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Biomedical subjects

T Tajimi

Publications and source records attributed to T Tajimi.

At least 19 recordsLinked to original sources
PubMed1995

Improvement of coronary vasomotion with eicosapentaenoic acid does not inhibit acetylcholine-induced coronary vasospasm in patients with variant angina.

Impaired function of the endothelium may be a mechanism of the coronary vasospasm induced by acetylcholine. We examined whether purified eicosapentaenoic acid (EPA), a major component of fish oil, improves the coronary vasomotion in response to acetylcholine, and the effect of purified EPA on acetylcholine (ACh)-induced coronary vasospasm in 22 patients with variant angina. ACh was infused into the coronary artery both before and after 4 months of EPA treatment (EPA 1.8 g/day, n = 12). In the control group (n = 10) that did not receive EPA, the response of the coronary diameter to ACh did not change over time. In the EPA-treated group, the cholinergic response in non-spastic sites changed from vasoconstriction to vasodilation, while ACh-induced coronary vasospasm persisted at the spastic sites. Therefore, EPA treatment improved the coronary vasomotor responsiveness to ACh, but did not inhibit ACh-induced coronary vasospasm.

Acetylcholine↗
PubMed1994

Effects of continuous intravenous infusion of isosorbide dinitrate on development of tolerance to vasodilating action in human epicardial coronary arteries.

This study was performed to determine the effects of long-term intravenous infusion on the coronary vasodilating actions of continuous intravenous and bolus intracoronary administration of isosorbide dinitrate (ISDN). With quantitative coronary angiography, the coronary diameter and the vasodilating response to intracoronary ISDN (1 mg) at angiographically normal segments were studied before and after intravenous administration of ISDN, 10 to 60 micrograms/min for 1 hour, 2 days, or 5 days. The vasodilating effects of intravenous ISDN were 72% +/- 13%, 65% +/- 21%, and 6% +/- 11% of the response to intracoronary ISDN in the baseline study in each group. Irrespective of the duration of intravenous infusion, subsequent intracoronary ISDN dilated coronary arteries to extent similar to that observed in each baseline study. In conclusion, significant coronary vasodilating effects of intravenous ISDN were observed after a 2-day infusion, whereas tolerance to the vasodilating effects apparently developed within 5 days of infusion. The vasodilating response to bolus intracoronary ISDN was preserved even when the vasodilating effects of intravenous ISDN were no longer present.

Angina Pectoris↗
PubMed1994

Prevalence and pathogenesis of silent myocardial ischemia following myocardial infarction.

The objective of this study was to examine the prevalence and pathogenesis of silent myocardial ischemia during exercise following myocardial infarction. Exercise-induced myocardial ischemia was assessed by 201Tl-SPECT (single photon emission computed tomography) 4.5 weeks after acute myocardial infarction in 229 patients. Exercise-induced myocardial ischemia occurred in 109 patients (48%), and 72 (32%) had silent ischemia. Although the prevalence of multivessel coronary artery disease was similar between patients with silent and symptomatic ischemia, the size of reversible myocardial ischemia was larger in patients with symptomatic ischemia than in those with silent ischemia (21.3 +/- 3.0% vs 13.2 +/- 1.9% of LV, p < 0.05). The incidence of reversible ischemia remote from the infarct area was higher in patients with symptomatic ischemia than in those with silent ischemia (30% vs 17%, p < 0.10). The cause of silent ischemia after myocardial infarction may be closely related to the smaller size of reversible myocardial ischemia. Ischemia remote from, or adjacent to, the infarct area could be a factor in determining the presence or absence of pain.

Coronary Angiography↗
PubMed1992

Preservation of endothelium-dependent vasodilation in the spastic segment of the human epicardial coronary artery by substance P.

The objective of this study was to determine if endothelium-dependent vasodilation is preserved in the spastic segment of the epicardial coronary artery. Segmental responses of the coronary artery to substance P were examined by the use of a quantitative angiographic technique in 21 patients with variant angina. Coronary diameter at the basal state did not differ between the spastic and the nonspastic segments (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, p greater than 0.05). Changes in coronary diameter in response to substance P did not differ between segments with ergonovine-induced spasm and nonspastic segments. Maximal dilation averaged 27.1 +/- 9.5% in the spastic segment and 24.4 +/- 9.6% in the nonspastic segment (expressed as a percent increase over the value before drug administration). It appears that both the potential of the endothelium to release endothelium-dependent relaxing factor and the dilating response of the smooth muscle to endothelium-dependent relaxing factor are preserved, even in the spastic segment.

