Biomedical subjects

Ichiro Nishio

Publications and source records attributed to Ichiro Nishio.

At least 55 records · Page 3Linked to original sources

PubMed2003

Oxidized low-density lipoprotein sensitizes human vascular smooth muscle cells to FAS (CD95)-mediated apoptosis.

1. It was investigated in the present study whether oxidized low-density lipoprotein (oxLDL) was implicated in the susceptibility of human vascular smooth muscle cells (VSMC) to Fas-mediated death. Human fetal aorta smooth muscle cells were treated with agonistic anti-Fas antibody (CH11) and oxLDL and cell death was then determined by viability and DNA fragmentation. 2. The results of the present study show that cross-linking of Fas receptor with anti-Fas antibody in the presence of oxLDL induced death and DNA fragmentation in human VSMC, which were blocked by the caspase inhibitor z-VAD.fmk, followed by the upregulation of cell surface Fas. 3. The data indicate that oxLDL is implicated in death in VSMC and provide evidence that oxLDL is involved in Fas signal transduction. The present study proposes a novel mechanism(s) by which VSMC become susceptible to Fas ligand. 4. One of the mechanisms proposed by which oxLDL upregulates cell surface Fas is by inhibiting the degradation of Fas through the ubiquitin-proteasome pathway.

Amino Acid Chloromethyl Ketones↗

PubMed2003

Oxidized low-density lipoprotein inhibits vascular endothelial growth factor-induced endothelial progenitor cell differentiation.

1. Bone marrow-derived endothelial progenitor cells (EPC) in the peripheral blood of adult animals and humans have been shown to be incorporated into neovascularization. In contrast, hypercholesterolaemia impairs angiogenesis and collateral vessel formation in response to regional tissue ischaemia. We investigated whether oxidized LDL (oxLDL) affected human EPC differentiation. 2. When isolated human mononuclear cells (MNC) were incubated with vascular endothelial growth factor (VEGF), the number of differentiated, adherent EPC, as assessed by an in vitro culture assay, was increased in a dose-dependent manner (P < 0.01). When MNC were incubated with oxLDL at 1, 5 and 10 microg/mL in the presence of 100 ng/mL VEGF for 24 h, oxLDL dose-dependently reduced the number of differentiated, adherent EPC. 3. Vascular endothelial growth factor-induced EPC differentiation was significantly inhibited by pharmacological phosphatidylinositol 3-kinase blockers (either 10 nmol/L wortmannin or 10 micromol/L LY294002). Interestingly, immunoblotting analysis revealed that oxLDL dose-dependently led to dephosphorylation and, thus, deactivation of Akt in the presence of VEGF. Finally, these inhibitory effects induced by oxLDL were abolished by pretreatment with 1 micromol/L atorvastatin (P < 0.01). 4. Our data indicate that oxLDL inhibits VEGF-induced EPC differentiation through the dephosphorylation of Akt.

Cell Differentiation↗

PubMed2003

Role of alpha2-adrenergic receptors and cyclic adenosine monophosphate-dependent protein kinase in the regulation of norepinephrine release in the central nervous system of spontaneously hypertensive rats.

There has been much evidence showing that the central sympathetic nervous system may be involved in the control of blood pressure. In the present study, we investigated the role of the presynaptic alpha2-adrenergic receptors and the cyclic adenosine monophosphate-dependent protein kinase (protein kinase A) in the regulation of norepinephrine release in the central nervous system in hypertension. The alpha2-adrenergic receptor agonists UK 14, 304 and clonidine inhibited the stimulation-evoked [3H]norepinephrine release in a dose-dependent manner in the medulla oblongata of Sprague-Dawley rats. Pretreatment of pertussis toxin (a potent inhibitor of the Gi-protein) attenuated the suppression of NE release by UK 14, 304. The protein kinase A inhibitor H-8 also reduced the stimulation-evoked [3H]norepinephrine release in rat medulla oblongata. In spontaneously hypertensive rats, the inhibitory effect of UK 14, 304 on the stimulation-evoked norepinephrine release was significantly less than in age-matched normotensive Wistar-Kyoto rats. By contrast, the protein kinase A inhibitor H-8 reduced the stimulation-evoked norepinephrine release to a greater extent in hypertension than in normotensive controls. The results of the present study showed that the alteration in the presynaptic alpha2-receptor-protein kinase A system might actively participate in the regulation of norepinephrine release in the central nervous system in hypertension.

