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Biomedical subjects

Koji Ohmori

Publications and source records attributed to Koji Ohmori.

At least 19 recordsLinked to original sources
PubMed2007

Differential impact of atorvastatin vs pravastatin on progressive insulin resistance and left ventricular diastolic dysfunction in a rat model of type II diabetes.

BACKGROUND: Controversy exists regarding the effects of statin therapy on progressive insulin resistance (IR) and its consequences, in the present study a rat model of spontaneously developing type II diabetes mellitus (DM) was used to examine the impact of atorvastatin (AS) vs pravastatin (PS). METHODS AND RESULTS: The Otsuka Long-Evans Tokushima Fatty rats were either untreated or treated with 100 mg/kg per day of AS or PS from 6 weeks of age for 24 weeks. AS achieved much greater lipid lowering than PS. Serial oral glucose tolerance tests revealed new-onset diabetes was delayed by PS only. The untreated rats exhibited a progressive decrease in plasma adiponectin, increases in plasma leptin and tumor necrosis factor-alpha, and reduction of plasma nitric oxide (NO), which were limited more by PS than AS. PS, but not AS, enhanced adiponectin mRNA expression in white adipose tissue at 30 weeks. Cardiac endothelial NO synthase expression was upregulated, and overexpression of both transforming growth factor-beta1 and monocyte chemoattractant protein-1 mRNA was limited more by PS than AS. Coronary perivascular fibrosis at 30 weeks was suppressed only by PS, which was accompanied by preserved left ventricular diastolic function assessed with Doppler echocardiography. CONCLUSIONS: The moderate lipid lowering by PS, but not the intensive lipid lowering by AS, prevented new-onset DM and diastolic dysfunction in a rat model of IR, and this was associated with preferable adipocytokine profiles and cardiac redox states.

Adiponectin↗
PubMed2006

Involvements of Rho-kinase and TGF-beta pathways in aldosterone-induced renal injury.

Recent studies have suggested a role for aldosterone in the pathogenesis of renal injury. This study investigated the potential contributions of Rho-kinase and TGF-beta pathways to aldosterone-induced renal injury. Rats were uninephrectomized and then treated for 5 wk with 1% NaCl in a drinking solution and one of the following: Vehicle (2% ethanol, subcutaneously; n = 9); aldosterone (0.75 microg/h, subcutaneously; n = 9); or aldosterone + fasudil, a specific Rho-kinase inhibitor (10 mg/kg per d, subcutaneously; n = 8). Phosphorylation of myosin phosphate target subunit-1 (MYPT1) and Smad2/3 in renal cortical tissue was measured by Western blotting with anti-phospho MYPT1 and Smad2/3 antibodies, respectively. Rats that received aldosterone infusion exhibited hypertension and severe renal injury characterized by proteinuria, glomerular sclerosis, and tubulointerstitial fibrosis with increases in alpha-smooth muscle actin staining and numbers of monocytes/macrophages in the interstitium. Renal cortical mRNA levels of types I and III collagen, TGF-beta, connective tissue growth factor, and monocyte chemoattractant protein-1 as well as Smad2/3 phosphorylation were significantly increased in rats that received aldosterone infusion. All of these changes were associated with an increase in renal tissue MYPT1 phosphorylation. Treatment with fasudil did not alter BP but significantly ameliorated proteinuria and renal injury in rats that received aldosterone infusion. Furthermore, fasudil prevented MYPT1 phosphorylation and markedly decreased alpha-smooth muscle actin staining, numbers of monocytes/macrophages, mRNA levels of types I and III collagen, TGF-beta, connective tissue growth factor and monocyte chemoattractant protein-1, and Smad2/3 activity in renal cortical tissues. These results provide evidence, for the first time, that Rho-kinase is substantially involved in aldosterone-induced renal injury through activation of a TGF-beta-dependent pathway.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2006

An antioxidant treatment potentially protects myocardial energy metabolism by regulating uncoupling protein 2 expression in a chronic beta-adrenergic stimulation rat model.

