PubMed Health⌕ Search

Biomedical subjects

T Inou

Publications and source records attributed to T Inou.

At least 37 records · Page 2Linked to original sources
PubMed1993

Impaired coronary blood flow response to acetylcholine in patients with coronary risk factors and proximal atherosclerotic lesions.

We examined whether coronary risk factors and atherosclerotic lesions in the study artery were associated with impaired endothelium-dependent dilation of coronary resistance arteries. Acetylcholine (ACH) at graded doses (1, 3, 10 and 30 micrograms/min) and papaverine (10 mg) were selectively infused into the left anterior descending coronary artery of 28 patients, in whom the study artery was angiographically normal (n = 16) or with mild stenosis < or = 40% (n = 12). Coronary blood flow (CBF) was estimated from the product of mean CBF velocity measured by an intracoronary Doppler catheter and the arterial cross-sectional area of the study artery determined by quantitative arteriography. ACH increased CBF in a dose-dependent manner. However, the maximum CBF response to ACH varied widely among patients (from 50% to 660%). By multivariate analysis, the presence of atherosclerotic lesions in the study artery was an independent predictor for impaired CBF response to ACH (P < 0.01). Hypertension (P < 0.001), hypercholesterolemia (r = -0.52, P < 0.005), age > or = 50 yr (P < 0.01) and total number of coronary risk factors (r = -0.62, P < 0.001) were associated with the impaired increase in CBF with ACH by univariate analysis. The percent increase in CBF evoked with papaverine did not correlate with these risk factors. The results suggest that mild atherosclerotic lesions in the study artery and coronary risk factors are accompanied by impaired endothelium-dependent dilation of coronary resistance arteries evoked with ACH. Endothelial dysfunction of coronary resistance arteries may result in altered regulation of myocardial perfusion in patients with mild coronary atherosclerosis and coronary risk factors.

Acetylcholine↗
PubMed1992

Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.

Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 micrograms/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 micrograms/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction.

Acetylcholine↗
PubMed1991

Effects of coronary artery occlusion in animals with hypertension and left ventricular hypertrophy.

Chronic arterial hypertension (HT) and left ventricular hypertrophy (LVH) increase the morbidity and mortality of acute myocardial infarction in patients. In this article, we discuss earlier studies from Koyanagi et al. in our laboratory that showed that when animals with chronic HT and LVH (HT-LVH) were subjected to acute coronary artery occlusion (CAO), there was a 3.5-fold increase in mortality and a 35% increase in infarct size expressed as a percent of the area at risk. We subsequently determined the effect of HT-LVH on the wavefront of myocardial infarction. Dogs were made hypertensive using a single-kidney, single-clip model of renovascular hypertension that produced mean arterial blood pressure (BP) = 141 +/- 3 mm Hg and left ventricular:body weight = 5.8 +/- 0.1 g/kg (p less than 0.05 vs. control animals). Conscious animals with HT-LVH and control animals were subjected to 1 or 3 h of CAO. Infarct and risk areas were measured using triphenyltetrazolium chloride (TTC) stain and barium angiography, respectively. The results suggested that the wavefront of infarction was accelerated in animals with HT-LVH. Further studies suggested that the wavefront of myocardial infarction could be markedly retarded by normalizing blood pressure (nitroprusside) 1 h following CAO. Recent studies in an animal model of HT-LVH suggested that electrophysiological abnormalities occur when these animals were subjected to CAO. Sixty-five percent of animals with HT-LVH had sudden death during CAO compared to 27% of the control group. We studied whether chronic beta-adrenergic blockade would reduce mortality associated with CAO in animals with HT-LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of synthetic human atrial natriuretic peptide on the human coronary circulation in subjects with normal coronary arteries.

