and V collagens increased compared to control at 2 and 4 weeks. In the left ventricles (LVs) of M-treated rats, similar but less remarkable MIE shifts were found without remodeling of collagen types at 2 and 4 weeks. Collagen concentrations of BVs treated with M did not show any significant changes compared to control at 2 and 4 weeks. Our results show remodelings of contractile and noncontractile proteins in RVs during the development of RVH, and also provide evidence for the changes in protein metabolism of the counterpart of RVs (i.e., LVs) during the development of cardiac hypertrophy.

Animals↗