Search PubMed⌕ Search

Biomedical subjects

C Kawai

Publications and source records attributed to C Kawai.

At least 235 records · Page 13Linked to original sources
PubMed1988

Relation of left ventricular perfusion and wall motion with metabolic activity in persistent defects on thallium-201 tomography in healed myocardial infarction.

Myocardial viability in persistent thallium (TI)-201 defect is a controversial subject. To assess metabolic activity in segments with persistent defect, stress TI-201 tomography and positron emission tomography using nitrogen-13 ammonia and fluorine-18 2-fluoro-deoxyglucose (FDG) were performed in 28 patients with healed myocardial infarction. The segments with TI-201 perfusion defect in electrocardiogram-determined infarcted areas were selected for assessment. Stress perfusion defect was detected in 61 segments by TI-201 tomography. Twenty-two patients (36%) showed transient defects with redistribution (group 1) and 39 showed persistent defects (group 2). Increase in FDG uptake was observed in 95% in group 1. Among group 2 patients, 15 segments (38%) showed an increase in FDG uptake (group 2A) while the remaining 24 (62%) did not have an increased uptake (group 2B). The decrease in nitrogen-13 ammonia perfusion was more severe in group 2B (-23 +/- 7%) than in group 2A (-13 +/- 9%) (p less than 0.005) and group 1 (-10 +/- 4%) (p less than 0.001). In addition, wall motion scores tended to be lower in group 2B (0.21 +/- 0.71), compared with group 2A (0.67 +/- 0.70) (p = 0.05) and group 1 (0.77 +/- 0.60) (p less than 0.01). These data indicate that metabolic viability was observed in approximately 40% of the segments with persistent TI-201 defect. Preservation of regional perfusion and wall motion in these areas was similar to that in areas with transient TI-201 defect.

Aged↗
PubMed1988

Prevention of atherosclerotic progression in Watanabe rabbits by probucol.

The foam cell has been recognized as a characteristic feature of xanthomas in skin and tendons, and also of atheromas. Many foam cells in these lesions share properties characteristic of the macrophages. Therefore macrophages may be the progenitor of certain foam cells that are involved in atherogenesis. Several investigators demonstrated in vitro that macrophages can ingest large amounts of certain chemically modified lipoproteins, such as acetylated low-density lipoprotein (LDL) and malondialdehyde-treated LDL, through the process of receptor-mediated endocytosis. By this process, macrophages become foam cells. But this process has not been demonstrated in vivo. Recently, oxidized LDL has been suggested to play an important role in atherogenesis by facilitating the accumulation of lipids in macrophages in vitro. Probucol, originally developed as an antioxidant, prevents this oxidative modification of LDL in vitro. Moreover, there are some clinical reports that probucol induces regression of cutaneous and tendon xanthomas in patients with homozygous familial hypercholesterolemia. A question was posed whether in vivo probucol could prevent the progression of atherosclerosis in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. At age 2 months, 8 WHHL rabbits were classified into 2 groups: group A rabbits were controls and group B rabbits were treated with 1% probucol. After 6 months of treatment, average plasma concentrations of cholesterol were 704 +/- 121 mg/dl in group A and 584 +/- 61 mg/dl in group B. The percentage of surface area of total thoracic aorta with visible plaques in group A vs group B was 54.2 +/- 18.8% vs 7.0 +/- 6.3%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Significance of technetium-99m/thallium-201 overlap on simultaneous dual emission computed tomography in acute myocardial infarction.