Excessive beta-adrenergic stimulation causes cardiac toxicity, which also contributes to cardiac oxidative stress. Although uncoupling protein 2 (UCP2), a member of the mitochondrial inner membrane carrier family, can regulate energy efficiency and oxidative stress in mitochondria, little data exist regarding interactions between UCP2 expression and beta-adrenergic stimulation induced cardiac oxidative damage. We investigated whether chronic beta-adrenergic stimulation induces myocardial energy metabolism abnormality via oxidative stress, including any role of UCP2. We also examined whether 3-methyl-1-phenyl-2-pyrazolin-5-one (MIC-186; edaravone), a potent free radical scavenger, has cardioprotective effects against beta-adrenergic stimulation. Male Sprague-Dawley rats received isoproterenol (1.2 mg/kg/day) subcutaneously or/and edaravone (30 mg/kg/day) orally. Isoproterenol increased the heart/body weight ratio, accompanied by an increase in the level of myocardial thiobarbituric acid reactive substances (TBARS) and a decreased phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. Isoproterenol also markedly increased expressions of UCP2 mRNA (1.74 fold vs. non-isoproterenol) and protein (1.93 fold vs. non-isoproterenol). Edaravone had no apparent effect in hypertrophic responses, but significantly prevented both increases in TBARS and decreases in the PCr/ATP ratio. Edaravone also prevented increases in UCP2 mRNA (0.76 fold vs. isoproterenol) and protein (0.62 fold vs. isoproterenol) expressions against isoproterenol administration. Our results suggest that chronic beta-adrenergic stimulation induces myocardial energy inefficiency via excessive oxidative stress. The antioxidant effect of edaravone has potential to improve energy metabolism abnormalities against beta-adrenergic stimulation. Adequate regulation of UCP2 expression through artificial reduction of oxidative stress may play an important role in protection of the myocardial energy metabolism.

Adrenergic beta-Agonists↗
PubMed2006

Synergistic effect of mechanical stretch and angiotensin II on superoxide production via NADPH oxidase in vascular smooth muscle cells.

OBJECTIVE: Mechanical forces and angiotensin II influence the structure and function of vascular cells, and play an important role in reactive oxygen species production. In this study, we examined the effects of mechanical stretch and angiotensin II on the expression of p22-phox and Nox-1, essential membrane components of NADPH oxidase, and superoxide production in rat vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: Neither a stretch force nor angiotensin II alone altered p22-phox and Nox-1 expression in VSMCs. Combined stimulation markedly increased p22-phox and Nox-1 mRNA, however, which was associated with increased NADPH oxidase activity, superoxide production and total 8-iso-prostaglandin F2alpha concentration. The increases in p22-phox mRNA levels induced by a stretch force in combination with angiotensin II were prevented by treatment with an angiotensin type I (AT1) receptor antagonist, RNH-6270 (100 nmol/l). Protein expression of the AT1 receptor was upregulated by a stretch force. CONCLUSIONS: These data indicate that mechanical stretch and angiotensin II synergistically increase NADPH oxidase expression in VSMCs, and suggest that part of this mechanism is mediated through an upregulation of the AT1 receptor induced by mechanical stretch. The combined effects of mechanical strain and angiotensin II might promote vascular damage through the production of superoxide in a hypertensive state.

Angiotensin II↗
PubMed2006

Contribution of reactive oxygen species to the pathogenesis of left ventricular failure in Dahl salt-sensitive hypertensive rats: effects of angiotensin II blockade.

OBJECTIVE: We investigated the contribution of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species (ROS) generation to the pathogenesis of diastolic heart failure (DHF) in Dahl salt-sensitive (DS) hypertensive rats, with the aim of testing our hypothesis that the cardioprotective effects of angiotensin II (Ang II) blockade are provided by the suppression of this pathway. METHODS: DS rats were maintained on high (H: 8.0% NaCl) or low (L: 0.3% NaCl) salt diets from age 7 to 17 weeks. DS/H rats were also treated with candesartan cilexetil (10 mg/kg per day, orally) or a superoxide dismutase mimetic, tempol (3 mmol/l in drinking water) from age 7 to 17 weeks. RESULTS: DS/H rats represented hypertension, left ventricular (LV) relaxation abnormality and myocardial stiffening with preserved systolic heart function. As compared with DS/L rats, DS/H rats showed higher levels of transforming growth factor-beta (TGF-beta), connective tissue growth factor (CTGF), p22phox and gp91phox mRNA expression, NADPH oxidase activity and thiobarbituric acid-reactive substance (TBARS) contents in LV tissues. Gene expression of uncoupling protein-2 (UCP-2), an inner mitochondrial membrane proton transporter, was also 2.8 +/- 0.5-fold higher. In DS/H rats, treatment with candesartan did not alter blood pressure, but resulted in a marked improvement of the hemodynamic deterioration; these therapeutic effects were accompanied by decreases in myocardial NADPH oxidase activity, TBARS contents and the expression of TGF-beta, CTGF, p22phox, gp91phox and UCP-2. Similar therapeutic effects were provided by treatment with tempol in DS/H rats. CONCLUSIONS: Our data suggest that NADPH oxidase-mediated ROS production contributes to the pathogenesis of DHF in DS hypertensive rats, and that the cardioprotective effects of AngII blockade are, at least partially, mediated through the suppression of this pathway.

