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Biomedical subjects

K Moriyama

Publications and source records attributed to K Moriyama.

At least 181 records · Page 10Linked to original sources
PubMed1989

Osteonectin inhibiting de novo formation of apatite in the presence of collagen.

The effect of bone matrix protein of osteonectin on de novo formation of apatite was studied in a wide range of calcium phosphate solutions in the presence of collagen. In every solution, from which amorphous calcium phosphate, octacalcium phosphate, or apatite precipitated as a possible initial phase, osteonectin at concentrations less than 1 microM retarded the precipitation, subsequent transformation to apatite, and ripening crystal growth of apatite. Collagen present as either reconstituted or denatured form had no effect on the osteonectin-associated reactions as well as osteonectin-free reactions, and no structural correlation was observed between collagen fibrils and any of the calcium phosphates that appeared in our system. Direct measurement of free calcium levels in the solutions suggested that the reduction in calcium activity due to complexing with osteonectin hardly explained the inhibitory activity of osteonectin in retarding the formation of apatite. Instead, our transmission electron microscopic (TEM) observation strongly suggested that the primary mechanism for osteonectin to inhibit the formation of apatite is to block growth sites of calcium phosphates nucleated. The apatite thus formed in the presence of osteonectin showed less resolved X-ray diffraction patterns, partly because of smaller crystallites as suggested by TEM.

Animals↗
PubMed1989

Caffeine-induced contraction in arteries from stroke-prone spontaneously hypertensive rats.

Differences in caffeine-induced contraction in smooth muscle of resistance vessels from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY) were investigated by using mesenteric artery preparations. The contraction induced by caffeine (10 mM) was greater in SHRSP preparations, both in the presence and absence of Ca (10 min after Ca removal). Caffeine-induced contraction was gradually decreased by the removal of extracellular Ca. No significant difference was observed in the time course of the decay of the contraction between SHRSP and WKY preparations, and the contraction disappeared when the time in Ca-free solution exceeded 80 min. The contraction induced by high-K-Tyrode's solution was completely abolished within 10 min after Ca removal, both in SHRSP and WKY preparations. Caffeine-induced contraction could be blocked by procaine or ryanodine. The results suggest that caffeine induces contraction by releasing Ca from sarcoplasmic reticulum, and that the release of Ca is greater in SHRSP vascular smooth muscle. It is also suggested that sarcoplasmic reticulum is leaky for stored Ca when extracellular Ca is removed, and that the rate of leakage does not differ between smooth muscle cells of SHRSP and WKY mesenteric arteries.

Animals↗
PubMed1989

Study of the pathogenesis of cardiac hypertrophy--biochemical differences of cultured heart cells from normotensive and spontaneously hypertensive rats.

To elucidate the metabolic properties of the heart of spontaneously hypertensive rats (SHR), we examined the uptakes of 3H-uridine (3H) and 14C-leucine (14C) into single cultured heart cells, as well as the total protein content and cell size of heart cells in the presence and absence of stimulation, and compared the findings with those obtained with Wistar Kyoto rat (WKY) cells. As a result, (1) Spontaneous uptakes of 3H and 14C into WKY heart cells increased rapidly from day 2 to days 5-6, and then decreased gradually. In contrast, in SHR heart cells a constant increase in the uptakes of 3H and 14C was observed until the 10th day. The uptakes of both 3H and 14C into 10-day-old SHR heart cells were significantly higher than those into WKY heart cells (p less than 0.05). (2) The total protein content of SHR heart cells cultured for 4 or 5 days was significantly less than that of WKY heart cells, but there was no significant difference between cells cultured for more than 6 days. As for cell size, no significant difference was observed regardless of how long the cells were cultured. However, the increment in SHR heart cell total protein and cell size during cultivation appeared to be higher than they were in WKY heart cells. (3) Stimulation of heart cells with 10(-8) - 10(-5) M L(-)-isoproterenol (ISO) for 1 hour increased the uptake of 3H into heart cells from both kinds of rats, with no significant difference between the two.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1989

Isovolumic relaxation period as an index of left ventricular relaxation under different afterload conditions--comparison with the time constant of left ventricular pressure decay in the dog.

