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S Arima

Publications and source records attributed to S Arima.

At least 55 records · Page 3Linked to original sources
PubMed1996

Increase in the delta ST/delta heart rate (HR) index: a new predictor of restenosis after successful percutaneous transluminal coronary angioplasty.

With the goal of improving the prediction of restenosis after percutaneous transluminal coronary angioplasty (PTCA), we evaluated the usefulness of the delta ST/delta heart rate (HR) index derived from serial exercise treadmill tests. Exercise treadmill tests were performed by 125 patients with single-vessel coronary artery disease before and several days after PTCA, and just before follow-up angiography 3 to 12 months later. Simple HR-adjusted indexes of ST-segment depression during exercise (delta ST/delta HR index) were derived. We compared the usefulness of the increase in delta ST/delta HR index at follow-up over the value obtained several days after PTCA for prediction of restenosis with that of a positive exercise treadmill test and a positive thallium scintigram at follow-up. At follow-up, 47 of the 125 patients showed restenosis. The delta ST/delta HR index increased in 43 of 47 patients in the restenosis group and in 18 of 78 patients without restenosis (p < 0.0001). Separate analysis of each criterion revealed the following respective values for sensitivity, specificity, and positive and negative predictive values for prediction of restenosis; increased delta ST/delta HR index of follow-up: 91%, 77%, 70%, and 94%; positive exercise treadmill test: 83%, 65%, 59%, and 86%; and positive thallium scintigram: 79%, 78%, 69%, and 86%. The increased delta ST/delta HR index had a significantly (p < 0.05) higher sensitivity than the positive thallium scintigram and a significantly (p < 0.01) higher specificity than the positive exercise treadmill test. An increased delta ST/delta HR index at follow-up identifies subgroups of patients who are at high risk for restenosis after PTCA.

Aged↗
PubMed1996

Right ventricular stiffness measured by a new method without volume estimation in coronary artery disease.

This study was designed to measure the right ventricular (RV) stiffness (delta P/ delta V) with a new method without estimating the RV volume itself. RV stiffness has rarely been measured due to the difficulty in estimating the RV volume. Without measuring RV volume itself, stiffness can be determined by measuring its volume change (delta V). Tricuspid filling flow volume, which is the diastolic RV delta V, is measurable by using Doppler echocardiography. Thus, RV stiffness may possibly be obtained from Doppler echocardiography combined with high-fidelity RV pressure. Subjects consisted of 8 controls, 8 patients with angina pectoris, 8 with anterior, 8 with posterior, and 8 with inferior prior myocardial infarction. Tricuspid annular dimension was measured by 2-dimensional echocardiography and the tricuspid annular area was calculated. Velocity-time integral of the tricuspid filling flow during the late diastole was measured by pulsed Doppler echocardiography. Then, the late diastolic RV delta V was obtained as the product of the tricuspid annular area and the integral. The late diastolic RV pressure rise (delta P) was also measured with a micromanometer catheter. The RV elastic chamber stiffness constant ([delta P/ delta V]/P) was obtained by dividing simple stiffness by the mean RV pressure during late diastole. The RV elastic chamber stiffness constant did not significantly differ among controls, patients with angina pectoris, and those with anterior and posterior myocardial infarction (0.0054 +/- 0.0009 vs 0.0057 +/- 0.0018 vs 0.0064 +/- 0.002 vs 0.0052 +/- 0.0019 ml-1). However, it was significantly increased in patients with inferior myocardial infarction (0.010 +/- 0.004 ml-1, p < 0.01 or 0.05) compared with those in the other 4 groups. These results suggest (1) that RV stiffness can be measured with a new method without RV volume estimation, and (2) that this new method is useful in evaluating RV diastolic pathophysiology in patients with coronary artery disease.

Aged↗
PubMed1996

Transesophageal Doppler echocardiographic assessment of left coronary blood flow velocity in chronic aortic regurgitation.