Angiotensin II↗
PubMed2005

Treatment of ischemic limbs based on local recruitment of vascular endothelial growth factor-producing inflammatory cells with ultrasonic microbubble destruction.

OBJECTIVES: We sought to clarify the mechanism for neovascularization by ultrasonic microbubble destruction (US/MB) and its ability to improve the function of ischemic limbs. BACKGROUND: In tissue, US/MB can cause capillary rupture, leading to angiogenesis and arteriogenesis. METHODS: Seven days after removal of the femoral artery (day 0) in mice, microbubble/ultrasound treatment was performed by intermittent insonation (1.6 MHz, mechanical index 1.1) to the ischemic limbs after intravenous infusion of phospholipid-stabilized microbubbles BR14 (US/MB group). Effects were compared with those in untreated mice with ischemic limbs (control group). RESULTS: Immunostaining of the treated muscles revealed a greater leukocyte (CD45-positive cell) count in the US/MB group on days 3 and 7. These cells included F4/80-positive cells (macrophages) and CD3-positive cells (T-lymphocytes), both of which were immunoreactive to vascular endothelial growth factor (VEGF) antibody. Muscular VEGF content by Western blotting was elevated in the US/MB group on day 3, which declined but remained greater until day 21. The US/MB group showed a greater capillary density by alkaline phosphatase stain on day 7 without further increase at day 21. Surface vascularity of the muscles and blood flow were greater in the US/MB group on day 7, which further increased by day 21. Moreover, the US/MB group showed a two-fold longer treadmill time compared with the untreated control group on day 21. None of these favorable effects were observed in mice treated with ultrasound only or microbubbles only. CONCLUSIONS: Ultrasonic destruction of microbubbles delivered to the ischemic limbs can recruit inflammatory cells producing VEGF, which is followed by neovascularization and functional improvement, and thus has a therapeutic potential.

Animals↗
PubMed2005

Spatial distribution of right ventricular perfusion abnormalities following acute right coronary artery occlusion: a study by myocardial contrast echocardiography and blue dye staining.

OBJECTIVE: Although echocardiography is used for diagnosing right ventricular (RV) infarction produced by right coronary artery (RCA) occlusion, there has been no data on the spatial distribution of RV perfusion abnormalities following acute RCA occlusion. We examined this distribution by myocardial contrast echocardiography (MCE) and blue dye staining in canine models. METHODS: The RCA was occluded in 10 open-chest dogs. MCE was performed with 0.27 g/min Levovist infusion by harmonic power Doppler with electrocardiogram gated intermittent triggered imaging at baseline and at 90 min after RCA occlusion. The opacification defects were assessed at the basal, middle, and apical levels of the RV free wall by short-axis view. The extent of the risk area of the occluded RCA, expressed as a percentage of the RV free wall, was measured at each level by injecting blue dye at the end of the experiments. In 10 other dogs, the left anterior descending coronary artery (LAD) was occluded by ligating the proximal portion of the LAD to examine the territory of the LAD on the same levels of the RV free wall by injecting blue dye. RESULTS: Although patchy opacification defects accompanying RV dilation were observed at the basal and middle levels during RCA occlusion, no apical defects were observed in any dogs by MCE. The risk area of the occluded RCA, as delineated by blue dye, was larger in the basal than apical level of the RV free wall in all 10 dogs (basal: 79 +/- 9%; middle: 48 +/- 14%; apical: 3 +/- 6%, p < 0.0001). The risk area of the occluded LAD (basal: 17 +/- 7%; middle: 12 +/- 6%; apical: 6 +/- 6%) was smaller than the risk area of the occluded RCA at the basal and middle levels of the RV free wall (p < 0.0001), and no significant difference was observed at the apical level. CONCLUSIONS: RV perfusion abnormalities produced by RCA occlusion are larger in the basal than apical level of the RV free wall. This finding elucidates the spatial distribution of the territory of the RCA on the RV free wall, and may help in identifying and assessing RV ischemia by echocardiography in humans. Moreover, the data in the current study indicate that RV infarction may be produced by occlusion of the coronary arteries except RCA, because the territory of the LAD on the RV free wall is clearly delineated.