To examine the significance of technetium-99m pyrophosphate/thallium-201 scintigraphic overlap as an indicator of identifying early coronary reperfusion (less than or equal to 3 hours), 32 patients, in whom coronary recanalization was attempted for acute myocardial infarction (AMI), underwent myocardial imaging 3 days after the onset of AMI. The imaging was performed by simultaneous dual emission computed tomography, which allows simultaneous recording of technetium-99m pyrophosphate and thallium-201 images and comparison between both images in the same slice. The patients were separated into 3 groups: 9 patients in whom reperfusion was successful and showed scintigraphic overlap (group A), 12 with successful recanalization but no overlap (group B) and 11 with neither coronary reflow nor overlap (group C). No patient in whom reperfusion failed showed scintigraphic overlap (p less than 0.05). Groups A and B were comparable in age, infarct vessel, collateral circulation, residual coronary stenosis and cumulative release of creatine kinase-MB isoenzyme. However, compared with group B, group A had a shorter interval between onset of AMi and reflow (2.5 +/- 0.8 vs 4.8 +/- 1.3 hours, p less than 0.001). The presence of scintigraphic overlap identified early coronary reflow with a sensitivity of 80%, specificity of 91%, positive predictive accuracy of 89% and negative predictive accuracy of 83%. Thus, technetium-99m/thallium-201 overlap on dual emission computed tomography can be used as an index of documenting early recanalization and might reflect the presence of salvaged myocardium adjacent to the necrotic tissue.

Clinical Enzyme Tests↗
PubMed1988

F-18 deoxyglucose and stress N-13 ammonia positron emission tomography in anterior wall healed myocardial infarction.

To evaluate myocardial blood flow and glucose utilization, N-13 ammonia (NH3) and F-18 deoxyglucose positron emission tomography scanning was performed in 22 patients with previous anterior wall myocardial infarction, using a high-resolution, multi-slice, whole-body scanner. The N-13 ammonia study was performed at rest and after exercise. The F-18 deoxyglucose study was performed at rest after fasting greater than 5 hours. The N-13 ammonia study revealed a hypoperfused area in 19 of the 22 patients (86%), that corresponded to the infarcted regions as diagnosed by electrocardiography, coronary arteriography and left ventriculography (21 patients). The hypoperfused areas expanded after exercise in 16 of 22 patients (73%). F-18 deoxyglucose uptake was observed in these hypoperfused areas, especially in patients with hypokinetic wall motion on left ventriculography and in exercise-induced hypoperfused areas. However, positron emission tomography demonstrated diffuse uptake of F-18 deoxyglucose in 3 of 8 patients with dyskinetic wall motion. Thus, metabolically active myocardium in infarcted areas or periinfarct ischemia can be visualized with F-18 deoxyglucose and stress N-13 ammonia studies.

Adult↗
PubMed1988

Acute hemodynamic effects of MDL19205 on conscious dogs with mitral regurgitation.

To assess the effects of MDL19205, a combined inotropic-vasodilating agent, or an inodilator, on the left ventricle with subacute volume overload due to mitral regurgitation (MR), seven dogs were instrumented with a left ventricular (LV) micromanometer and a pair of ultrasonic crystals for the measurement of LV circumferential segment length. After examining the effects of this drug in the normal hearts, its effects were observed in the same dogs in which MR was produced by sectioning chordae tendineae. Mitral regurgitation caused increases in LV peak dP/dt (2,384 +/- 256 to 3,090 +/- 622 mmHg/sec; p less than 0.05), mean circumferential shortening velocity (Vcf; 1.41 +/- 0.25 to 1.85 +/- 0.20 sec-1; p less than 0.05), LV end-diastolic pressure (LVEDP; 8.2 +/- 1.6 to 15.8 +/- 3.7 mmHg; p less than 0.001), and LV end-diastolic length (LVEDL; 10 to 10.6 +/- 0.2mm; p less than 0.01). The dogs were intravenously administered MDL19205 7 to 14 days after they had completely recovered from the first and second operations. With 3 mg/kg of MDL19205, peak changes of hemodynamic indices occurred within 5 minutes in the hearts with MR LV dP/dt and mean Vcf significantly rose (from 3,090 +/- 622 to 5,356 +/- 811 mmHg/sec; p less than 0.001, 1.85 +/- 0.20 to 2.65 +/- 0.36 sec-1, p less than 0.001). LVEDP and LVEDL were returned to the control values obtained in the normal hearts (15.8 +/- 3.7 to 6.4 +/- 2.4 mmHg; p less than 0.001, 10.6 +/- 0.2 to 10 +/- 0.4; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Recurrent left ventricular mural thrombi in a patient with acute myocarditis.