Angina Pectoris, Variant↗
PubMed1992

[A mediating role of physiological arousal in social facilitation].

An experiment was conducted to examine the mediating role of physiological arousal in social facilitation. It was hypothesized that the elevation of arousal level by the presence of other persons or evaluative apprehension would facilitate task performance. Twenty-four male and 24 female college students performed simple task alone, with a cooperative person, or with a competitive person. One half of the subjects was given an instruction which would produce evaluative apprehension. Subjects' skin potential responses were measured as the indices of physiological arousal. Although the hypothesis was supported by the analysis of psycho-physiological index, but it was not at all by the self-reported index of arousal.

Adult↗
PubMed1992

[Myocardial infarct size and left ventricular function in diabetic patients].

We determined the relationship between myocardial infarct size (MIS) estimated by electrocardiographic measurements of infarct size (QRS score) and left ventricular function estimated by angiographically left ventricular ejection fraction (EF). MIS estimated by QRS score were the same in both DM and NDM (5.2 +/- 0.5 vs 4.3 +/- 0.4: p greater than 0.05), but EF in DM was significantly lower than in NDM (43.1 +/- 1.4 vs 51. +/- 1.1%: p less than 0.05). There was clear linear correlation between MIS and EF in NDM (r = -0.71) but not in DM. EF was much lower in DM than in NDM even at the same QRS score level. There were no differences in blood pressure, serum lipid levels, age, and the site of the myocardial infarction. The most likely explanation for this appears to be due to a previous left ventricular disease in DM.

Aged↗
PubMed1991

IgG-kappa type multiple myeloma in alcoholic cirrhosis--a case report.

Transition from polyclonal to monoclonal gammopathy resulted in myeloma in the course of cirrhosis is rare but of interest. We treated such a case of multiple myeloma of IgG-kappa type associated with alcoholic cirrhosis. The case was a 72-year-old Japanese male patient who was admitted because of ascites and edema. Physical examination and laboratory findings including liver histology were compatible with alcoholic cirrhosis. Serum electrophoresis revealed monoclonal hypergammaglobulinemia of IgG-kappa. Bence Jones protein in urine was positive. Bone scintigraphy and roentgenography revealed small punched out lesions in the skull. A bone marrow clot section showed marked infiltration of atypical plasma cells. From these findings multiple myeloma associated with alcoholic cirrhosis was diagnosed. On the basis of a review of the reported cases, the possible relationship between monoclonal gammopathy and chronic liver diseases was discussed.

Aged↗
PubMed1988

Early diastolic filling dynamics during experimental mitral regurgitation in the conscious dog.

Diastolic flow into the left ventricle during mitral regurgitation must increase as total stroke volume increases in response to the volume overload. The mechanisms that allow augmented diastolic filling are not fully defined. Accordingly, the left ventricle of five dogs was instrumented with a micromanometer and sonomicrometers and studied during the conscious state before (control) and after the creation of significant mitral regurgitation. Serial measurements were made at control and up to 4 weeks after the creation of the volume overload. Heart rate, peak systolic wall stress, and peak positive dP/dt showed no significant changes between control and subsequent observations. End-diastolic volume and total stroke volume progressively and significantly increased during the 4-week course. When compared with the control state (51 +/- 4, mean +/- SD), the filling fraction during the first 40% of diastolic time was increased at 4 days (67 +/- 10%, p less than 0.001), 2 weeks (72 +/- 6%, p less than 0.001), and 4 weeks (76 +/- 10%, p less than 0.001). During the period of adaptation to the volume overload, filling fraction correlated with end-diastolic volume (r = 0.52, p less than 0.02) and total stroke volume (r = 0.80, p less than 0.001). Compared with the control state (0.81 +/- 0.04), eccentricity of the left ventricle at end systole decreased at 4 weeks (0.79 +/- 0.06, p less than 0.05); the absolute change in this ratio during the first 40% of diastolic time was significantly augmented at 2 weeks (0.09 +/- 0.02, p less than 0.05) and 4 weeks (0.11 +/- 0.04, p less than 0.005) compared with control (0.05 +/- 0.02). Ventricular elastance (pressure/volume) at end systole (minimum volume) was 1.70 +/- 0.50 mm Hg/ml at control, 1.09 +/- 0.46 at 4 days (p less than 0.05), 0.96 +/- 0.42 at 2 weeks (p less than 0.01), and 0.99 +/- 0.22 at 4 weeks (p less than 0.01). Moreover, the elastance change during the rapid-filling phase was significantly diminished after creation of mitral regurgitation. Thus, during the volume overload of mitral regurgitation, the left ventricle accommodates a higher percentage of its total stroke volume during early diastole; this adaptation can be correlated with augmented systolic shortening, and thereby with increased restorative forces or elastic recoil, and with reduced chamber elastance and eccentricity during the early part of diastole. Other potential mechanisms include altered systolic and relaxation loading, augmented elastic recoil of the left atrium, left atrium and left ventricular pressure gradient, accelerated myocardial inactivation, and increased adrenergic stimulation.