Animals↗
PubMed2004

Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type II diabetes model.

OBJECTIVES: We examined the effects of early treatment with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin on the progression of glucose intolerance and cardiovascular remodeling in a model of spontaneously developing type II diabetes mellitus (DM), the Otsuka Long-Evans Tokushima Fatty (OLETF) rats. BACKGROUND: Clinical trials showed that pravastatin prevented new-onset DM in hypercholesterolemic patients, and that it was effective in prevention of cardiovascular events in diabetics. METHODS: The OLETF rats were treated with pravastatin (100 mg/kg/day) from 5 weeks of age and compared with age-matched untreated OLETF rats and normal Long-Evans Tokushima Otsuka (LETO) rats on serial oral glucose tolerance tests (OGTT) and Doppler echocardiography and on histopathological/biochemical analyses of the heart at 30 weeks. RESULTS: The OGTT revealed that 40% and 89% of untreated OLETF rats were diabetic at 20 and 30 weeks, respectively, but 0% and only 30%, respectively, were diabetic in the treated OLETF. Left ventricular diastolic function was found impaired from 20 weeks in untreated OLETF but remained normal in the treated-OLETF. The wall-to-lumen ratio and perivascular fibrosis of coronary arteries were increased in untreated-OLETF but were limited in the treated-OLETF at 30 weeks. Moreover, cardiac expressions of a fibrogenic growth factor, transforming growth factor-beta1 (TGF-beta1), and a proinflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), were increased in untreated-OLETF. However, in the treated-OLETF, overexpressions of TGF-beta1 and MCP-1 were attenuated, which was associated with overexpression of endothelial nitric oxide synthase (eNOS) (2.5-fold of control LETO). CONCLUSIONS: Early pravastatin treatment prevented cardiovascular remodeling in the spontaneous DM model by retarding the progression of glucose intolerance, overexpressing cardiac eNOS, and inhibiting overexpressions of fibrogenic/proinflammatory cytokines.

Animals↗
PubMed2004

Treatment of acute myocardial infarction by hepatocyte growth factor gene transfer: the first demonstration of myocardial transfer of a "functional" gene using ultrasonic microbubble destruction.

OBJECTIVES: We examined whether ultrasonic microbubble destruction (US/MB) enables therapeutic myocardial gene transfer of hepatocyte growth factor (HGF) for acute myocardial infarction (MI). BACKGROUND: Hepatocyte growth factor gene transfer provides cardioprotective effects in MI, which requires direct intramyocardial injection or special vectors. Although US/MB was used in myocardial gene transfer, its feasibility in transfer of a therapeutic gene with non-viral vector remains unknown. METHODS: In a rat model of acute MI, naked plasmid (pVaxl) encoding human HGF (1,500 microg) was infused into the left ventricular (LV) chamber during US/MB (HGF-US/MB) or insonation only (HGF-US) or alone (HGF-alone), while control MI rats received empty pVaxl during US/MB (pVaxl-US/MB). For US/MB, transthoracic intermittent insonation with a diagnostic transducer (1.3 MHz) was performed for 2 min at a peak negative pressure of -2,160 kPa during intravenous 20% Optison. RESULTS: Baseline risk area was comparable among the groups. Immunohistology seven days after treatment revealed significant myocardial expression of HGF protein only in HGF-US/MB. At three weeks, LV weight in HGF-US/MB (0.89 +/- 0.03 g) was significantly lower than those in HGF-alone (1.09 +/- 0.08 g), HGF-US (1.04 +/- 0.07 g), and pVaxl-US/MB (1.04 +/- 0.05 g). Moreover, scar size was significantly smaller (16 +/- 6% vs. 39 +/- 5%, 41 +/- 6%, and 40 +/- 4% of total myocardial circumferential length, respectively), while capillary density (49 +/- 8 vs. 34 +/- 5, 37 +/- 6, and 36 +/- 4 capillaries/high-power field, respectively) and arterial density (37 +/- 7 vs. 15 +/- 9, 18 +/- 4, and 14 +/- 11 arterioles/high-power field, respectively) in the risk area were higher in HGF-US/MB than the other groups. CONCLUSIONS: Ultrasound-mediated microbubble destruction may enable myocardial HGF gene transfer with systemic administration of naked plasmid, which enhances angiogenesis, limits infarction size, and prevents LV remodeling after MI.