Atrial natriuretic peptide (ANP) is recognized as an "endogenous vasodilator". The purpose of this study was to determine the effects of a clinical therapeutic dose of synthetic alpha-human ANP on the coronary circulation in 15 subjects with normal coronary arteries and normal ventricular function. The epicardial coronary arterial diameter was measured by selective coronary arteriography. Coronary blood flow was estimated from the arterial cross-sectional area and the flow velocity determined using an subselective intracoronary Doppler catheter. ANP, 0.03 micrograms/min/kg given intravenously over 15 minutes, caused a dilation of the large epicardial coronary artery (n = 8): the diameter of the proximal left anterior descending artery dilated from 2.6 +/- 0.4 to 3.1 +/- 0.5 mm (p less than 0.01). Mean arterial pressure decreased from 89 +/- 5 to 83 +/- 5 mmHg (p less than 0.01); heart rate did not change during ANP infusion. Estimated coronary blood flow significantly increased (n = 6, p less than 0.01), and thus the coronary vascular resistance decreased after ANP infusion, suggesting an ANP-induced dilation of resistance vessels. The present study demonstrates that in human subjects a clinical dose of ANP by intravenous infusion dilates both the large epicardial and small resistance coronary vessels. These results suggest a potentially beneficial role for ANP in reducing the severity of myocardial ischemia in patients with ischemic heart disease.

Adult↗
PubMed1991

Acute myocardial infarction with a hemodynamic pattern resembling constrictive pericarditis.

A 49-year-old woman experienced acute myocardial infarction with a hemodynamic pattern resembling constrictive pericarditis. To clarify its mechanism, we performed right atrial pacing and volume challenge test during the chronic state. Although these two interventions elevated diastolic pressures of the both ventricles, the dip and plateau pattern was not reproduced. Factors other than ischemia may be important in producing a hemodynamic pattern resembling constrictive pericarditis in acute myocardial infarction.

Blood Pressure↗
PubMed1991

[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension].

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.

Angiography, Digital Subtraction↗
PubMed1990

[Coronary artery disease and the results of coronary bypass surgery in diabetics].

To evaluate the influence of diabetes mellitus on coronary artery disease and the results of coronary bypass surgery, a review was made of 63 consecutive patients undergoing isolated saphenous vein aortocoronary bypass, of whom 38 patients (G-1) were nondiabetic, 9 patients (G-2) had impaired glucose tolerance, and 16 patients (G-3) were diabetic. The severity of coronary artery disease was assessed using an angiographic grading system. Among three patient groups, there was no difference in total coronary score per patient reflecting total extent of disease (G-1; 15.7 +/- 5.5, G-2; 14.1 +/- 5.9, G-3; 17.1 +/- 6.3, mean +/- S.D.) and the incidence of diffusely diseased vessels. The mean number of diseased vessels (greater than 50% stenosis) per patient was 2.5 +/- 0.6 in G-1, 2.6 +/- 0.7 in G-2, and 2.5 +/- 0.7 in G-3, and the mean number of bypass grafts per patient was 2.3 +/- 0.9, 2.2 +/- 0.9, and 2.1 +/- 0.7, respectively. Coronary luminal diameters and the severity of atherosclerotic changes of coronary arteries at the site of graft anastomosis, studied intraoperatively, were similar in all groups. Vein graft blood flows and early graft patency in diabetics (112 +/- 55 ml/min, 96.9%, respectively) were also similarly good as those in the other groups (98 +/- 49 ml/min, 91.4% in G-1, and 92 +/- 39 ml/min, 94.1% in G-2). Overall hospital mortality was 1.6% (one of 63). The only death from meningoencephalitis occurred in the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1989

[Quantification of myocardial infarct size by technetium-99m pyrophosphate single photon emission computed tomography].

Myocardial infarct size in 41 patients with the first attack of acute transmural myocardial infarction (MI) was assessed by technetium-99m pyrophosphate single photon emission computed tomography (99mTcPYP-SPECT). A ratio of the number of voxels of 99mTcPYP uptake into the infarct area to that into the thorax was calculated as a parameter of MI size. The ratio was positively correlated with both peak CPK activity (r = 0.53, p less than 0.005, n = 24) and extent score in 201TI-SPECT (r = 0.70, p less than 0.005, n = 14) significantly in patients with anterior MI but not in patients with inferior MI. There was also significant negative correlation between the ratio and the left ventricular ejection fraction (LVEF) measured by RI angiography in both acute (r = -0.67, p less than 0.005, n = 18) and chronic (r = -0.75, p less than 0.005, n = 25) phases in patients with anterior MI. Recovery in LVEF at chronic phase was noted in patients with small anterior MI but not with large anterior MI. 8 of 14 patients with inferior MI had right ventricular MI, that might have affected evaluation of MI size and resulted in no correlation between variables. It was suggested that 99mTcPYP-SPECT was a useful method to evaluate MI size and to predict prognosis of cardiac function in patients with anterior MI but not in patients with inferior MI.