Animals↗
PubMed1988

The usefulness of equilibrium radionuclide ventriculography in the diagnosis of arrhythmogenic right ventricular dysplasia and a report of cases of a familial occurrence.

Arrhythmogenic right ventricular dysplasia (ARVD) is a recently identified clinical entity and its diagnosis rests on documentation of ventricular tachycardia (VT) of right ventricular origin and morphologic changes of the right ventricle. However, the diagnosis of ARVD is difficult noninvasively and often requires angiography. The usefulness of equilibrium radionuclide ventriculography as a noninvasive method for the diagnosis of ARVD has not been fully evaluated. We performed equilibrium radionuclide ventriculography in 7 patients with ARVD, 10 normal subjects and 9 patients with dilated cardiomyopathy (DCM). The right ventricular ejection fraction (EF) in patients with ARVD (25 +/- 8%, mean +/- SD) was lower (p less than 0.001) than that in normal subjects (56 +/- 7%) but was not significantly different from that in patients with DCM (32 +/- 10%). The left ventricular EF in patients with ARVD (57 +/- 12%) was lower (p less than 0.05) than that in normal subjects (70 +/- 7%), but higher (p less than 0.001) than that in patients with DCM (27 +/- 7%). These findings suggest that ARVD is a specific form of DCM which predominantly affects the right ventricle and that equilibrium radionuclide ventriculography may be a useful noninvasive method for the diagnosis of this disorder. In addition, we present a family in which 3 of 6 siblings were affected by ARVD, suggesting that some genetic factors may be involved in the etiology of this disorder.

Adolescent↗
PubMed1988

Isolated right heart purulent pericarditis forming a large mediastinal mass.

A 40-year-old man developed cardiomegaly with protrusion of the right heart border following staphylococcal endocarditis. Computed tomography of the chest revealed a large anterior mediastinal mass. Hemodynamic pressure curves presented features similar to those of constrictive pericarditis. At operation, 150 ml of purulent fluid was encapsulated within the thickened pericardium and separated from the rest of the pericardial sac. The encapsulated abscess was resected.

Adult↗
PubMed1987

Application of end-systolic pressure-volume and pressure-wall thickness relations in conscious dogs.

The usefulness of end-systolic measures of ventricular function was compared with that of standard contractility indexes in conscious dogs. End-systolic relations between left ventricular pressure and volume and between pressure and wall thickness were analyzed in dogs previously instrumented with ultrasonic crystals. Progressive angiotensin infusions were used to generate computer-averaged pressure-volume and pressure-wall thickness loops. Both relations were linear in every study and highly reproducible. With low and high dose dobutamine, the end-systolic pressure-volume relations were significantly displaced, with increased slope and inconsistent changes in intercept. This relation was more useful than the ejection fraction for detecting contractility increases at different afterloads, but it showed no advantage over maximal left ventricular dP/dt at all ranges of preload and afterload. The end-systolic pressure-volume relations were insensitive for detecting mild decreases in inotropic state produced by propranolol, and maximal dP/dt was superior for detecting such mild acutely reduced contractility. The end-systolic pressure-wall thickness relations showed displacement with dobutamine, although slope and intercept changes were not significant; these relations did not detect mild decreases in contractility produced by propranolol. It is concluded that the end-systolic pressure-volume relation and a simplified end-systolic measure using pressure and wall thickness provide sensitive, load-independent and reproducible approaches for defining acute increases in left ventricular contractility in conscious animals. Maximal dP/dt was equally effective for defining these increases in contractility and more sensitive for detecting slight acute decreases in contractility.

Angiotensin II↗
PubMed1987

The development of the entire end-systolic pressure-volume and ejection fraction-afterload relations: a new concept of systolic myocardial stiffness.