Adrenergic alpha-Agonists↗

PubMed2003

Estrogen attenuates the emotional stress-induced cardiac responses in the animal model of Tako-tsubo (Ampulla) cardiomyopathy.

Reduction of estrogen levels may underlie the high incidence of 'Tako-tsubo (Ampulla) cardiomyopathy in postmenopausal females. Ovariectomized (OVX) and estradiol-supplemented ovariectomized female rats (OVX + E) were subjected to immobilization stress, an animal model of Tako-tsubo cardiomyopathy. In order to evaluate cardiac changes, left ventriculography and electrocardiography were performed under anesthesia (control). Next day, the conscious rats were exposed to immobilization stress, and left ventriculography was performed (stress). In OVX rats, percentage contraction in left ventriculography was significantly reduced in response to stress, while it was not significantly changed in OVX + E rats. In both groups, heart rate was significantly increased in response to stress. However, heart rate in stress was significantly higher in OVX than in OVX + E rats. In summary, these data suggest that increase of serum estradiol levels can diminish the pathological changes in the heart induced by emotional stress.

Animals↗

PubMed2003

Role of protein kinase C in the regulation of acetylcholine release in the central nervous system of spontaneously hypertensive rats.

Previous studies have shown that the central cholinergic nervous system may be involved in blood pressure control. In the present study, we investigated the role of protein kinase C in the regulation of cholinergic nervous activity in the central nervous system in hypertension. In superfused slices of the striatum obtained from spontaneously hypertensive rats and age-matched Wistar-Kyoto rats, we examined the effects of the protein kinase C inhibitor H-7 on the release of [3H]-acetylcholine in vitro. The stimulation-evoked [3H]-acetylcholine release was not different between spontaneously hypertensive rats and Wistar-Kyoto rats. The protein kinase C inhibitor H-7 reduced the stimulation-evoked [3H]-acetylcholine release to a greater extent in spontaneously hypertensive rats than in Wistar-Kyoto rats. The results of the present study showed that the enhanced calcium-protein kinase C system might actively participate in the regulation of cholinergic nervous activity in the central nervous system in hypertension.

Acetylcholine↗

PubMed2003

Molecular mechanism of emotional stress-induced and catecholamine-induced heart attack.

Emotional or physical stress triggers 'tako-tsubo' cardiomyopathy or 'transient left ventricular apical ballooning', but the pathogenesis is unclear. In response to the immobilization stress of rats, a useful model of emotional stress, rapid activation of p44/p42 mitogen-activated protein kinase was observed in the heart, followed by a transient upregulation of immediate early genes in the smooth muscle cells of coronary arteries, the endothelial cells and the myocardium. Heat shock protein 70 was induced in the aortic and coronary arterial smooth muscle cells and in the myocardium. Natriuretic peptide genes were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to emotional stress. Blocking of both alpha-adrenoceptors and beta-adrenoceptors eliminated the upregulation of immediate early genes induced by stress, while alpha-agonists and beta-agonists upregulated immediate early genes in the perfused heart. Activation of alpha-adrenoceptors and beta-adrenoceptors is the primary trigger of emotional stress-induced molecular changes in the heart.

Animals↗

PubMed2002

Leptin improves membrane fluidity of erythrocytes in humans via a nitric oxide-dependent mechanism--an electron paramagnetic resonance investigation.

Abnormalities in physical properties of the cell membranes may underlie the defects that are strongly linked to hypertension, stroke, and other cardiovascular diseases. Recently, there has been an indication that leptin, the product of the human obesity gene, actively participates not only in the metabolic regulations but also in the control of cardiovascular functions. In the present study, to assess the role of leptin in the regulation of membrane properties, the effects of leptin on membrane fluidity of erythrocytes in humans are examined. The membrane fluidity of erythrocytes in healthy volunteers by means of an electron paramagnetic resonance (EPR) and spin-labeling method is determined. In an in vitro study, leptin decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (ho/h-1) for 16-NS obtained from EPR spectra of erythrocyte membranes in a dose-dependent manner in healthy volunteers. The finding indicated that leptin increased the membrane fluidity and improved the microviscosity of erythrocytes. The effect of leptin on the membrane fluidity was significantly potentiated by the nitric oxide (NO) donors, L-arginine and S-nitroso-N-acetylpenicillamine (SNAP), and a cyclic guanosine monophosphate (cGMP) analog, 8-bromo-cGMP. In contrast, the change evoked by leptin was significantly attenuated in the presence of the NO synthase inhibitors, N(G)-nitro-L-arginine-methyl-ester (L-NAME) and asymmetric dimethyl-L-arginine (ADMA). The results of the present study showed that leptin increased the membrane fluidity and improved the rigidity of cell membranes to some extent via an NO- and cGMP-dependent mechanism. Furthermore, the data also suggest that leptin might have a crucial role in the regulation of rheological behavior of erythrocytes and microcirculation in humans.