A case of acute myocarditis with recurrent left ventricular mural thrombi in a 59-year-old man is reported. Two-dimensional echocardiogram demonstrated left ventricular mural thrombus with apical dyskinesis on the 2nd day after the onset of chest oppression. No hemoagglutination abnormalities were present. Anticoagulation treatment with heparin was initiated. A two-dimensional echocardiogram obtained on the 15th day showed that the left ventricular wall motion had become normal and that the thrombus had disappeared. However, on the 38th day, a new pedunculated free mobile thrombus was found in the apical part of the left ventricle despite the normal wall motion. By the 46th day, the new thrombus had disappeared. The present case suggests that mural thrombi can occur in the absence of left ventricular dyskinesis and dilatation. Anticoagulation therapy resolved the mural thrombi but could not prevent the recurrence at the apex. Thus, in acute myocarditis, a mural thrombus may appear as a result of the endocardial damage, even when blood stasis is absent.

Acute Disease↗
PubMed1988

Protective effect of recombinant alpha interferon on coxsackievirus B3 myocarditis in mice.

The effects of recombinant human leukocyte interferon alpha-A/D on experimental myocarditis caused by coxsackievirus B3 were investigated. Four-week-old male C3H/He mice were inoculated intraperitoneally with 10(5.5) 50% tissue culture infective dose (TCD50) in 0.1 ml of coxsackievirus B3 (Nancy strain). Interferon alpha-A/D, 10(4) U/gm/day, was administered subcutaneously daily, starting 1 day before (group 1) or on the day of (group 2) infection. Animals were killed on day 7. The infectivity of myocardial virus was significantly lower in group 1 (0.7 +/- 0.1 log10TCD50/mg, p less than 0.005) and in group 2 (2.5 +/- 1.2 log10TCD50/mg, p less than 0.005) than in control mice (4.4 +/- 0.9 log10TCD50/mg). Results of histologic examination showed extensive myocardial necrosis and cellular infiltration in all mice in the untreated group, but significantly less severe necrosis and infiltration in the treated groups. Thus, interferon alpha-A/D, when given before and simultaneously with virus, effectively inhibited replication of myocardial virus and reduced the inflammatory response and myocardial damage in an experimental model of viral myocarditis.

Animals↗
PubMed1988

Non-Q wave versus Q wave myocardial infarction: regional myocardial metabolism and blood flow assessed by positron emission tomography.

This study compared regional myocardial blood flow at rest and during supine exercise as well as regional myocardial glucose utilization in the fasting condition in 22 patients, 11 with antecedent non-Q wave and 11 with antecedent Q wave infarction. With use of N-13 (nitrogen-13) ammonia and F-18 (fluorine-18) deoxyglucose as tracers of blood flow and exogenous glucose utilization and positron emission tomography, hypoperfused areas were noted at rest and during exercise in all 11 patients (100%) with Q wave infarction. Among the 11 patients with non-Q wave infarction such areas were noted in only 5 (45%) at rest and in 8 (73%) during exercise. Furthermore, segmentally enhanced F-18 deoxyglucose uptake corresponding to the infarcted areas (identified electrocardiographically) was seen in 10 (91%) of the 11 patients with non-Q wave infarction but in only 4 (36%) of the 11 patients with Q wave infarction (p less than 0.01). In conclusion, segmental F-18 deoxyglucose uptake as a possible sign of myocardial viability was seen more frequently in non-Q wave than in Q wave infarction and, importantly, regionally enhanced F-18 deoxyglucose uptake occurred even in the absence of segmental rest or exercise blood flow abnormalities, or both, in 5 (45%) of 11 patients with non-Q wave infarction.