Animals↗
PubMed2004

Latent abnormal fatty acid metabolism in apparently normal perfusion during stress in patients with restenosis after coronary angioplasty: assessment by exercise stress thallium-201 and iodine-123-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid-dual myocardial single-photon emission computed tomography.

Restenosis is a major problem in patients undergoing coronary angioplasty. Reduced uptake of iodine-123-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (I-BMIPP-123) relatively to thallium-201 (Tl-201) has been attributed to the metabolic damage in the myocardium in patients with coronary artery disease. Therefore, we performed exercise stress Tl-201 and I-BMIPP-123 dual myocardial single-photon emission computed tomography (SPECT) to detect coronary restenosis in 48 patients (35 men and 13 women, mean age 66 +/- 8 years), followed by coronary angiography at follow-up. Patients were divided into 2 groups: those with (n = 24) and without (n = 24) restenosis. Redistribution of Tl-201 was seen more frequently in the restenosis group than in no-restenosis group (58% [14 of 24] vs 8% [2 of 24], p <0.05). Five of 10 patients (50%) with restenosis but without Tl-201 redistribution had Tl-201/I-BMIPP-123 discrepancy during stress. In patients without restenosis, only 1 patient had this discrepancy during stress. Incorporation of Tl-201/I-BMIPP-123 uptake discrepancy during stress significantly improved the sensitivity (58% [14 of 24] to 79% [19 of 24]) with preserved specificity (92% [22 of 24] to 88% [21 of 24]). Exercise stress Tl-201 and I-BMIPP-123 dual myocardial SPECT revealed that latent abnormal fatty acid metabolism may exist in apparently normal perfusion during stress in patients with restenosis after coronary angioplasty. Use of I-BMIPP-123 together with Tl-201 during stress SPECT substantially improved the diagnostic accuracy of restenosis based on Tl-201 redistribution (from 75% to 83%).

Aged↗
PubMed2004

Leukocyte-targeted myocardial contrast echocardiography can assess the degree of acute allograft rejection in a rat cardiac transplantation model.

BACKGROUND: Repetitive endomyocardial biopsies are necessary to monitor the effects of immunosuppressants after cardiac transplantation. Contrast ultrasound with microbubble targeting of leukocytes detects acute leukocyte infiltration. We examined whether leukocyte-targeted myocardial contrast echocardiography (MCE) could provide for the quantitative assessment of acute cardiac rejection. METHODS AND RESULTS: Hearts from Brown Norway rats or Lewis rats were transplanted into other Brown Norway rats. Isografts and groups of allografts either untreated or treated with cyclosporin A (CsA) at a low dose (3 mg x kg(-1) x d(-1)) or high dose (10 mg x kg(-1) x d(-1)) from 3 days before transplantation were compared at posttransplantation day 3. Echocardiography-derived left ventricular wall thickening was comparable among the 4 groups. Myocardial blood flow assessed with MCE, relating pulsing intervals with signal intensity (SI), was slightly decreased only in untreated allografts. However, myocardial SI (in gray levels) obtained after a 10-minute period allowing microbubble-leukocyte interactions after contrast injection exhibited a clear gradient in these groups (12+/-2 in untreated allografts, 9+/-5 in allografts treated with low-dose CsA, 6+/-3 in allografts treated with high-dose CsA, and 2+/-1 in isografts, P<0.001). The pattern of difference in SI among the groups agreed well with that in ED-1-positive cell (macrophage) count (25+/-7, 12+/-4, 5+/-3, and 1+/-0 cells per high-power field, respectively, P<0.001), which correlated with CD3-positive cell (T lymphocyte) count (33+/-5, 22+/-5, 9+/-4, and 1+/-0 cells per high-power field, respectively, P<0.001). CONCLUSIONS: Leukocyte-targeted MCE can noninvasively assess the degree of rejection in transplanted hearts by directly revealing the magnitude of intramyocardial infiltration of macrophages and T lymphocytes.