Arginine↗

PubMed2002

Leukemia inhibitory factor relaxes arteries through endothelium-dependent mechanism.

Leukemia inhibitory factor (LIF) is a cytokine, which inhibits angiogenesis and decreases endothelial cell proliferation and migration, suggesting that LIF may modulate vascular tone. In this study, we examined the effects of LIF on the tone of rat arteries. The isometric tension of ring preparations from rat superior mesenteric arteries was continuously measured. LIF relaxed the mesenteric arteries in a dose-dependent manner, when the arterial rings were precontracted with phenylephrine. The relaxation was totally inhibited by mechanical removal of endothelium. N(G)-nitro-L-arginine methyl ester did not affect the relaxation by LIF. Ca(2+)-dependent K channel (KCa) blockers, apamin with charybdotoxin, inhibited the relaxation by LIF. Catalase, an enzyme which scavenges hydrogen peroxide, also inhibited the relaxation by LIF. Endothelium-derived hyperpolarizing factor relaxes smooth muscle cells and the effect is blocked by KCa and catalase. Our results suggest that LIF regulates vascular tone through the effect of this factor.

Animals↗

PubMed2002

Blood pressure response to heart rate during exercise test and risk of future hypertension.

Previous works have shown that exaggerated blood pressure response to exercise is a valid risk marker for future hypertension, yet the use of an exercise test as a means of early prediction of hypertension still requires methodological development and confirmation. The purpose of this study was to determine abnormal ranges of blood pressure responses in relation to heart rate increase during exercise and to examine the clinical utility of exercise blood pressure measurement in evaluating individual risk for developing hypertension. We examined exercise test data from a population-based sample of 1033 nonmedicated normotensive men (mean age, 42.9+/-8.5 years; range, 20 to 59 years). Percentile curves of systolic and diastolic blood pressure responses to relative heart rate increments during submaximal exercise were constructed using a third-order polynomial model with multiple regression analysis. Of the original study sample, a cohort of 726 subjects was followed for hypertensive outcome for an average period of 4.7 years. Progression to hypertension, defined as a blood pressure of > or =140/90 mm Hg or the initiation of antihypertensive therapy, was found in 114 subjects (15.4%). Kaplan-Meier survival estimates showed that the cumulative incidence of hypertension increased progressively with higher percentiles of systolic and diastolic blood pressure response (both, P<0.01). A Cox proportional survival analysis revealed a significantly increased risk for developing hypertension associated with exaggerated blood pressure response to exercise after multivariable adjustments for traditional risk factors (relative risk, 3.8; 95% confidence interval, 2.3 to 6.1). These results suggest that an exaggerated blood pressure response to heart rate during exercise is predictive of future hypertension independent of other important risk factors and lend further support to the concept that blood pressure measurement during exercise test is a valuable means of identifying normotensive individuals at high risk for developing hypertension.

Adolescent↗

PubMed2002

Apoptosis of vascular smooth muscle cells is induced by Fas ligand derived from monocytes/macrophage.

