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S Tomimoto

Publications and source records attributed to S Tomimoto.

17 recordsLinked to original sources
PubMed2000

Synergistic induction of pituitary adenylate cyclase-activating polypeptide (PACAP) gene expression by nerve growth factor and PACAP in PC12 cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) gene expression was analyzed in PC12 cells. PC12 cells transfected with a PACAP promoter-luciferase reporter construct were utilized to investigate the effects of PACAP, either alone or in combination with nerve growth factor (NGF), on PACAP transcriptional response. PACAP induced transcription from the PACAP promoter through PACAP type I receptor (PAC1 receptor). PACAP gene transcription was also induced by NGF. Simultaneous treatment with PACAP and NGF resulted in a synergistic transcriptional response that was more than three times the predicted response, based on a simple additive effect of both agents. This synergism in transcriptional response paralleled the PACAP mRNA levels, as determined by RT-PCR and northern blotting. The level of PACAP mRNA peaked 3 h after stimulation and gradually returned to basal levels by 48 h. PC12 cells are known to express predominantly the hop isoform of the PAC1 receptor, which positively couples to both adenylate cyclase and phospholipase C. To determine the role of the cyclic AMP and protein kinase C pathways in PACAP gene expression, the effects of forskolin and phorbol 12-myristate 13-acetate (PMA) were then examined. PMA did not alter PACAP mRNA levels but enhanced forskolin-induced PACAP mRNA expression. Down-regulation of protein kinase C blocked the ability of PACAP to stimulate PACAP mRNA expression. The mitogen-activated protein kinase extracellular signal-regulated kinase (ERK) kinase 1/2 (MEK1/2) inhibitor PD98059 also blocked the PACAP mRNA expression induced by either PACAP or NGF but not that induced by a combination of PACAP and NGF. These results suggest that PACAP stimulates the PACAP gene expression in PC12 cells at least in part through activation of adenylate cyclase and protein kinase C signaling pathways and that the ERK1/2 cascade is involved in PACAP and NGF-induced PACAP gene expression, although redundant signaling pathways may also be involved. The present finding showing that PACAP in combination with NGF causes a synergistic increase in PACAP gene expression in PC12 cells supports the idea that PACAP acts as an autocrine regulatory factor.

Animals↗
PubMed1999

Evaluation of adjunctive intracoronary administration of acetylcholine following intravenous infusion of ergonovine to provoke coronary artery spasm.

A dilemma arises in patients with chest pain or other symptoms suggestive of coronary artery disease but without significant coronary artery stenosis or spasm even after the spasm provocation test by either ergonovine or acetylcholine. Incremental doses of intracoronary acetylcholine (up to 100 micrograms for left coronary artery and 50 micrograms for right coronary artery) were administered when intravenous infusion of ergonovine 0.4 mg showed negative results. A total of 39 patients were studied. Provocation test was performed because of chest pain suggestive of coronary artery disease (n = 19), atypical chest pain (n = 6), post balloon angioplasty status (n = 6), silent ischemia (n = 4), Adams-Stokes syndrome (n = 3), and dead-on-arrival (n = 1). Characteristics of chest pain indicated variant angina (n = 11), rest angina (n = 4), and effort angina (n = 4). No electrocardiographic evidence of ischemia was detected before this test in any patient. Spasm was induced in 23 patients (59.0%) with complete obstruction in 7 (30.4%), diffuse vasoconstriction (90-99%) in 14 (60.9%), and focal spasm in 2 (8.7%). The patients with chest pain showed the highest positive rate of 78.9%. Further, the patients with atypical chest pain and miscellaneous reasons also revealed positive rates of 33.3% and 42.9%, respectively. One ventricular tachycardia and 2 atrial fibrillations occurred but terminated spontaneously. This test is useful for detecting spasm in a variety of patients in whom intravenous ergonovine infusion fails to induce spasm.