Assessment of systolic and diastolic coronary blood flow velocities (FVs) in patients with aortic regurgitation (AR) has remained a clinical challenge. We recorded left anterior descending coronary blood FV in 21 patients with chronic AR an in 6 control subjects using transesophageal pulsed Doppler echocardiography. In 7 patients FV was measured 4.0 +/- 5.2 months after aortic valve replacement. Peak and mean FVs during systole and diastole and systolic/diastolic ratios of these FVs were determined. Left ventricular (LV) mass index was calculated by means of standard M-mode echocardiography. In patients with severe AR, peak and mean systolic FVs were significantly increased (34 +/- 8 cm/sec and 21 +/- 6 cm/sec, respectively) compared with FVs in the control group (15 +/- 4 and 12 +/- 3 cm/sec, respectively) and in patients with mild AR (17 +/- 3 cm/sec and 13 +/- 2 cm/sec, respectively). Peak and mean systolic FVs were also significantly increased in severe AR (54 +/- 13 cm/sec and 33 +/- 9 cm/sec, respectively) compared with FVs in the control (30 +/- 8 cm/sec and 21 +/- 5 cm/sec, respectively) and mild AR groups (30 +/- 5 cm/sec and 21 +/- 4 cm/sec, respectively). Peak systolic and diastolic FVs were correlated significantly with LV mass index (r = 0.72 and r = 0.73, respectively). Systolic and diastolic FVs and LV mass index were significantly decreased, normalized or both after aortic valve surgery. In conclusion, LV mass seems to have an effect on the significantly increased systolic and diastolic left coronary blood FV pattern in patients with chronic, severe AR. Increased systolic and diastolic FV appears to be normalized in the late period after surgery.

Adult↗
PubMed1996

High serum concentration of lipoprotein(a) is a risk factor for restenosis after percutaneous transluminal coronary angioplasty in Japanese patients with single-vessel disease.

To determine the relation between the concentration of lipoprotein(a) [Lp(a)] and restenosis after percutaneous transluminal coronary angioplasty (PTCA) in Japan, we studied 80 consecutive patients with single-vessel disease who successfully underwent PTCA. All were evaluated by follow-up angiography a mean of 6.9 months after PTCA and were divided into the restenosis (30 patients) and the non-restenosis (50 patients) groups. The serum Lp(a) concentration of 29 +/- 17 mg/dl in the restenosis group was significantly higher than that of 17 +/- 14 mg/dl in the nonrestenosis group (p < 0.01). Multiple logistic regression analysis for risk factors revealed a significant correlation between restenosis and Lp(a) (p < 0.003). The serum Lp(a) concentration was positively correlated with the coronary artery percent stenosis at the time of follow-up angiography (r = 0.32, p < 0.01). High serum concentration of Lp(a) is therefore a risk factor for restenosis after PTCA in Japan.

Adult↗
PubMed1996

Angiotensin II action in isolated microperfused rabbit afferent arterioles is modulated by flow.

We have recently presented evidence that endogenous nitric oxide (NO) and prostaglandins (PGs) modulate angiotensin II (Ang II) action in microperfused afferent arterioles (Af-Arts). Because flow may be a physiological stimulus of endothelial release of NO and PGs, we tested the hypothesis that flow through the lumen of the Af-Art stimulates the endothelium to produce NO and PGs, which in turn modulate the action of Ang II. We microdissected the terminal segment of an interlobular artery together with two Af-Arts, their glomeruli and efferent arterioles (Ef-Art). The two Af-Arts were perfused simultaneously from the interlobular artery, while one Ef-Art was occluded. Since the arteriolar perfusate contained 5% albumin, oncotic pressure built up in the glomerulus with the occluded Ef-Art and opposed the force of filtration, resulting in little or no flow through the corresponding Af-Art. Thus this preparation allowed us to observe Ang II action in free-flow and non-flow Af-Arts simultaneously. Ang II-induced constriction was weaker in free-flow than non-flow Af-Arts, with the luminal diameter decreasing by 8 +/- 2% and 23 +/- 3% at 10(-9) M, respectively (P < 0.013 free-flow vs. non-flow; N = 9). Disrupting the endothelium augmented Ang II action in free-flow (33 +/- 5.1%; P < 0.01 vs. intact endothelium) but not non-flow Af-Arts (31 +/- 5.3%), thus abolishing the differences between them (N = 8). Pretreatment with an inhibitor of either NO synthase (N-nitro-L-arginine methyl ester) or cyclooxygenase (indomethacin) augmented Ang II action more in free-flow than non-flow Af-Arts, likewise abolishing the differences between them. These results suggest that intraluminal flow modulates the vasoconstrictor action of Ang II in Af-Arts via endothelium-derived NO and PGs. Thus flow may be important in the fine control of glomerular hemodynamics.

Angiotensin II↗
PubMed1996

20-HETE requires increased vascular tone to constrict rabbit afferent arterioles.