Fas and its ligand (FasL), are a receptor-ligand pair identified as promoting cell death in several tissues. Apoptosis of vascular smooth muscle cells (VSMCs) in human atherosclerotic plaque may contribute to weakening of the fibrous cap, ultimately resulting in plaque rupture. We investigated the ability of monocytes to induce apoptosis of cultured VSMCs through Fas/FasL pathway. In addition, we examined the association of FasL with apoptosis in human coronary plaques. Both activated monocytes and the supernatant obtained from activated monocytes were able to kill cultured VSMCs. The apoptotic response of VSMCs was almost completely blocked by the caspase inhibitor z-VAD-fmk and was partially blocked by incubation with antagonistic anti-Fas IgG1 which suggests that Fas/FasL system was involved in the induction of cell death. An approximate 30 kDa protein, which represents a cleaved, soluble form of FasL, was identified in culture medium from activated monocytes, but not in culture medium from control, unactivated monocytes. Immunohistochemical analysis of human atherosclerotic coronary lesions showed that FasL is expressed by macrophages, and microvessels in the adventitia as well as in the plaque. Finally, double-staining with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and FasL antibody showed that FasL enriched lesions always included a number of TUNEL-positive cells. These data suggest that Fas/FasL pathway can be employed by monocytes/macrophages to induce VSMC apoptosis in the atherosclerotic lesions.

Antigen-Antibody Complex↗

PubMed2002

Synergistic role of progesterone and nitric oxide in the regulation of membrane fluidity of erythrocytes in humans: an electron paramagnetic resonance investigation.

BACKGROUND: It has been shown that progesterone may actively participate in the regulation of blood pressure and other cardiovascular regulations. However, the precise mechanism underlying its effects is unclear. METHODS: In the present study, we examined the effects of progesterone on membrane fluidity of erythrocytes in healthy volunteers by means of an electron paramagnetic resonance (EPR) and spin-labeling method. RESULTS: In an in vitro study, progesterone significantly decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (ho/h-1) for 16-NS obtained from EPR spectra of erythrocyte membranes. The finding indicates that progesterone might increase the membrane fluidity and improve the membrane microviscosity of erythrocytes. The effect of progesterone was significantly potentiated by the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP) and a cyclic guanosine monophosphate (cGMP) analogue, 8-bromo-cGMP. In contrast, the change in the membrane fluidity evoked by progesterone was attenuated in the presence of the NO synthase inhibitors, N(G)-nitro-L-arginine-methyl-ester (L-NAME) and asymmetric dimethyl-L-arginine (ADMA). CONCLUSIONS: The results of the present study showed that progesterone increased the membrane fluidity of erythrocytes and ameliorated the rigidity of cell membranes, at least in part, by an NO-dependent mechanism. Furthermore, the data strongly suggest that progesterone might be involved in the regulation of rheological behavior of erythrocytes and have a crucial role in the improvement of microcirculation in humans.

Analysis of Variance↗

PubMed2002

Effect of oestrone on membrane fluidity of erythrocytes is mediated by a nitric oxide-dependent pathway: An electron paramagnetic resonance study.

1. It has been recognized that hormone replacement therapy (HRT) may have a beneficial effect on protection against cardiovascular diseases. Oestrone is the major component of conjugated equiline oestrogens, which are commonly used in HRT. The present study was performed in order to investigate the effects of oestrone on the membrane fluidity of erythrocytes by means of an electron paramagnetic resonance (EPR) and spin-labelling method. 2. In an in vitro study, oestrone significantly decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (ho/h-1) for 16-nitroxide stearate (16-NS) obtained from EPR spectra of erythrocyte membranes. This finding indicated that oestrone may increase the membrane fluidity and improve the membrane microviscosity of erythrocytes. 3. The effect of oestrone was significantly potentiated by the nitric oxide (NO) donor s-nitroso-N-acetylpenicillamine and the cGMP analogue 8-bromo-cGMP. 4. In contrast, the change in membrane fluidity induced by oestrone was antagonized by the NO synthase inhibitors NG-nitro-l-arginine methyl ester and asymmetric dimethyl-l-arginine. 5. The results of the present study show that oestrone significantly increases membrane fluidity and improves the rigidity of cell membranes, which is partially mediated by a NO- and cGMP-dependent pathway. Furthermore, the data may be consistent with the hypothesis that oestrone could have a beneficial effect on the rheological behaviour of erythrocytes and have a crucial role in the regulation of the microcirculation.

Analysis of Variance↗

PubMed2002

Oxidized low density lipoprotein potentiation of Fas-induced apoptosis through lectin-like oxidized-low density lipoprotein receptor-1 in human umbilical vascular endothelial cells.