Acetylcholine↗
PubMed1998

Hemodynamic effect of amrinone depends on pretreatment vascular resistance in patients with evolving congestive heart failure: correlation between vascular resistance and neurohormonal activity.

We investigated the hemodynamic effects of amrinone and assessed its effects on neurohormonal factors in 15 patients with evolving congestive heart failure with various origins. We serially determined the pulmonary and systemic vascular-resistance indices after amrinone infusion and examined the relation between changes in hemodynamic parameters and changes in concentrations of norepinephrine, atrial natriuretic peptide, angiotensin II, and endothelin-1 in the pulmonary capillary wedge region (PCWR) and in the peripheral veins. Amrinone significantly reduced pulmonary vascular-resistance index (PVRI; Wood x m2) in patients with high PVRI (> or =15) before the infusion, significantly reduced systemic vascular-resistance index (SVRI; Wood x m2) in patients with high SVRI (> or =50) before the infusion, and had little effect on vascular resistances in patients with low PVRI (<15) and low SVRI (<50). The reduction in PVRI was correlated with the reduction in the endothelin-1 level (r = 0.75) in the PCWR, and the reduction in SVRI with norepinephrine level (r = 0.70) in the peripheral veins. The angiotensin II level did not change throughout the study. These findings suggest that amrinone had selective hemodynamic effects on pulmonary and systemic circulations with neurohormonal effects, according to PVRI and SVRI before infusion.

Aged↗
PubMed1998

Pulmonary capillary hemangiomatosis: a unique feature of congestive vasculopathy associated with hypertrophic cardiomyopathy.

A 34-year-old man with an 18-year history of hypertrophic cardiomyopathy died of worsening right-sided heart failure. Central venous pressure was greatly increased to 25 cm H2O before death. Postmortem examination revealed features of severe congestive vasculopathy, including those of pulmonary capillary hemangiomatosis in the lungs. Marked proliferation of capillaries was seen chiefly in alveolar septa and extending into pulmonary veins and arteries, causing severe luminal occlusion with recanalization. Diffusely distributed intra-alveolar edema and hemorrhage with collections of hemosiderin-laden macrophages were also seen, which suggested that the pulmonary capillary hemangiomatosis was associated with longstanding chronic passive congestion of the lung. It is possible that severe pulmonary passive congestion may be one of the causes of development of idiopathic pulmonary capillary hemangiomatosis.

Adult↗
PubMed1997

Plasma concentrations of adrenomedullin correlate with the extent of pulmonary hypertension in patients with mitral stenosis.

OBJECTIVE: To examine the pathophysiological significance of adrenomedullin in the pulmonary circulation by investigating the relation between plasma concentrations of adrenomedullin and central haemodynamics in patients with mitral stenosis. METHODS: Plasma concentrations of adrenomedullin in blood samples obtained from the femoral vein, pulmonary artery, left atrium, and aorta were measured by a newly developed specific radio-immunoassay in 23 consecutive patients with mitral stenosis (16 females and seven males, aged 53 (10) years (mean (SD)) who were undergoing percutaneous mitral commissurotomy. RESULTS: Patients with mitral stenosis had higher concentrations of adrenomedullin than age matched normal controls (3.9 (0.3) v 2.5 (0.3) pmol/l, p < 0.001). There was a reduction in adrenomedullin concentrations between the pulmonary artery and the left atrium (3.8 (0.2) v 3.2 (0.4) pmol/l, p < 0.001). The venous concentrations of adrenomedullin correlated with mean pulmonary artery pressure (r = 0.65, p < 0.001), total pulmonary vascular resistance (r = 0.83, p < 0.0001), and pulmonary vascular resistance (r = 0.65, p < 0.001). Plasma concentrations of adrenomedullin did not change immediately after percutaneous mitral commissurotomy; however, they decreased significantly one week later. CONCLUSIONS: Plasma concentrations of adrenomedullin are increased in patients with mitral stenosis. This may help to attenuate the increased pulmonary arterial resistance in secondary pulmonary hypertension due to mitral stenosis.