In this study we introduce a new concept of systolic myocardial stiffness that extends the Suga-Sagawa maximum ventricular elastance concept to the myocardium. End-systole is defined as the time of maximum systolic myocardial stiffness (max Eav), which we examined for its load independence and sensitivity to changes in the inotropic state and to heart rate. Seven adult mongrel dogs were instrumented with ultrasonic crystals for measurements of long and short axes and left ventricular wall thickness, and a high-fidelity micromanometer was inserted for measurement of left ventricular pressures. Preload and afterload were altered by inferior vena cava occlusion, nitroprusside, angiotensin II, atropine, propranolol, and various combinations with propranolol. End-systolic stress-strain relations (slope: max Eav) were linear in all seven dogs, implying that end-systolic myocardial stiffness is independent of end-systolic stress. Changes in max Eav (for constant preload and afterload) reflected changes in the ejection fraction; max Eav was also insensitive to propranolol and to changes in heart rate over the range from 120 to 180 beats/min. End-systolic pressure-volume relations (ESPVRs), derived analytically from these stress-strain relations, were nonlinear, and estimates of volume at zero stress (Vom) were always positive. On the other hand, ESPVRs obtained on the basis of the Suga-Sagawa maximum ventricular elastance concept, were linear, and volume at zero pressure (Vop) estimated by linear extrapolation was negative in one case. Based on the concept of systolic myocardial stiffness, the slope of the ESPVR varies with end-systolic volume and attains its maximum value (Emax) at zero end-systolic pressure. Normalization of Emax with Vom demonstrated a close relationship to max Eav. Thus both max Eav and Vom and Emax are ideal variables for assessing changes in myocardial contractility when preload and afterload are constant. Furthermore, Vom and max Eav permit development of the entire ejection fraction-afterload relationship for a given preload, thus providing a method for comparing myocardial contractile states between ventricles.

Animals↗
PubMed1986

Experimental exercise-induced ischemia: drug therapy can eliminate regional dysfunction and oxygen supply-demand imbalance.

The purpose of this study was to test the hypothesis that moderately severe exercise-induced regional myocardial ischemia can be prevented by combined pharmacologic intervention. Eight chronically instrumented dogs were studied using an ameroid constrictor to produce critical stenosis of the left circumflex coronary artery. The dogs were studied during steady state treadmill exercise that induced regional myocardial dysfunction (reduced systolic wall thickening; sonomicrometers) and ischemia (reduced subendocardial blood flow; microspheres). During a control exercise run, wall thickening in the ischemic posterior wall decreased from 21.4 to 13.3% whereas subendocardial blood flow failed to increase normally (36% of that in the normal zone). In the control anterior wall, both wall thickening and subendocardial blood flow increased significantly during the control run. Wall thickness-left ventricular pressure loop areas were calculated as an index of regional work; this index increased abruptly with the onset of exercise in both regions but became significantly depressed in the ischemic region during the steady state exercise. Therapy with a combination of atenolol (0.3 mg/kg body weight orally), diltiazem (0.3 mg/kg intravenously) and isosorbide dinitrate (2.0 mg/kg orally) effectively prevented regional myocardial ischemia and regional dysfunction. After drug therapy, wall thickening in the posterior wall increased from 17.3% at rest to 18.8% during exercise, and the regional transmural blood flow pattern was markedly improved. The initial overshoot of the regional work index during exercise was blunted by the drug therapy, and at steady state no differences between the ischemic and control regions were detected. Thus, combined drug therapy can eliminate exercise-induced regional myocardial ischemic dysfunction and appears to normalize the oxygen supply-demand imbalance.

Adrenergic beta-Antagonists↗
PubMed1986

Preload reserve and mechanisms of afterload mismatch in normal conscious dog.

Preload reserve and mechanisms of afterload mismatch were examined in 10 normal conscious dogs. The left ventricular (LV) pressure, wall thickness, and external major and minor axis diameters (sonomicrometry) were measured during sinus rhythm, and beat-averaged pressure-volume loops were generated. With maximum angiotensin II infusion, LV end-diastolic volume (EDV) increased by 13 +/- 2% (SEM), LV peak pressure (LVSP) increased by 44 +/- 6%, and stroke volume decreased by 12 +/- 3% (P less than 0.01), demonstrating an apparent descending limb of LV performance. With volume load alone, EDV increased by 9 +/- 2% from control (P less than 0.01), and stroke volume increased by 13 +/- 2%; mean wall stress during ejection was not increased, and heart rate and end-systolic pressure-volume relations showed no changes. To test whether the descending limb of function was due to maximum use of preload reserve or to inadequate venous return, angiotensin infusion was repeated during volume load. The descending limb relating LVEDV to stroke volume was always shifted upward and to the right after volume load, and the stroke volume at a comparable wall stress was 12 +/- 3% higher than during control angiotensin infusion (P less than 0.01). During pressure loading plus volume loading, the maximum EDV increase was 16 +/- 2%, and assuming unchanged afterload and end-systolic volume, an average maximum stroke volume reserve of 31 +/- 4% is calculated. 1) We conclude that sizable preload and stroke volume reserves exist in the normal resting dog; and 2) we describe a mechanism for the descending limb of LV performance curves produced by pressure loading in the intact circulation, which is related to inadequate venous return.