Adult↗
PubMed1987

Relative importance of hypertension after coronary occlusion in chronic hypertensive dogs with LVH.

We have shown that there was a 50% increase in infarct size and a threefold increase in the incidence of sudden death following coronary occlusion in dogs with hypertension and left ventricular hypertrophy (LVH). To further investigate this problem, we separated the effects of hypertension from those of LVH by decreasing arterial pressure either by renal anastomosis or intravenous administration of nitroprusside in dogs with chronic renal hypertension and LVH. In 123 conscious dogs, the circumflex coronary artery was acutely occluded. Hemodynamics were monitored, myocardial perfusion was measured with labeled microspheres, the risk area was defined by postmortem angiography, and infarct size was determined pathologically 48 h after occlusion. The incidence of sudden death following acute coronary occlusion decreased dramatically in dogs with LVH if the arterial pressure was decreased with either nitroprusside or renal anastomosis. In addition, if arterial pressure was decreased with nitroprusside or renal anastomosis, infarct size in dogs with LVH was not augmented. In conclusion, normotension induced by renal anastomosis or nitroprusside returned infarct size and the incidence of sudden death in dogs with chronic hypertension and LVH toward control values. Thus it is likely that hypertension, as opposed to LVH, is the critical factor responsible for the increase in infarct size and the high incidence of sudden death observed in dogs with hypertension and LVH following sudden coronary occlusion.

Animals↗
PubMed1987

A new method for early detection of renal allograft rejection. Gel high-performance chromatography of urinary IgM.

We developed a new device utilizing high-performance chromatography to measure urinary IgM protein in renal transplant recipients. With this device we were able to obtain a reliable result in less than 2 h, requiring much less time than using the conventional method. Urinary IgM was found in 22 of 23 posttransplantation patients (96%) during acute rejection. An increase in urinary IgM excretion was noted 2-3 days before the appearance of clinical signs of acute rejection.

Adult↗
PubMed1987

Alterations in the coronary circulation in hypertrophied ventricles.

During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.

Animals↗
PubMed1986

Failure of pyruvate to salvage myocardium after prolonged ischemia.

Thrombolytic therapy for acute coronary occlusion may be more effective if combined with substrate-enhanced reperfusion. In this study, we examined the utility of pyruvic acid, an important metabolic substrate, in salvaging ischemic myocardium. Twenty-six anesthetized dogs underwent 3 h of circumflex coronary occlusion followed by 90 min of reperfusion with administration of intracoronary pyruvate or vehicle. To test the sensitivity of the model in detecting differences in infarct size, eight additional dogs underwent coronary occlusion of shorter duration (45 min), an intervention that is known to reduce infarct size. Collateral perfusion to the ischemic zone during coronary occlusion was similar in experimental and control groups. Whereas a shorter duration of occlusion (45 min) decreased the infarct-to-risk area ratio by 54% compared with a longer duration of occlusion (90 min), neither early (15 min prior to occlusion) nor late (3 h after occlusion) onset of intracoronary infusion of pyruvate shifted the infarct-risk relationship (control: y = 74x - 8.7, r = 0.99; early infusion: y = 0.76x - 9.5, r = 0.85; late infusion: y = 0.58x - 5.5, r = 0.79). The failure of intracoronary administration of pyruvate to limit infarct size raises questions as to its potential clinical utility in the setting of acute myocardial ischemia.

Animals↗
PubMed1985

Chronic instrumentation and its lack of effect on the hemodynamics and regional myocardial blood flow of conscious dogs.