Adrenomedullin↗
PubMed1997

[Lesion-related factors associated with restenosis after percutaneous transluminal coronary angioplasty in the absence of patient-related factors].

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is one of the biggest problems in the treatment of coronary artery disease. Although many studies have been performed on lesion-related factors, they are influenced by patient-related factors such as smoking, hyperlipidemia, and the presence of acute coronary syndrome. In this study, lesion-related factors were assessed in the absence of other factors by univariate and multivariate analysis. One hundred and nine lesions were reviewed in 37 consecutive patients with both restenotic lesion(s) and non-restenotic one(s) confirmed by coronary arteriography performed 4.4 +/- 2.2 months after PTCA. Angiographic findings before and immediately after angioplasty were compared between restenotic and non-restenotic lesions. The overall lesion-restenosis rate was 42%. Univariate analysis revealed that calcified lesions (p < 0.05), multiple irregularities (p < 0.01) before angioplasty, residual percentage stenosis (p < 0.05), and angiographical intraluminal haziness (p < 0.05) were related to restenosis. Intimal dissection after PTCA was not associated with restenosis. Multivariate analysis with multiple logistic regression revealed that multiple irregularities (t = 2.8) was the most predictive of restenosis before PTCA and residual percent stenosis (t = 2.6) after the procedure. Coronary lesions with calcification or multiple irregularities indicate high risk of restenosis after PTCA. Optimal dilatation of the lesions without intraluminal haziness regardless of intimal dissection is important to prevent restenosis.

Aged↗
PubMed1997

[Captopril test].

Explore the source record for details and available documents.

Adrenal Cortex Function Tests↗
PubMed1996

Adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone.

A case of adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone is reported. A 55-year-old woman had hypertension, hypokalemia, low plasma renin activity and an adrenal tumor. The plasma level of aldosterone was normal, and the levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were extremely high. After the tumor removal, the plasma level of aldosterone decreased and plasma levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were normalized. The tumor was benign adenoma and the production of steroid hormones was under control of adrenocorticotropic hormone. The enzyme activity of 21-hydroxylation in the tumor was elevated and that of 11 beta-hydroxylation was decreased compared with the adjacent tissue.

18-Hydroxydesoxycorticosterone↗
PubMed1995

[Feasibility of the left ventricular volume measurement by acoustic quantification method: comparison with ultrafast computed tomography].

Acoustic quantification (AQ: the real-time automated boundary detection system) allows instantaneous measurement of cardiac chamber volumes. The feasibility of this method was evaluated by comparing the left ventricular (LV) volumes obtained with AQ to those derived from ultrafast computed tomography (UFCT), which enables accurate measurements of LV volumes even in the presence of LV asynergy, in 23 patients (8 with ischemic heart disease, 5 with cardiomyopathy, 3 with valvular heart disease). Both LV end-diastolic and end-systolic volumes obtained with the AQ method were in good agreement with those obtained with UFCT (y = 1.04 x - 16.9, r = 0.95; y = 0.87x + 15.7, r = 0.91; respectively). AQ was reliable even in the presence of LV asynergy. Interobserver variability for the AQ measurement was 10.2%. AQ provides a new, clinically useful method for real-time accurate estimation of the left ventricular volume.

Feasibility Studies↗
PubMed1991

Single-beat estimation of the slope of the end-systolic pressure-volume relation in the human left ventricle.