In order to determine whether isovolumic relaxation period (IRP) reflects left ventricular relaxation under different afterload conditions, 17 anesthetized, open chest dogs were studied, and the left ventricular pressure decay time constant (T) was calculated. In 12 dogs, angiotensin II and nitroprusside were administered, with the heart rate constant at 90 beats/min. Multiple linear regression analysis showed that the aortic dicrotic notch pressure (AoDNP) and T were major determinants of IRP, while left ventricular end-diastolic pressure was a minor determinant. Multiple linear regression analysis, correlating T with IRP and AoDNP, did not further improve the correlation coefficient compared with that between T and IRP. We concluded that correction of the IRP by AoDNP is not necessary to predict T from additional multiple linear regression. The effects of ascending aortic constriction or angiotensin II on IRP were examined in five dogs, after pretreatment with propranolol. Aortic constriction caused a significant decrease in IRP and T, while angiotensin II produced a significant increase in IRP and T. IRP was affected by the change of afterload. However, the IRP and T values were always altered in the same direction. These results demonstrate that IRP is substituted for T and it reflects left ventricular relaxation even in different afterload conditions. We conclude that IRP is a simple parameter easily used to evaluate left ventricular relaxation in clinical situations.

Angiotensin II↗
PubMed1989

Improvement of right ventricular systolic performance by long-term domiciliary oxygen therapy in patients with chronic respiratory failure.

Eight patients with clinically stable chronic respiratory failure, hypoxemia (PaO2 less than or equal to 60 mmHg) and pulmonary hypertension (mean pulmonary arterial pressure greater than or equal to 20 mmHg) were allocated to long-term domiciliary oxygen therapy, and were followed for three months. Oxygen was supplied for from 15 to 18 hours daily from an oxygen concentrator at a flow rate sufficient to raise the PaO2 to 60 to 80 mmHg. We examined the effects of this therapy on right ventricular performance both at rest and during exercise in these patients. Hemodynamic data were obtained by right heart catheterization. Right ventricular ejection fractions (RVEF) were ascertained using first-pass quantitative radionuclide 81mKr angiocardiography. Thirty minutes of oxygen inhalation at rest had no significant effect on cardiac function, both before therapy (T0) and after 3 months of therapy (T1). The mean pulmonary arterial pressure and the pulmonary vascular resistance during exercise were not significantly different between T0 and T1. On the other hand, at T0, the RVEF tended to decrease from 51.6 +/- 4.9% (during oxygen inhalation at rest) to 48.7 +/- 7.9% (during exercise), whereas at T1 it significantly (p less than 0.05) increased from 48.8 +/- 6.8% (during oxygen inhalation at rest) to 54.2 +/- 8.2% (during exercise). Thus, while 3 months of long-term domiciliary oxygen therapy did not reduce the right ventricular afterload either at rest or during exercise, it was found to improve the right ventricular systolic performance during exercise. This suggested that long-term oxygen therapy could be useful in improving the quality of daily life of patients with chronic respiratory failure.

Aged↗
PubMed1989

Study of cardiac hypertrophy--humoral factors that stimulate protein metabolism of cultured rat heart cells.