Adult↗
PubMed1988

Cholesteryl ester accumulation in macrophages incubated with low density lipoprotein pretreated with cigarette smoke extract.

Although cigarette smoking is one of the major risk factors for atherosclerosis and coronary heart disease, the precise mechanisms of its adverse effects have not been fully elucidated. We incubated low density lipoprotein (LDL) with cigarette smoke (CS) extract and examined the incorporation of the lipoprotein by macrophages in vitro. When incubated with macrophages, LDL pretreated with CS extract (100 micrograms/ml) stimulated cholesteryl [14C]oleate synthesis approximately equal to 12.5-fold that with unmodified LDL and transformed macrophages to cells rich in lipid droplets positively stained with oil red O. Enhancement in cholesteryl ester synthesis was dependent on the concentration of CS-modified LDL and exhibited saturation kinetics. When subjected to electrophoreses, CS-modified LDL migrated to a more anionic position than did unmodified LDL and showed extensive fragmentation of apolipoprotein B. This LDL modification depended upon the incubation time and concentration of the CS extract. Superoxide dismutase inhibited modification of LDL by 52%, suggesting that superoxide anion is, at least in part, involved. These results suggest that CS extract alters LDL into a form recognized and incorporated by macrophages. Such modification if it occurs in vivo, could explain the increased incidence of atherosclerosis and coronary heart disease in smokers.

Animals↗
PubMed1988

Detection of low molecular kininogen messenger RNA in human kidney.

The purpose of the present study was to confirm expression of kininogen in human kidneys. As the human kininogen gene is alternatively transcribed to high molecular weight and low molecular weight kininogen messenger (m)RNA, we constructed a probe which can discern these two transcripts by the S1 nuclease mapping analysis. The low molecular weight kininogen mRNA was detected in human kidney cortex and medulla. This finding strongly supports the existence of a local kinin-kallikrein system in human kidneys.

Blotting, Northern↗
PubMed1988

Electrophysiological effects of melperone on isolated rabbit heart muscles.

1. Electrophysiological effects of melperone on isolated atrial and ventricular muscle preparations of the rabbit were studied by a conventional microelectrode technique. 2. Melperone (3.3 microM) prolonged the action potential duration and effective refractory period of the atrial preparations without affecting the maximum rate of depolarization (Vmax). These effects of melperone on action potential duration and effective refractory period were inhibited by a low potassium perfusate (2.7 mM). 3. A high concentration of melperone (16.6 microM) decreased Vmax of atrial preparations. In ventricular muscles, melperone at either concentration decreased Vmax, although the increase in action potential duration was greater than in the atrium. 4. Depression of Vmax of ventricular muscles by melperone was found to be augmented by an increase of stimulation frequency and drug concentration. 5. The rate of onset of rate-dependent block of Vmax in ventricle was increased with drug concentration and frequency of stimulation. However, the time constant of recovery from rate-dependent block was almost constant. The kinetics of rate-dependent block of Vmax by melperone were approximately similar to those of quinidine and disopyramide. Consequently it is concluded that melperone possesses class 1a antiarrhythmic activity as well as class 3 activity.

Action Potentials↗
PubMed1988

Effects of hypoxia and reoxygenation on maximum rate of early left ventricular filling.

Left ventricular early filling during hypoxia and reoxygenation was examined in isolated working rat hearts that contracted 300 times/min when perfused with Krebs-Henseleit solution at 37 degrees C. Left ventricular short-axial diameter (LVD = D) was measured with a pair of ultrasonic crystals. The maximum lengthening velocity of LVD [(dD/dt)max] decreased with hypoxia and recovered after reoxygenation (from a control of 20.3 +/- 6.7 to 7.3 +/- 1.7 mm/s after 15 min of hypoxia and to 16.3 +/- 8.1 mm/s after 15 min of reoxygenation; n = 7). However, (dD/dt)max/delta D (where delta D is systolic shortening) showed no significant change with either hypoxia or reoxygenation (from a control of 21.0 +/- 2.9 l/s to 22.2 +/- 2.7 l/s after 15 min of hypoxia and to 22.5 +/- 3.7 l/s after 15 min of reoxygenation; n = 7). Therefore, we concluded that the changes of (dD/dt)max with hypoxia and reoxygenation were caused by the changed systolic shortening and that left ventricular myocardial recoil, expressed by (dD/dt)max/delta D, showed no change with either hypoxia or reoxygenation.