Acute Disease↗
PubMed2004

Interaction with leukocytes: phospholipid-stabilized versus albumin-shell microbubbles.

PURPOSE: To confirm that BR14 microbubbles (MBs) can be phagocytosed by activated leukocytes, to determine their stability after phagocytosis, and to evaluate how such characteristics influence the fate of neutrophils containing MBs after insonation. MATERIALS AND METHODS: BR14 and human albumin MBs (2 x 10(7)/mL) were incubated with activated human neutrophils (2 x 10(6)/mL) to allow phagocytosis. Deflation rate of the phagocytosed MBs after pulsed insonation (one burst per second for 5 seconds) at 1.8 MHz with peak negative pressure of -540 kPa or -1,340 kPa, lactate dehydrogenase (LDH) leakage, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain-positive cell count after insonation were compared between the two agents. RESULTS: At -540 kPa, phagocytosed MBs remained nearly unchanged for both agents after insonation. At -1,340 kPa, although human albumin MBs were disrupted on the first or second burst, BR14 MBs remained undisrupted. After -540-kPa insonation, a similar number of apoptotic cells appeared in neutrophils containing human albumin and BR14 MBs. At -540 kPa, LDH leakage was limited in human albumin MBs and BR14 MBs. At -1,340 kPa, LDH leakage was significantly increased in human albumin MBs and BR14 MBs (P <.01, both vs -540 kPa). Apoptotic cells were significantly decreased in human albumin MBs and BR14 MBs (P <.01, both vs -540 kPa). LDH leakage was lower and apoptotic cell count was greater in BR14 MB-containing neutrophils than in human albumin MB-containing neutrophils (both P <.01). CONCLUSION: Compared with human albumin MBs, BR14 MBs were more stable after phagocytosis with insonation. This stability is associated with less disruption and greater induction of apoptosis in leukocytes after relatively high-pressure insonation in the range for diagnostic use.

Adult↗
PubMed2004

Usefulness of brain natriuretic peptide as a marker for separating cardiac and noncardiac causes of syncope.

We retrospectively evaluated the feasibility of measuring brain natriuretic peptide to identify cardiac syncope in 148 consecutive patients with syncope. Sixty-one patients with cardiac syncope were identified. A cut-off value of 40 pg/ml was used to determine the cardiac causes of syncope; the sensitivity and specificity for identification of cardiac syncope were 82% and 92%, respectively. Thus, measurement of brain natriuretic peptide concentrations may help confirm cardiac causes of syncope, and merits consideration for incorporation into the algorithm used to diagnose syncope.

Aged↗
PubMed2004

Potential pitfalls of visualization of myocardial perfusion by myocardial contrast echocardiography with harmonic gray scale B-mode and power Doppler imaging.