Recent extensive studies suggested that some humoral factors may contribute to the development and/or reversal of cardiac hypertrophy in hypertension. The purpose of this study is to examine whether there exists humoral factor(s) for cardiac hypertrophy in experimental perinephritic hypertension in dogs. Hypertension was induced by the method of Page with some modifications. Humoral factors were studied using a microassay system that was independent of pressure overload, hemodynamic effects, and other factors. L(-)-isoproterenol (ISO) and angiotensin II (AngII) increased the uptake of 3H-uridine into 10-day-old cultured heart cells. The maximal response to ISO or AngII was obtained by 10(-5) M ISO or 10(-10) M AngII, and the percent increments in the uptake of 3H-uridine was 38.4 +/- 20.4%, and 45.1 +/- 22.5%, respectively. Moreover, ISO, DL-noradrenaline, and AngII stimulated protein synthesis of 7-day-old or 14-day-old cultured heart cells in this order (9.5 +/- 1.5, 7.3 +/- 1.2, 2.0 +/- 0.5 micrograms/6 x 10(5) by 7-day-old heart cells; 23.8 +/- 8.3, 19.0 +/- 9.4, 4.4 +/- 1.1 micrograms/6 x 10(5) by 14-day-old heart cells). Heart and kidney extracts were obtained from experimental perinephritic hypertensive dogs and sham-operated dogs. The heart extract obtained from hypertrophied left ventricle (LV) of the experimental hypertensive dogs, but not of the sham-operated dogs, increased the uptake of 3H-uridine into 10-day-old heart cells. The mean percent increment in uptake of 3H-uridine induced by the hypertrophied LV heart extract at a final concentration of 5 x 10(-3)% V/V (1-3 micrograms) in different experiments was about 15%. High performance liquid chromatography (HPLC) demonstrated that the LV heart extract obtained from the perinephritic hypertensive dogs contained at least 16 molecules. Among them, one with a molecular weight of approximately 11,200 daltons stimulated uptake of both 3H-uridine and 14C-leucine into cultured heart cells. These results demonstrated that heart extract obtained from hypertrophied LV of perinephritic hypertensive dogs contained at least one factor which may induce and/or modulate myocardial hypertrophy in this model for hypertension.

Angiotensin II↗
PubMed1989

[Cardiovascular response to cerebral circulatory regulation during shifts in head position].

Cardiovascular response and its effect on cerebral regulation was examined in groups of young and old people by putting pressure on the cerebral circulatory system through rapid changes in head position. A transient increase in blood pressure was observed in both the young and old people's groups when the head was tilted up. In the old group, there was less change in both systolic blood pressure and diastolic blood pressure. A transient reduction in blood pressure was observed in both groups when the head was tilted down. However, there was less change in diastolic blood pressure in the old group. The number of heart beats before a maximum change in blood pressure was 5 to 9 beats when the head was tilted up, and there was no significant difference between the two groups. The corresponding figure when the head was tilted down was 17.1 +/- 3.51 beats in the young group, and 27.1 +/- 11.5 beats in the old group, significantly higher among the old group. All were early responses observed within 1-2 minutes. Looking at the change of pulse after the head was tilted up or down among the young group, the number of heart beats increased to reach a peak when the head was tilted up, and when the head was tilted down the number of heart beats fell to its lowest level. The affect of these two cardiovascular responses tended to compensate for cerebral perfusion pressure, which indicates the possible existence of a cerebral perfusion pressure regulatory mechanism, assisted by a carotid sinus reflex. A reduction of this function was suggested in the old group.

Adult↗
PubMed1989

[Effects of growth factors on scar fibroblasts derived from rat palatal mucosa].

Many growth factors are known to play important roles in the early wound healing process. However, their roles in the subsequent scar formation phase are relatively unexplored. The aim of this study is to investigate how these factors affect DNA and collagen synthesis by scar fibroblasts in the scar formation process. Experimental wounds were made by excising palatal mucosa of eight-week-old SD rats. One month later, immature scar tissues were secured from the palate and scar fibroblasts (SF) were obtained from explant cultures of these tissues. Normal fibroblasts (NF), used for control, were obtained from palatal mucosa of untreated animals by the same culture procedure. SF had more slender shape than NF in stationary phase. SF showed longer doubling time, higher collagen synthesis and relatively higher type III collagen formation compared with NF. PDGF and EGF stimulated [3H] Thymidine uptake less effectively in SF than in NF. TGF-beta had no effects on [3H] Thymidine uptake when it was added alone. However, when TGF-beta was administrated in combination with EGF, the EGF-induced stimulation in DNA synthesis was suppressed dose-dependently. TGF-beta stimulated collagen synthesis more effectively in SF than in NF. These data may explain the reason for the accumulation of collagen and the increase in cell number during the scar formation process.

Animals↗
PubMed1989

Herpes simplex virus in oral mucosal ulcers in patients with hematological malignancy.