Animals↗
PubMed1988

Randomized, double-blinded multicenter study. Comparison of intracoronary single-chain urokinase-type plasminogen activator, pro-urokinase (GE-0943), and intracoronary urokinase in patients with acute myocardial infarction.

Coronary recanalization rates and changes in the coagulation and fibrinolysis system were evaluated in a randomized fashion in patients with acute myocardial infarction after intracoronary administration of single-chain urokinase-type plasminogen activator (pro-urokinase: GE-0943) or urokinase. Three groups of patients were studied: group H (n = 50), 6,000 units pro-urokinase i.c.; group L (n = 44), 3,000 units pro-urokinase i.c.; and group U (n = 54), 960,000 IU urokinase i.c. Coronary recanalization rates determined angiographically after 45 minutes of intracoronary infusion averaged 90% in group H, 59% in group L, and 61% in group U. The differences were statistically significant between group H and the latter two groups. Pro-urokinase affected plasma proteins of the fibrinolytic system to a lesser degree than urokinase. Bleeding complications were present in one patient in group L, in none in group H, and in five in group U. Thus, intracoronary administration of 6,000 units pro-urokinase is more effective in coronary thrombolysis and causes less systemic fibrinogenolysis than intracoronary administration of urokinase.

Adult↗
PubMed1988

Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs.

The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of excessive central blood volume by buffering pressure rise in the atrium and by providing an adequate ventricular filling volume.

Adaptation, Physiological↗
PubMed1988

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Changes in arachidonate metabolism were examined in mouse peritoneal macrophages incubated with various types of lipoproteins. Oxidized low density lipoprotein (LDL) was incorporated by macrophages and stimulated macrophage prostaglandin E2 (PGE2) and leukotriene C4 syntheses, respectively, 10.8- and 10.7-fold higher than by the control. Production of 6-keto-PGF1 alpha, a stable metabolite of prostacyclin, was also stimulated. No stimulation was found with native LDL, which was minimally incorporated by the cells. Acetylated LDL and beta-migrating very low density lipoprotein (beta-VLDL), though incorporated more efficiently than oxidized LDL, also had no stimulatory effect. When oxidized LDL was separated into the lipoprotein-lipid peroxide complex and free lipid peroxides, most of the stimulatory activity was found in the former fraction, indicating that stimulation of arachidonate metabolism in the cell is associated with uptake of the lipoprotein-lipid peroxide complex. These results suggest that peroxidative modification of LDL could contribute to the progression of atheroma by stimulating arachidonate metabolism during incorporation into macrophages.

Animals↗
PubMed1988

Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Serum PGI2 stabilizing factor (PSF) was purified from human serum to a single protein with a molecular weight of 28,000 D by SDS-PAGE. Analyses of NH2-terminal sequence (32 residues), COOH-terminal sequence (3 residues) and the composition of amino acids disclosed its homology with human apolipoprotein A-I (Apo A-I), a major apolipoprotein of HDL. Apolipoprotein A-II, C-I, C-II, C-III, D and E, as well as LDL, and VLDL did not possess this activity. The alpha-helix structure of Apo A-I is necessary for the binding of PGI2. HDL and nascent HDL reconstituted from Apo A-I and phospholipid significantly prolonged the half-life of PGI2. PGI2 stabilization by HDL and Apo A-I may be an important protective action against the accumulation of platelet thrombi at sites of vascular damage. The beneficial effect of HDL in the prevention of coronary artery disease may be partly due to this action.

Amino Acid Sequence↗