Renal production of 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P-450-dependent arachidonate metabolite, increases during development of hypertension in spontaneously hypertensive rats, and inhibition of its production prevents hypertension. Since 20-HETE is a potent vasoconstrictor, these findings suggest that 20-HETE may contribute to the development of hypertension by elevating renal vascular resistance. In this study we examined the direct action of 20-HETE on the afferent arteriole, a vascular segment crucial to the control of renal vascular resistance. Rabbit afferent arterioles were microperfused at 60 mm Hg in vitro, and 20-HETE was added to the lumen. Although 20-HETE (10(-10) to 10(-6) mol/L) had no effect on the diameter of non-treated afferent arterioles (n=6), it caused dose-dependent constriction when vascular tone was increased with norepinephrine (0.3 micromol/L); 20-HETE at 10(-6) mol/L decreased diameter by 43 +/- 4% (n=6, P < .001). This constriction was abolished by disrupting the endothelium (n=5). Moreover, pretreatment with the cyclooxygenase inhibitor indomethacin (50 micromol/L) or the thromboxane/endoperoxide receptor antagonist SQ29548 (1 micromol/L) significantly (P < .03) attenuated 20-HETE-induced constriction: 20-HETE at 10(-6) mol/L constricted norepinephrine-treated afferent arterioles by 28 +/- 3% (n=6) and 25 +/- 4% (n=5), respectively. These results demonstrate that an increase in afferent arteriolar tone is required for the vasoconstrictor action of 20-HETE, which is partly mediated by the endothelial cyclooxygenase pathway. THus, increased production of 20-HETE in the kidney and increase in afferent arteriolar tone, both of which often precede the development of hypertension, may synergistically contribute to the development of hypertension by elevating renal vascular resistance.

Animals↗
PubMed1996

Platelet-activating factor dilates efferent arterioles through glomerulus-derived nitric oxide.

UNLABELLED: Despite evidence that platelet-activating factor (PAF) is produced by the glomerulus, its direct action on the glomerular microcirculation is poorly understood. It was recently reported that at picomolar concentrations, PAF dilates isolated microperfused afferent arterioles (Af-Art) via nitric oxide (NO). The present study tested the hypothesis that PAF acts on the glomerulus to release NO, which in turn controls the resistance of the efferent arteriole (Ef-Art). Rabbit Ef-Art were perfused from the distal end (retrograde perfusion [RP]) to eliminate the influence of the glomerulus, or through the glomerulus from the end of the Af-Art (orthograde perfusion [OP]) to maintain the influence of the glomerulus. Ef-Art were preconstricted by approximately 40% with norepinephrine and increasing doses of PAF were added to both the arteriolar perfusate and bath. Only with OP did PAF at picomolar concentrations cause significant dilation: at 400 pmol, the diameter increased by 64 +/- 11% from the preconstricted level (N = 6, P < 0.01). This dilation was completely abolished by pretreatment with an NO-synthesis inhibitor. To study its possible constrictor action, PAF was added to nonpreconstricted Ef-Art. At nanomolar concentrations, PAF constricted Ef-Art similarly in both RP and OP: at 40 nM, the diameter decreased by 24 +/- 4% (N = 6, P < 0.01) and 20 +/- 2% (N = 6, P < 0.01), respectively. This constriction was attenuated by pretreatment with indomethacin (Indo) in both RP (14 +/- 2%, N = 7; P < 0.02 versus without Indo) and OP (10 +/- 2%, N = 6; P < 0.02 versus without Indo). IN CONCLUSION: (1) at picomolar concentrations, PAF stimulates the glomerulus to release NO, which in turn dilates the Ef-Art; and (2) at nanomolar concentrations, PAF constricts the Ef-Art partly through release of cyclooxygenase metabolites. Thus, PAF may play a role in glomerular hemodynamics under various physiological and pathological conditions.

Animals↗
PubMed1996

Diverse effects of calcium antagonists on glomerular hemodynamics.

This study examined the direct effects of calcium antagonists on glomerular hemodynamics. Rabbit afferent (Af-) or efferent arterioles (Ef-Arts) were microperfused in vitro at constant pressure. Ef-Arts were perfused from the distal end of Af-Art through the glomerulus. Increasing doses (10(-10) to 10(-7) M) of nifedipine (Nif), nicardipine (Nic) or manidipine (Man) were added into the lumen of Af- or Ef-Arts preconstricted (by about 40%) with norepinephrine. Although Nif and Nic dilated Af-Arts in a dose-dependent manner, they did not cause any dilation in Ef-Arts. In contrast, Man dilated both Af- and Ef-Arts in a dose dependent manner; Man at 10(-7) M dilated Af- and Ef-Arts by 71 +/- 12% (N = 7) and 38 +/- 3% (N = 6), respectively. Although Man's dilator effect on Ef-Art was not affected by inhibiting nitric oxide (NO) synthesis (N = 6), it was markedly attenuated by eliminating the influence of glomerulus (14 +/- 3% by Man at 10(-7) M, N = 5). These results demonstrate that in addition to dilating Af-Art, Man, but not Nif or Nic, dilates Ef-Art through a glomerulus-derived vasodilator(s) other than NO. Such diverse actions should be taken into consideration when calcium antagonists are used in the treatment of patients with cardiovascular and renal diseases.