Developments of oral mucosal ulcers induced by herpes simplex virus (HSV) were studied in patients with hematologic malignancy. Herpes simplex virus type-1 (HSV-1) was identified by immunological staining using virus-specific monoclonal antibodies in the epithelial cells of such ulcers from two patients with malignant lymphoma (ML), three with acute myeloblastic leukemia (AML), one with refractomy anemia with excess blasts, two with chronic myelocytic leukemia (CML), one with acute lymphoblastic leukemia (ALL) and one with aplastic anemia (AA). Herpes simplex virus type-2 (HSV-2) was also identified in an ulcer from a patient with AML. Isolation of HSV-1 was successful in the two patients with ML, one with CML, one with AML, the one with ALL and the one with AA. The ulcers developed on the tongue (four cases), buccal membrane (five cases), hard palate (one case), soft palate (one case), soft palate (one case) and gingiva (two cases). Only one patient with CML and one with AML had accompanying labial vesicular lesions. All patients except the one with AA had previously been given combination chemotherapy with anti-neoplastic agents. The results indicate that HSV may have an important role to play in the development of chemotherapy-related oral mucosal ulcers in patients with hematological malignancy.

Adult↗
PubMed1989

[Evaluation of mid-ventricular obstruction of hypertrophic cardiomyopathy by real-time two-dimensional Doppler flow imaging: a case report].

Mid-ventricular obstruction was evaluated in a case of hypertrophic cardiomyopathy using a real-time two-dimensional Doppler flow imaging system. A 60-year-old woman was referred to our hospital because of oppressive precordial sensation., I-mode echocardiography showed asymmetric septal hypertrophy: thickness of the end-diastolic left ventricular posterior wall was 9 mm, and that of the interventricular septum was 19 mm. However, there was no systolic anterior motion of the mitral apparatus. Doppler color flow imaging showed a mid-left ventricular narrowing in late-systole and a mosaic pattern was depicted from the mid-ventricle to the outflow tract. Continuous wave Doppler echocardiography disclosed a peak velocity of 2.0 m/sec (pressure gradient (PG) = 16 mmHg). In the right ventricular outflow tract, a mosaic pattern was also seen and a peak velocity of 1.5 m/sec was detected (PG = 9 mmHg). These results were nearly identical with the data measured by cardiac catheterization. Thus, it was concluded that intraventricular obstruction of hypertrophic cardiomyopathy is diagnosed by observing the flow image and flow velocities in the ventricle using a real-time two-dimensional Doppler flow imaging system.

Cardiomyopathy, Hypertrophic↗
PubMed1988

Mechanism of prolongation of pre-ejection period in the hypertrophied left ventricle with normal systolic function in unanesthetized hypertensive dogs.

To determine the mechanism for prolongation of pre-ejection period (PEP) in the hypertensive heart with normal systolic function, cardiac catheterizations, echocardiograms, and electrocardiograms were performed at the baseline period (CS, control stage) and eight weeks (HS, hypertensive stage) after the induction of systemic hypertension by Page's method in unanesthetized dogs. Mean aortic blood pressure increased significantly (96 +/- 12 to 137 +/- 26 mmHg) (p less than 0.05). Diastolic aortic pressure also increased significantly (80 +/- 12 to 118 +/- 24 mmHg) (p less than 0.01). Left ventricular (LV) PEP of HS was significantly prolonged (72 +/- 12 vs. 87 +/- 22 ms, CS vs. HS). The ratio of LV pre-ejection period to ejection time (PEP/ET) also increased significantly (0.33 +/- 0.04 to 0.42 +/- 0.07) (p less than 0.05). LV end-diastolic wall stress as an index of preload decreased significantly (7.7 +/- 2.5 vs. 5.9 +/- 1.8 10(3) dynes/cm2, CS vs. HS). Heart rate, mean velocity of circumferential fiber shortening (VCF) and end-systolic wall stress of HS did not change. That is, myocardial contractility in the hypertensive heart of HS most likely is not depressed. At autopsy, left ventricle to body weight ratio of HS was significantly (p less than 0.01) greater than the sham-operated dogs (5.7 +/- 0.8 vs. 4.3 +/- 0.5 g/kg). From these findings, there are two possible factors responsible for prolongation of PEP of HS. First, elevated diastolic aortic pressure may influence PEP. Second, the prolonged PEP is possibly caused by the decrease of preload.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Extra- and intracellular calcium in vanadate-induced contraction of vascular smooth muscle.