The effects of chronic instrumentation on regional myocardial performance and regional myocardial blood flow were studied in 8 mongrel dogs. Regional segment lengths were measured by an ultrasonic dimension gauge technique at two areas of the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX). Regional myocardial blood flow was measured by a tracer microsphere technique. These measurements were repeated while the animals were conscious on the 4th, 11th, 21st and 28th days after instrumentation. On the 4th day, the heart rate was rather high and regional shortening at both the LAD and LCX areas remained suppressed. After the 11th day, hemodynamic variables such as heart rate, left ventricular pressure and regional wall motion were fairly constant. Regional myocardial blood flow and its distribution were also constant throughout the experimental period. Fibrosis of the epicardium invariably induced by surgical procedures did not affect the distribution of regional blood flow as compared with that of the interventricular septum. Thus, a stable hemodynamic state was recorded after the 11th day following surgical manipulation and the implantation of sensors and catheters did not affect the level of regional myocardial blood flow or its distribution at rest. Such long term reproducible measurements of regional wall motion and regional myocardial blood flow may facilitate chronic studies of cardiovascular physiology.

Animals↗
PubMed1984

Renal allografts with glomerulonephritic change and proteinuria.

Eight cases of renal allografts with glomerulonephritic change and proteinuria were classified into three groups according to the morphological features of the glomerular lesions. Group I (3 cases): By light microscope, remarkable reduplication of glomerular basement membrane (GBM), widening of mesangial region, and slight increase in mesangial cells, were observed. Electron microscopy revealed thickening of subendothelial space by deposition of electron-lucent material, mesangial interposition, and dense deposits in various regions (mainly in the subendothelial space). Group II (3 cases): By light microscope, crescent formation and reduplication of GBM were observed, while by electron microscope, changes of GBM similar to group I, but less remarkable, were seen. Group III (2 cases): Light microscope revealed spike formation in one case, but not in the other. With an electron microscope, subepithelial dense deposits were observed in both cases. Thickening of subendothelial space by deposition of electron-lucent material was noted in one case, while thickening of lamina densa was observed in the other case. Morphological change caused by rejection was observed in all eight cases, with six cases showing massive proteinuria and the other two showing slight proteinuria.

Adult↗
PubMed1983

Functional significance of collaterals during ameroid-induced coronary stenosis in conscious dogs. Interrelationships among regional shortening, regional flow and grade of coronary stenosis.

We studied the relationships among collateral flow, regional myocardial shortening and the grade of coronary stenosis during ameroid-induced chronic coronary constriction in 22 conscious dogs. A radiolucent ameroid, a Doppler flow probe and a cuff occluder were placed on the left circumflex coronary artery (LCx). Regional myocardial shortening and regional myocardial blood flow were assessed simultaneously using ultrasonic dimension gauges and the tracer microsphere technique, respectively, during temporary occlusion of the LCx. Regional hypokinesia and ischemia were attenuated as a function of time during progressive coronary stenosis. Fifty percent recovery and full recovery of regional shortening during occlusion were observed 19 +/- 3 and 25 +/- 4 days after instrumentation, respectively, when the endocardial blood flow recovered from 0.42 +/- 0.07 ml/min/g at 7 days to 0.56 +/- 0.07 and 0.80 +/- 0.05 ml/min/g, respectively. Greater than 75% coronary stenosis coincided with collateral development, as estimated from regional shortening rate and the appearance of angiographically opacified collaterals. Our study confirms that the development of collateral vessels reduces regional ischemia and hypokinesia induced during abrupt coronary occlusion in a canine model.

Animals↗
PubMed1982

Multiple atherosclerotic coronary aneurysms in association with acute myocardial infarction.

A 60-year-old woman with multiple coronary aneurysms, complicated with acute infero-posterior myocardial infarction is presented. The cine-coronary arteriogram disclosed a diffuse dilatation of epicardial coronary arteries associated with multiple aneurysms, fusiform ones in the right coronary and the left circumflex coronary arteries and saccular ones in the left anterior descending coronary artery. Distal run-off was poor. Ventriculography revealed a decrease in the ejection fraction (36%) and segmental abnormal wall motion at the apical and infero-posterior regions. The cause of the aneurysms appeared to be atherosclerotic. We suggested that coronary embolization was the cause of acute myocardial infarction in this case.

Aneurysm↗