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C Kawai

Publications and source records attributed to C Kawai.

At least 145 records · Page 8Linked to original sources
PubMed1991

[Definitive myocardial blood flow evaluated by contrast echocardiography: experimental and A-C bypass flow studies].

We evaluated the feasibility of a new method for calculating definitive myocardial flow using contrast echocardiography in canine experiments and in patients who had undergone ACBG surgery. The principle for calculating flow was based on Kety-Schmidt method using time-intensity curve analysis between the epicardial and endocardial aspect. Inlet and outlet flows were hypothesized at the epicardium and endocardium, respectively. Analysis of time-contrast-intensity curves between the epicardium and endocardium, the difference of the area to the saturated point between epicardium and pericardium (A), and the saturated value (H) theoretically lead to the equation: Flow = 100 x (H/A) (Kety-Schmidt) in a 100-gram myocardium. No factors of intensity and time were included. Using this equation, the flow in 7 experimental canine and the flow of 9 patients who had ACBG surgery were compared to the electromagnetic flow. In the canine experiments, the left circumflex coronary artery was dissected free and was connected with contrast injector, a magnetic flowmeter and pneumatic occluder, proximal to distal in this order. Flow was controlled either by the occluder or drugs (papaverin and dipyridamole). Manually-agitated contrast media were injected rapidly (1 ml/2.5 sec), and M-mode echocardiographic recordings were densitometrically translated into time-intensity curves. Thirty-eight trials in 7 dogs showed close correlations (r = 0.901) between the electromagnetic flow and contrast echo flow. For the patients with ACBG, M-mode contrast echo recordings were made using transesophageal echo during the operations with contrast injections via the bypass grafts. Analysis of time-intensity curves was made and recorded in the same way as during the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Different appearance and pathogenic roles of serum IgA against autologous IgG Fc and Fab in patients with IgA nephropathy.

The serum levels of IgA class antibodies against autologous IgG Fc and Fab fragments were measured by ELISA in 62 patients with primary IgA nephropathy (IgAN) and 20 normal healthy volunteers. Both antibodies were significantly higher in the patients (P less than 0.01). The total IgA levels were correlated with those of IgA anti-IgG Fc antibodies (IgA anti-Fc) (rs = 0.57, P less than 0.001), but not with those of the IgA anti-IgG Fab antibodies (IgA anti-Fab). A histopathological comparison revealed that the sera of patients with severe glomerulonephritis had significantly higher levels of IgA anti-Fc than those with milder lesions (P less than 0.01). On the other hand, no correlation was observed between the serum levels of IgA anti-Fab and the histopathological severity. A comparison before and after treatment in 12 patients demonstrated a significant decrease of IgA anti-Fc (P less than 0.01) and an increase of IgA anti-Fab (P less than 0.05) after the treatment. Size analysis in serial sera from 3 patients was performed using HPLC under neutral (pH = 7.0) and under acid (pH = 3.5) buffer conditions. A markedly increased ratio of both antibodies with the polymeric form was observed in the active phase. In the remission phase, the amounts of acid-dissociable polymeric form IgA anti-Fc were decreased. In contrast, high levels of polymeric form IgA anti-Fab continued to be observed in 2 patients at this phase. These results suggest that abnormally stimulated production of IgA class autoantibodies especially with the polymeric form against both IgG Fc and Fab fragments, occurs in IgAN, involving separate regulation with differing reactions to treatment and a distinct relationship between IgA anti-Fc and active histopathological lesions.

Adolescent↗
PubMed1991

[A bull's eye subtraction polar map for assessing thallium redistribution (1). Comparison with quantitative redistribution].