This study assessed a new method of estimating the slope (Ees) of the end-systolic pressure-volume relation (ESPVR) from a single beat of the human heart. Left ventricular pressure was recorded with a high-fidelity micromanometer in patients with heart disease during left ventriculography. Peak isovolumic pressure at the end-disastolic volume was estimated by a curve-fitting technique from an isovolumic left ventricular pressure curve. The ESPVR line was drawn from the estimated peak isovolumic pressure-volume point tangential to the left upper corner of the pressure-volume loop. The slope of this estimated ESPVR line from single-beat analysis was compared with the slope of the ESPVR line obtained from three pressure-volume loops in 16 patients given angiotensin II or nitroglycerin infusion. The estimated Ees was 5.0 +/- 2.2 mm Hg/ml/m2, and the conventional Ees was 4.9 +/- 2.7 mm Hg/ml/m2. The estimated Ees showed a positive correlation with the conventional Ees (r = 0.91, p less than 0.001, SEE = 1.2 mm Hg/ml/m2). In the other 13 patients, after dobutamine infusion (5 micrograms/kg/min i.v.) the estimated Ees increased significantly from 5.6 +/- 1.4 to 7.4 +/- 2.0 mm Hg/ml/m2 (p less than 0.01). Thus, the estimated Ees approximated the conventional Ees and was sensitive to a positive inotropic intervention. We conclude that this single-beat analysis method facilitates assessment of the beat-by-beat ESPVR of the human heart.

Angiotensin II↗
PubMed1991

[Transmitral flow velocity patterns as influenced by preload, afterload and heart rate alterations: pulsed Doppler echocardiographic study].

The influences of preload, afterload and heart rate alterations on the pattern of left ventricular filling were investigated using pulsed Doppler echocardiography (PDE) in humans. Transmitral flow at the level of the valvular tip was recorded during dextran infusion, lower body negative pressure, angiotensin II infusion, and atrial and atrioventricular sequential pacings. Peak velocity of rapid filling (R), peak velocity of atrial contraction (A), the ratio of peak velocities (A/R), flow velocity integrals of the rapid filling phase (IR) and atrial contraction (IA) were obtained. PDE and the measurement of hemodynamics during lower body negative pressure (0, -10 mmHg, -20 mmHg) and dextran infusion (100 ml, 200 ml) were studied in 22 patients with ischemic heart disease. R decreased significantly after lower body negative pressure, and increased significantly during dextran infusion. Before and during angiotensin II infusion, PDE and the measurement of hemodynamics were studied in 14 patients with ischemic heart disease. The patients were categorized into 2 subgroups according to left ventricular function. During afterload stress, the A/R and IA increased in patients with normal left ventricular function; whereas, the A/R decreased in patients with poor left ventricular function. PDE was recorded during right atrial and atrioventricular sequential pacings at the heart rates of 60 to 100 beats/min in 29 patients with ischemic heart disease. When the heart rates increased, R decreased during atrial and atrioventricular sequential pacings. The A increased after the occurrence of the summation between the rapid and atrial filling waves. The A/R gradually increased with incremental heart rate. These results indicate that changes in the preload alter the peak velocity of left ventricular filling pattern of transmitral flow. The effects of the increasing afterload depend on the basal left ventricular function, with an increase in the peak velocity of atrial contraction being observed in the presence of normal left ventricular function. Both the peak velocity of rapid filling and atrial contraction were related to the heart rate and atrioventricular conduction delay. In assessing left ventricular filling dynamics using PDE, the influence of the preload, afterload and heart rate must be considered.

Angiotensin II↗
PubMed1989

Noninvasive assessment of left ventricular diastolic filling in coronary artery disease by Doppler dipyridamole-stress testing.

To evaluate left ventricular diastolic function during dipyridamole-provoked myocardial ischemia, transmitral flow was studied in 73 patients with coronary artery disease and 8 normal subjects using pulsed Doppler echocardiography. Coronary vasodilating agents like dipyridamole can provoke myocardial ischemia in patients with coronary artery disease. The peak flow velocity of left ventricular rapid filling (R), that of atrial contraction (A) and the ratio of A to R (A/R) in each cardiac cycle were measured. The rapid filling phase was divided into two subphases at the point of R. The integral of the two subphases and atrial contraction were computed and designated IR1, IR2 and IA. The time intervals of the two subphases of rapid filling were designated TR1 and TR2. Of the 73 patients with coronary artery disease, 41 patients developed ischemia (positive responder = PR) and 32 patients did not (negative responder = NR) after dipyridamole infusion. In PR, A/R increased (p less than 0.05), IR2 decreased (p less than 0.01) and TR2 shortened (p less than 0.01) significantly. In NR and normal subjects, these indices remained unchanged. We observed mitral regurgitation (MR) in 13 PR patients during acute myocardial ischemia. A/R increased in patients without MR but A/R remained unchanged in patients with MR. These results suggest that in acute myocardial ischemia, changes in Doppler indices (A/R, IR2 and TR2) reflect a left ventricular diastolic abnormality, and that the masking of the diastolic abnormality was ascribed to the presence of MR.