Angiotensin II↗
PubMed1986

Exercise-induced regional dysfunction with subcritical coronary stenosis.

The hypothesis was tested that regional myocardial contractile dysfunction can detect subtle regional coronary blood flow maldistribution induced by exercise. In seven dogs, left ventricular pressure (micromanometer), regional systolic wall thickening (WTh, sonomicrometry), and myocardial blood flow (MBF, microspheres) were measured when mild degrees of coronary artery stenosis were produced during treadmill exercise. During exercise without coronary stenosis, WTh increased by 21 +/- 12% (SD), and transmural MBF increased uniformly. In each dog, two levels of coronary stenosis were produced during exercise by adjusting the coronary hydraulic cuff: (1) St-Ex I, where WTh during exercise failed to increase significantly (average change 0 +/- 7%), and (2) St-Ex II, where WTh during exercise decreased moderately from the resting control value (average -20 +/- 8%). In the potentially ischemic zone coronary hyperemia occurred with each run: resting subendocardial MBF was 1.09 +/- 0.30 mg/g/min, and it was 3.04 +/- 0.83 during control exercise, 2.48 +/- 0.75 during St-Ex I, and 1.55 +/- 0.59 ml/g/min during St-Ex II (p less than .01 compared with control exercise and control area). The subendocardial-subepicardial blood flow ratio fell from 1.32 +/- 0.27 during control exercise to 1.07 +/- 0.20 (p less than .05) during St-Ex I, and to 0.64 +/- 0.15 (p less than .01) with St-Ex II. Changes in the subendocardial electrogram and reactive hyperemia occurred more consistently during St-Ex II than St-Ex I. Thus, failure of regional function to increase during exercise detected slight maldistribution of regional MBF, whereas reduction of regional function during exercise of 10% or more below the resting value was a reliable marker of a regional flow defect and was always associated with other evidence of ischemia. Therefore, regional dysfunction during exercise can detect subcritical but functionally significant coronary stenosis, which may allow regional wall motion to be used for detecting coronary artery disease at a relatively early stage.

Animals↗
PubMed1985

Effect of the combination of diltiazem and atenolol on exercise-induced regional myocardial ischemia in conscious dogs.

The effect of combination therapy with diltiazem and atenolol on the regional myocardial blood flow-function relationship was studied in eight conscious dogs with chronic coronary artery stenosis. An ameroid constrictor and hydraulic occluder were placed around the left circumflex coronary artery, sonomicrometers were implanted for measuring wall thickness in control and ischemic regions, and regional myocardial blood flow was measured with the microsphere method. Eighteen days (average) after surgery, resting regional myocardial function and blood flow were normal, but treadmill exercise induced severe regional myocardial dysfunction in the posterior wall (wall thickening during systole reduced from 25.5% to 2.7%, a 90% reduction). Subendocardial blood flow decreased by 68% from the control standing value, while subepicardial flow increased. An identical exercise bout was performed 3 hr after administration of atenolol (1.0 mg/kg orally) and 15 min after administration of diltiazem (0.3 mg/kg iv). Heart rate during running was significantly lower as were left ventricular peak systolic pressure, end-diastolic pressure, and peak dP/dt. Wall thickening in the control region was not augmented during exercise after atenolol and diltiazem. There was less dysfunction in the ischemic region (35% reduction) and the improved performance was accompanied by a substantial increase in subendocardial perfusion (0.31 +/- 0.14 vs 0.61 +/- 0.30 ml/min/g, a 36% reduction from rest). Epicardial flow was unchanged, and the endocardial/epicardial ratio increased (0.27 +/- 0.13 vs 0.62 +/- 0.29). Recovery time for regional wall thickening also improved. The beneficial effects of the combination of atenolol and diltiazem in a preparation of single-vessel chronic coronary stenosis were shown to be significantly greater than those of either drug alone.

Animals↗