OBJECTIVE: The present study compared the regional variation of myocardial signal intensity in visualizing myocardial perfusion by myocardial contrast echocardiography (MCE) between harmonic gray scale and power Doppler imaging. METHODS: MCE was performed in 12 patients by electrocardiographic (ECG)-gated intermittent triggered MCE with harmonic gray scale and power Doppler imaging following slow intravenous injection of 0.5 ml contrast agent (Optison). The interval between the ECG triggers (pulsing interval) was increased from every heart beat (1:1) to every 2 (1:2), 4 (1:4), and 8 (1:8) cardiac cycles to allow incremental microbubble (contrast agent) replenishment. The MCE images were recorded when attenuation produced by the left ventricular cavity was minimal. The background-subtracted videointensity was measured in 7 segments in an apical 4-chamber view: 3 (apical, mid, and basal) septal segments, 3 (apical, mid, and basal) lateral segments, and 1 apex segment (apical cap). RESULTS: The background-subtracted videointensity for each segment was greater with the power Doppler than the gray scale imaging (p < 0.01). With the gray scale imaging, the background-subtracted videointensity in the basal septal segment demonstrated a negative value at all pulsing intervals, and the value (-9 +/- 13) was significantly lower than that (22 +/- 20) in the apical lateral segment at a pulsing interval of 1:8 (p < 0.01). With power Doppler imaging, the background-subtracted videointensity was high even in the basal septal segment (112 +/- 33), and no significant difference was observed among each segment. CONCLUSIONS: The findings indicate that quantitative assessment of myocardial perfusion based upon background-subtracted video-intensity may be difficult in the far field with harmonic gray scale imaging although the attenuation is not apparent by visual analysis. Harmonic power Doppler is more sensitive for detecting basilar perfusion in the far field compared with harmonic gray scale imaging.

Aged↗
PubMed2004

A comparison of video and digital data in the assessment of myocardial perfusion abnormalities by myocardial contrast echocardiography.

OBJECTIVE: The objective of the present study was to compare the digital and video data of myocardial contrast echocardiography (MCE) to assess altered myocardial blood flow produced by graded coronary stenoses. METHODS: Three grades of left anterior descending (LAD) coronary artery stenosis and occlusion were created in eight open-chest canine models. MCE was performed with BR1 infusion by harmonic power Doppler with ECG gated intermittent triggered imaging at pulsing intervals ranging from 1:1 to 1:10. For images that were recorded simultaneously on both a videotape (video data) and an optical disk (digital data), myocardial signal intensity in the LAD region was plotted vs. pulsing intervals and was fitted to an exponential function: y = A(1 - e(-bt)), where A is the peak plateau signal intensity, and b is the rate of signal intensity rise for quantification of myocardial blood flow. RESULTS: Both values for A and b progressively decreased with a greater level of stenosis. The correlation of A with myocardial blood flow (determined by use of fluorescent microspheres) was weak with digital data (r = 0.38, p = 0.037), and was insignificant with video data (r = 0.16, p = 0.38). The correlation of b with microsphere-derived myocardial blood flow was better than that of A with both video and digital data, and was similar between the two kinds of data (video: r = 0.69, p < 0.0001; digital: r = 0.68, p < 0.0001). CONCLUSIONS: Video and digital MCE data are equivalent in their ability to quantify altered myocardial blood flow produced by graded coronary stenoses.

Analysis of Variance↗
PubMed2004

Leptin kinetics during peritoneal dialysis in acutely uraemic rats.

BACKGROUND: Leptin has been shown to function as an inhibitor of appetite and energy expenditure accelerator. However, it was recently reported that leptin has other important functions as a fibrogenetic factor and a novel, independent risk factor for coronary heart disease. The present study aimed to assess the blood concentration of leptin in acute uraemic rats by using various peritoneal dialysis (PD) solutions. METHODS: To induce acute renal failure, the bilateral renal arteries were ligated via a mid-abdominal incision 1 h before starting PD. Rats were divided into four groups: 13.6 g/L glucose-containing dialysate (group L); 38.6 g/L glucose-containing dialysate (group H); 13.6 g/L glucose and 25 g/L mannitol-containing dialysate with equal osmotic pressure to the dialysate of group H (group M); and renal failure without PD (group F). The concentrations of glucose, urea nitrogen (UN), leptin and insulin were measured at 0, 2 and 4 h after starting PD. RESULTS: We observed significant blood UN suppression in all dialysed groups. Blood glucose was significantly higher in rats treated with the high glucose solution than in those treated with the low glucose solution. Insulin and leptin significantly increased in the high glucose solution group. There was a strong correlation between the blood glucose and insulin levels. We also found a strong correlation between the percentage changes in blood glucose and leptin. The relationship between the percentage changes in insulin and leptin were weak but significant. CONCLUSION: The high glucose PD solution resulted in increased circulating levels of leptin, glucose, and insulin, suggesting that these changes are linked with PD performed with glucose-based dialysis fluid.

Acute Kidney Injury↗