Blood Flow Velocity↗
PubMed1989

[Influence of preload alteration on the transmitral flow velocity in patients with old myocardial infarction: effects of nitroglycerin and lower body negative pressure].

We studied the influence of preload alteration on the pattern of transmitral flow as obtained by pulsed Doppler echocardiography. In protocol I, 14 patients with old myocardial infarction (OMI) were observed by simultaneous measurements of transmitral flow by PDE and left ventricular end-diastolic dimension (LVDd) using M-mode echocardiography during the control period and after sublingual nitroglycerin. In protocol II, eight patients with OMI were similarly observed during stepwise lower body negative pressure (LBNP: 0, -10 and -20 mmHg). The rapid filling phase was categorized in two subphases at peak R as the first half and second half phases. The integrals of each half phase and the atrial systolic phases (IR1, IR2 and IA) were measured by planimetry. After the administration of nitroglycerin, LVDd decreased significantly; whereas the mean arterial pressure decreased and heart rate increased significantly. The peak R and IR1 decreased significantly, but the peak A, IR2 and IA remained unchanged. During LBNP, LVDd decreased stepwise; whereas there was no change in the mean arterial pressure or heart rate. The changes in the peak R and IR1 paralleled the preload reduction during LBNP. The peak A, IR2, and IA remained unchanged. In conclusion, the first and second half volumes during the LV rapid filling phase can be influenced by various factors. The patterns of the transmitral flow velocity, the maximal velocity and first half volume in the LV rapid filling phase may be influenced by preload alteration.

Adult↗
PubMed1987

Effects of percutaneous transluminal coronary angioplasty on segmental left ventricular function in patients with acute myocardial infarction.

In order to investigate the usefulness of percutaneous transluminal coronary angioplasty (PTCA) on subsequent left ventricular (LV) function in patients with acute myocardial infarction (AMI), regional ejection fraction (REF) was calculated from the left ventriculogram and compared in the acute and chronic phases (4 weeks after infarction) in 19 successful cases of PTCA (group A). In addition, 15 successful cases of intracoronary thrombolysis (PTCR) (group R) and 14 unsuccessful cases (group U) were also analyzed in this study. From the results, the following points were elucidated. (1) REF of group A in the chronic phase showed a significant increase compared to that in the acute phase (10 +/- 18% vs 20 +/- 19%, p less than 0.01), and this was similar to that observed in group R (9 +/- 19% vs 21 +/- 16%, p less than 0.01). (2) All cases in group A showed a significant increase in REF (p less than 0.02), if recanalization occurred within 3 hours after the onset of AMI. Some cases in the 3-6 hour recanalization group showed a decrease in REF. (3) In group A, only patients with subtotal occlusion on the initial coronary angiogram showed a significant increase in REF 4 weeks later (p less than 0.01), whereas patients with total occlusion on the initial coronary angiogram showed no significant increase in REF. (4) In group A, only patients recanalized between 3 and 6 hours showed a severe degree of prolonged contrast staining immediately after successful recanalization following PTCA. Thus, chronic phase regional wall motion was markedly improved by PTCA in those cases with residual flow. In contrast, abrupt recanalization after PTCA might causally decrease regional wall motion due to hemorrhagic infarction, if it is performed in cases with total occlusion.

Angioplasty, Balloon↗