Animals↗
PubMed1995

Neuronal differentiation of Neuro 2a cells by lactacystin and its partial inhibition by the protein phosphatase inhibitors calyculin A and okadaic acid.

Lactacystin (1.3 microM), a metabolite from an actinomycete, induced the formation of bipolar projections at both sides of the cell body of Neuro 2a cells 1 day after treatment and networks at and after 3 days and enhanced acetylcholinesterase activity (a marker of neuronal differentiation). Thus, the neuronal differentiation was characterized both morphologically and functionally. The experiments with various inhibitors of protein kinases and phosphatases revealed that the protein phosphatase inhibitors calyculin A (0.5 nM) and okadaic acid (0.6 nM) inhibit the formation of bipolar projections at 1 day, but does not inhibit the network formation at and after 3 days.

Acetylcholinesterase↗
PubMed1995

Echocardiographic diagnosis of partial anomalous pulmonary venous connection from right upper lobe to the coronary sinus.

A 36-year-old woman was admitted because of an enlarged right heart. Echocardiographic examination revealed an abnormal vessel connecting to the dilated coronary sinus. The abnormal vessel traveled in the direction from the right axillary to the left epigastric region. Partial anomalous pulmonary venous connection (PAPVC) from the right upper lobe to the coronary sinus was initially considered as a possible diagnosis by echocardiography. At surgery, diagnosis of an isolated PAPVC of the right upper pulmonary vein to the coronary sinus was confirmed.

Adult↗
PubMed1995

Cardiac dystrophin abnormalities in Becker muscular dystrophy assessed by endomyocardial biopsy.

Duchenne and Becker muscular dystrophy (DMD/BMD) are allelic variants caused by mutations in gene-encoding dystrophin. Abnormal expression of dystrophin in skeletal muscle has been shown to correlate with severity of disease. However, in BMD the severity of skeletal and cardiac involvement are not well correlated. We studied the immunostaining pattern of cardiac dystrophin in endomyocardial biopsy specimens from 83 patients with heart disease. Immunohistochemical assessment of dystrophin in four patients with BMD and cardiomyopathy showed a variable distributions of myocytes with continuous, discontinuous, or absent membrane immunostaining patterns. These patterns were obviously different from patterns of other heart diseases. We conclude that the discontinuous immunostaining pattern of cardiac dystrophin is characteristic of BMD and that an absent pattern may be associated with more severe cardiac dysfunction. Because genetic analysis cannot determine the correct diagnosis in 35% of DMD/BMD cases, we recommend routine examination of immunostaining patterns of dystrophin in endomyocardial biopsy specimens in patients with cardiomyopathy suspected to be the result of BMD.

Adult↗
PubMed1995

High glucose augments angiotensin II action by inhibiting NO synthesis in in vitro microperfused rabbit afferent arterioles.

Preglomerular afferent arteriole (Af-Art) is a crucial vascular segment in the control of glomerular hemodynamics. We have recently reported that vascular reactivity of Af-Art is modulated by nitric oxide (NO). However, little is known about its reactivity under pathophysiological conditions such as diabetes, which is often accompanied by abnormal glomerular hemodynamics. In the present study, we examined the direct effects of high glucose, the hallmark of diabetes, on the vascular reactivity of Af-Art. Rabbit Af-Arts were microperfused for three hours with medium 199 containing either normal (5.5 mM; NG-Af-Arts) or high concentrations (30 mM; HG30-Af-Arts) of glucose, and then vascular reactivity was examined. Sensitivity to angiotensin II (Ang II) was significantly higher in HG30-Af-Arts than in NG-Af-Arts. Ang II began to cause significant constriction from 10(-9) M in NG-Af-Arts (18 +/- 3%, N = 6, P < 0.01) and from 10(-11) M in HG30-Af-Arts (9 +/- 2%, N = 6, P < 0.01). NO synthesis inhibition with 10(-4) M nitro-L-arginine methyl ester (L-NAME) increased the sensitivity to Ang II in NG-Af-Arts without affecting Ang II action in HG30-Af-Arts. In L-NAME-pretreated NG-Af-Arts, Ang II began to cause constriction from 10(-11) M (11 +/- 3%, N = 6, P < 0.01). Thus, pretreatment with L-NAME abolished the difference in sensitivity to Ang II between NG- and HG30-Af-Arts, suggesting impaired NO synthesis in HG30-Af-Arts.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

[Receptors and its signal transduction pathway in the renal interstitial cells].