Under normal conditions, vascular endothelial cells are resistant to Fas-mediated apoptosis, although they express detectable Fas on their cell surface. Because oxidized Low density lipoprotein (Ox-LDL) is thought to promote atherogenesis, the potential role that Ox-LDL may play in Fas-mediated apoptosis was investigated in human umbilical vascular endothelial cells (HUVECs), focusing particularly on the involvement of the lectin-like Ox-LDL receptor-1 (LOX-1). HUVECs were treated with agonistic anti-Fas antibody (CH11) and Ox-LDL and then the degree of apoptosis was determined by cell death ELISA. Ox-LDL concentration-dependently sensitized Fas-mediated apoptosis. Flow cytometry demonstrated that Ox-LDL dose-dependently up-regulated cell surface Fas expression. On the other hand, treating HUVECs with Ox-LDL did not lead to any significant change in the expression of death mediators, including Fas, Fas ligand (FasL), FADD, and FLICE as assessed by multiplex polymerase chain reaction amplification. More importantly, these effects of Ox-LDL on Fas-mediated apoptosis were significantly blocked by a neutralizing LOX-1 monoclonal antibody, which can block LOX-1-mediated cellular uptake of Ox-LDL. Ox-LDL may be an important factor involved in the regulation of Fas-induced apoptosis via Ox-LDL/LOX-1 interaction in vascular endothelial cells. The results may provide insights into the pathogenesis of accelerated atherosclerosis in patients with hyperlipidemia.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Emotional stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors: a possible animal model of 'tako-tsubo' cardiomyopathy.

The etiology of a novel cardiac syndrome 'tako-tsubo' cardiomyopathy, otherwise known as 'transient left ventricular (LV) apical ballooning' and which mimics acute myocardial infarction, is not clear; however, emotional or physical stress is known to precede the attack. Left ventriculography of rats experiencing emotional stress induced reversible LV apical ballooning, which was normalized by pretreatment with adrenoceptor blockade. Together with results of previous studies, activation of cardiac adrenoceptors in the absence of ischemia-reperfusion is proposed as the primary cause of this syndrome.

Animals↗

PubMed2002

Acute effect of endothelin AB antagonist on sympathetic outflow in conscious rats with heart failure.

Although ET-1 antagonists have been beneficial in the treatment of heart failure (HF), their involvement in the effect on the sympathetic nervous system in HF remains unknown. The present study investigated the role of endogenous endothelin (ET) in the sympathetic nervous system in HF by observing the effect of ET AB antagonist (TAK-044) on renal sympathetic nerve activity (RSNA) in conscious rats with HF (n = 7). HF was induced by left coronary artery ligation and 6 weeks later, TAK-044 was intravenously administered in the conscious and freely moving rats. RSNA, mean arterial pressure (MAP) and heart rate were compared with rats with sham operations (sham; n = 7). MAP was significantly decreased in both groups; however, RSNA was significantly decreased only in the HF group at 5 min after administration, and this change continued until 10 min. There was also an effect of TAK-044 on the arterial baroreflex function indicated by the slope of RSNA to the changes in MAP during phenylephrine and nitroprusside injection in both groups. Compared with the sham group, the HF group showed impaired arterial baroreflex control of RSNA during phenylephrine injection, and intravenous administration of TAK-044 normalized this abnormality, whereas the function in the sham group was not changed. These data show that ET AB antagonist suppressed renal sympathetic activity in rats with HF, and improved arterial baroreflex function. The beneficial effect of endothelin antagonist on heart failure may involve improvement of the increased sympathoexcitation and impaired arterial baroreflex function in HF.

Animals↗

PubMed2002

Antihypertensive effects of aerobic exercise in middle-aged normotensive men with exaggerated blood pressure response to exercise.

An exaggerated blood pressure (BP) response to physical exertion among normotensive subjects is considered a significant risk factor for future hypertension. The purpose of this study was to examine whether regular aerobic exercise can lead to a reduction in hypertensive risks in patients with such a high-risk profile. Thirty-five sedentary men (46 +/- 2 years old) with normal BP at rest but an exaggerated BP response during exercise were randomly assigned to an exercise or control group for 12 weeks followed by an 8-week washout period. The subjects were then crossed over to the alternate group for an additional 12-week period. The exercise training consisted of 3 days per week of stationary bicycling for 45 min at 50-60% of the heart rate reserve. The treatment effects were evaluated using the method of Hills and Armitage. The training-induced reduction in resting BP was not statistically significant. In ambulatory BP monitoring, the averages of 24-h and daytime systolic and diastolic BP were significantly lower, but nighttime BP remained unchanged after training. During ergometric exercise, significant decreases were observed in systolic and diastolic BP and plasma norepinephrine concentration measured at the submaximal workloads. M-mode echocardiographic and Doppler-derived left ventricular variables were not significantly affected by training. These findings suggest that regular aerobic exercise attenuates BP elevations during physical exertion and daytime activities mainly as a result of the reduction in enhanced sympathetic nervous tonus, which may in turn play a role in lowering the risk for hypertension in normotensive subjects with an exaggerated BP response to exercise.