The effects of extracellular Ca and Ca antagonists on vanadate-induced contractions of vascular smooth muscles of aortae and mesenteric arteries from rabbits, guinea pigs, and Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied. Vanadate-induced contractions of aortae were greatly diminished by extracellular Ca removal; the size of the remaining contraction was variable. Vanadate-induced contractions of mesenteric arteries, which were only observed in the presence of elevated K, were suppressed by the removal of Ca. Verapamil and nifedipine depressed vanadate-induced contractions of aortae from WKY and SHRSP, whereas they produced no or only slight inhibition of responses in guinea pig and rabbit aortae. Ca uptake into smooth muscle cell increased in the presence of vanadate, but the increase was much less than that induced by high K. In saponin-skinned smooth muscle, vanadate depressed the Ca-induced contraction. It is concluded that the vanadate-induced contraction utilizes both extracellular and intracellularly bound Ca, the relative contribution of which varies from preparation to preparation.

Animals↗
PubMed1988

Soluble factor from the hypertrophied left ventricle of dogs in experimental hypertension: ability to stimulate protein metabolism of cultured heart cells.

Our study concerned the existence of humoral factor(s) in cardiac hypertrophy arising from experimental perinephritic hypertension in dogs. Hypertension was induced by the method of Page with some modifications. A microassay technique was used on cultured neonatal rat heart cells. Heart extract from the hypertrophied left ventricle of dogs with experimentally induced renal hypertension, but not sham-operated dogs, increased the uptake of 3H-uridine by cultured rat heart cells. At a final heart extract concentration of 5 X 10(-3)% v/v (1-3 micrograms/ml), 3H-uridine was increased by a mean of about 15%, from four experiments. High performance liquid chromatography showed that the heart extract contained at least 16 molecules. Among them, a molecule of approximately 11,200 molecular weight stimulated the uptake of both 3H-uridine and 14C-leucine by cultured rat heart cells. These results indicate that the heart extract from the hypertrophied left ventricle of dogs with experimentally induced renal hypertension contained a factor that might induce and/or modulate myocardial hypertrophy in the model of hypertension.

Animals↗
PubMed1988

Left ventricular end-systolic wall stress--dimension relationship in unanesthetized dogs with perinephritic hypertension.

To study myocardial contractility in hypertensive hearts with normal wall motion, we examined left ventricular end-systolic wall stress-dimension relationships (ESWDR) during a baseline period (CS: control stage) and in the eighth week after induction of systemic hypertension by Page's method (HS: hypertensive stage) in unanesthetized dogs. The mean aortic blood pressure increased from 94 +/- 11 to 142 +/- 26 mmHg (p less than 0.01). The end-diastolic left ventricular posterior wall thickness increased significantly during the HS (9.4 +/- 1.3 vs 7.3 +/- 1.3 mm; HS vs CS), and its dimension was significantly (p less than 0.05) smaller than it was during the CS (37.0 +/- 4.2 vs 39.9 +/- 4.6 mm; HS vs CS). There were no significant differences between the 2 stages in left ventricular fractional shortening (31.9 +/- 5.0 vs 32.6 +/- 2.8; HS vs CS), in end-systolic meridional left ventricular wall stress (75.3 +/- 10.8 vs 68.3 +/- 15.6 10(3) dynes/cm2; HS vs CS), or in the ESWDR slopes (98.6 +/- 17.7 vs 94.0 +/- 19.7; HS vs CS). The ESWDR dimension intercepts significantly decreased from 2.0 +/- 0.3 to 1.8 +/- 0.3 cm during the HS; that is, the relationship shifted to the left with no significant change in the slope. At autopsy, the ratio of left ventricular weight to body weight of the hypertensive dogs was significantly (p less than 0.01) greater than that of sham-operated control dogs (6.0 +/- 0.9 vs 4.3 +/- 0.5 g/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