There are several types of renal interstitial cells, such as fibroblast, monocyte/macrophage, lymphocyte, dendritic cell, and so on. These cells in the interstitium probably modulate changes in tubular repair, including cell proliferation, cell mitosis, fibrosis, immune cell infiltration and interstitial fibrosis through a complex cytokine and/or mediator network. These factors bind to cellular receptors, and then they activate signal transduction pathways, and result in expression of several information such as cell proliferation, mitosis and so on. In this paper, we attempt to describe some receptors and its signal transduction pathway in the renal interstitial cells.

Animals↗
PubMed1995

[A case of remarkable response of colon cancer with multiple liver and bone metastasis treated with tegafur and cisplatin].

A 47-year-old man with ascending colon cancer with multiple liver metastases and bone metastasis (VII thoracic vertebra) showed a remarkable response to the combination therapy of tegafur and cisplatin. Tegafur (1,200 mg/day) was administered through continuous intravenous infusion mixed with IVH, and cisplatin was given every two weeks at a dose of 100 mg. The total dose of tegafur was 39.6g and that of cisplatin was 300mg. After therapy, primary and metastatic lesions were remarkably reduced according to various imaging techniques, and the serum CEA level of 34ng/ml at diagnosis decreased 3.7 ng/ml. Various tumor-related symptoms were improved. Drug toxicity caused slight nausea and leucopenia. Right hemicolectomy with R2 lymph node dissection was performed after chemotherapy. Histologically, primary lesion and regional lymph nodes showed diffuse fibrosis and necrosis, and only a few cancer cells remained some vessels. These results suggested that the combination chemotherapy of tegafur and cisplatin is useful for the treatment of colon cancer.

Adenocarcinoma↗
PubMed1994

Production of two novel monoclonal antibodies against human renal glomeruli and their application to the immunohistochemical investigation of crescentic glomerulonephritis.

Two monoclonal antibodies (MAbs) against human renal glomeruli, HEP1 and HBM1, were produced using isolated human glomeruli as an antigen. Immunohistochemical and immunoelectron microscopic analyses revealed that the recognition site of HEP1 is the cell surface of the visceral glomerular epithelial cells. HEP1 showed no reaction in the renal interstitium or in other tissues. HBM1 recognized an antigen present in the basal lamina of the renal glomeruli, Bowman's capsule, and partly in the basement membrane of renal tubules, but it was not reactive with the mesangial matrix or renal interstitium. The isotype of both MAbs was IgG1, k. The molecular weights of their corresponding antigens were 127-177 and 220 kD, respectively. Besides human tissues, HEP1 also showed cross-reactions with antigens in the visceral glomerular epithelial cells of various animals other than mice. HBM1 recognized human antigen only. Using both MAbs, eight cases of crescentic glomerulonephritis were examined immunohistochemically. As a result, it was demonstrated that the crescents may not be formed by visceral glomerular epithelial cells. From this study, these two MAbs appear to be useful markers for the evaluation of renal glomerular disorders.

Animals↗
PubMed1994

Increased heparin-releasable platelet factor 4 and D dimer in patients one month after the onset of acute myocardial infarction: persistent activation of platelets and the coagulation/fibrinolytic system.

To evaluate the activity of platelets and the coagulation/fibrinolytic system 1 month after the onset of acute myocardial infarction, we measured the plasma levels of molecular markers, i.e. beta-thromboglobulin, platelet factor 4, thrombin-antithrombin III complex and D dimer, in 16 patients with acute myocardial infarction and in 11 normal subjects. Blood was drawn through a catheter placed in the pulmonary artery before heparin injection. The heparin-releasable platelet factor 4 was calculated by subtracting the level before the injection of 5000 U of heparin, from the level 5 min after injection. The plasma beta-thromboglobulin, thrombin-antithrombin III complex and the D dimer levels in the acute phase of myocardial infarction were 134.9 +/- 121.2, 11.2 +/- 7.1 and 164.4 +/- 115.3 ng/ml, respectively. These values were significantly higher than those in the normal subjects. The plasma levels of beta-thromboglobulin and thrombin-antithrombin III complex, 1 month after the onset (36.6 +/- 16.4 and 4.6 +/- 2.3 ng/ml, respectively) were not significantly different from those of the normal subjects. In contrast, D dimer and heparin-releasable platelet factor 4 were 216.9 +/- 176.9 and 80.5 +/- 29.3 ng/ml, respectively, and significantly higher than in the normal subjects. These findings suggest a latent but persistent activation of the platelets and the coagulation/fibrinolytic system 1 month after the onset of acute myocardial infarction.

Adult↗