Blood Pressure↗

PubMed2002

[Statement of initial therapy of elderly patients with hypertension in Wakayama prefecture].

In order to evaluate the characteristics of initial therapy for elderly hypertensive patients in Wakayama prefecture, a case-card survey was performed in February 1997. The investigation consisted of blood pressure when starting therapy, initial physical examination and laboratory tests, and the initial drug therapy, and it's effects 3 months later. The initial physical examination and laboratory tests were the diagnostic procedures for determining the presence of target organ damage, they included electrocardiogram (ECG), chest X-rays, echocardiogram (UCG), funduscopy and urinalysis. Data of 7,647 cases from 156 facilities were obtained. These cases were divided into 2 groups, a non-elderly group (under 65 years, 3,396 cases) and an elderly group (65 years or over, 4,012 cases). The blood pressure at the start of pharmacological treatment was 174.9 +/- 17.4/93.7 +/- 11.0 mmHg (mean +/- SD) in the elderly group, and 170.6 +/- 17.8/98.6 +/- 11.2 mmHg in the non-elderly group. Systolic blood pressure in the elderly group was higher than in that the non-elderly group and diastolic blood pressure was lower in the elderly group than that in the non-elderly group. Cases of ECG (98.3% vs 71.3%; the non-elderly group vs the elderly group), chest X-ray (86.5% vs 65.2%), UCG (27.1% vs 23.7%), urinary test (96.0% vs 69.3%), examination of ophthalmic fundi (27.0% vs 24.3%), were much lower in the elderly group than in the non-elderly group. The rate of positive findings of left ventricular hypertrophy by ECG criteria (24.8% vs 20.3%), cardiomegaly by chest X-p (35.3% vs 26.6%), proteinuria by urinary test (14.8% vs 12.9%) was lower in the elderly than non-elderly. Details of drug use in non-elderly vs elderly were as follows; calcium antagonists (47.3% vs 51.9%), angiotensin converting enzyme inhibitor (ACE-I) (14.2% vs 12.2%), diuretics (6.3% vs 10.2%), beta-blockers (11.2% vs 4.7%), alpha-blockers (1.4% vs 1.3%), others (1.5% vs 2.4%), multiple (13.7% vs 12.5%), undefined (4.2% vs 4.7%). Sufficient hypotensive effects were obtained in 61.5% of the non-elderly, and 68.5% of the elderly. Initial physical examination to assess target organ damage was lower in the elderly than the non-elderly. It was thought necessary to be corrected. The incidence of main antihypertensive drugs in the elderly were Ca antagonists, ACE-I and diuretics. Treatment trends met the Japanese guideline on treatment of hypertension in the elderly.

Aged↗

PubMed2002

[Assessment of left ventricular function by thallium-201 quantitative gated cardiac SPECT].

PURPOSE: Present study was designed to evaluate the accuracy of the measurement of left ventricular volume by quantitative gated SPECT (QGS) software using 201T1 and the effect of cutoff frequency of Butterworth prereconstruction filter on the calculation of volume. METHODS: The RH-2 type cardiac phantom and 20 patients with ischemic heart disease were studied. Left ventricular end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) were calculated by the QGS software using the various frequency of Butterworth filter. These parameters were evaluated by Simpson's method using left ventriculography (LVG). RESULTS: The volume of the phantom calculated by QGS was under-estimated by 14%. In the clinical study, EDV and ESV measured by QGS were smaller than those obtained from LVG by 10%. When the cutoff frequency of Butterworth filter was 0.43 cycles/cm, the values measured by QGS were best correlated with those by LVG (EDV: r = 0.80, p < 0.001; ESV: r = 0.86, p < 0.001; EF: r = 0.80, p < 0.001). CONCLUSION: These data suggest that 201Tl quantitative gated cardiac SPECT can estimate myocardial ischemia and left ventricular function simultaneously.

Adult↗