A new bull's eye subtraction polar (BS) map has been developed for quantitative assessment of redistribution on stress-delayed thallium-201 SPECT studies. BS map was created after subtraction of a normalized stress bull's eye polar map from a normalized delayed polar map in 10 normal subjects and 33 patients with coronary artery disease to compare BS map with qualitative redistribution scores. The BS map showed less than 15% in all of the 50 segments in the normal subjects. Of 27 segments exhibiting persistent defect without redistribution, the BS map showed less than 10% in 20 segments (74%) and 10-15% in 6 segments (22%). On the other hand, of 34 segments exhibiting redistribution, the BS map showed greater than or equal to 15% in 25 segments (74%) and 10-15% in the remaining 9 segments (26%). Thus, significant redistribution was evident in the areas showing greater than or equal to 10-15% on the BS map. We conclude that the BS map is valuable for quantitative assessment of redistribution on stress-delayed thallium-201 SPECT imaging.

Adult↗
PubMed1991

Simple quantification of regional myocardial uptake of fluorine-18-deoxyglucose in the fasting condition.

Quantitative measurement of myocardial uptake of fluorine-18-deoxyglucose (FDG) is required for assessing tissue viability in the fasting state due to suppressed FDG uptake in the normal myocardium. A simple FDG uptake index (% dose per 100 ml tissue) has been introduced to compare with the fractional FDG uptake in 21 patients who underwent serial arterial blood sampling (14 under fasting and 7 under post-prandial conditions) and to measure the normal range in each myocardial segment in the study of 10 normal subjects (all in the fasting condition). Since the integral of plasma FDG values correlated with the body-weight corrected injected FDG dose (r = 0.82), an excellent correlation was observed between the FDG uptake index and the fractional FDG uptake (r = 0.98) in the fasting condition. In addition, the FDG uptake index correlated well with the regional metabolic rate of glucose calculated with the Patlak graphic analysis (r = 0.99). But this correlation was different in the postprandial condition and in the fasting condition in diabetic patients. In the study of normal subjects, the FDG uptake index was slightly higher in the lateral and inferior segments, as compared to the septal and anterior segments (p less than 0.05, each). We conclude that the FDG uptake index is considered as a simple and reliable parameter for quantitative assessment of myocardial FDG uptake in the nondiabetic patients in the fasting condition. Since its uptake was heterogeneous, FDG uptake should be carefully evaluated for assessing myocardial viability by comparing normal values in each segment.

Blood Glucose↗
PubMed1991

A new type of vasodilator, HA1077, an isoquinoline derivative, inhibits proliferation of bovine vascular smooth muscle cells in culture.

The effects of a newly developed vasodilator agent, HA1077 [1-(5-isoquinolinesulfonyl)-homopiperazine hydrochloride], were investigated on the proliferation of cultured bovine aortic vascular smooth muscle cells (VSMC). HA1077 (10-100 microM) inhibited both fetal calf serum-induced proliferation and [3H]thymidine incorporation into DNA of the growth-arrested VSMC in a dose-dependent manner. When quiescent cells were stimulated with platelet-derived growth factor followed by insulin, HA1077 (1-30 microM), administered together with either stimulation, showed dose-dependent inhibition of [3H]thymidine incorporation. Further reduction of [3H]thymidine incorporation was observed when HA1077 was present at both stimulations, suggesting that HA1077 suppresses DNA synthesis acting in both competence and progression stages. After stimulation with fetal calf serum, quiescent VSMC started and ceased DNA synthesis in 15 to 18 hr and 24 hr, respectively. HA1077 inhibited [3H]thymidine incorporation when it was added either from 12 hr to 15 hr or from 21 hr to 24 hr after serum stimulation. In addition, when percent inhibition of [3H]thymidine incorporation by continuous exposure to HA1077 was examined as a function of the time it was added, reductions of the value were observed at 0 to 3 hr, 12 to 18 hr and 21 to 24 hr. Thus, we concluded that HA1077 suppresses DNA synthesis of bovine VSMC acting at the G0/G1 and the G1/S phase transitions and also in the S phase of the cell cycle. It is suggested that this agent may act as a potent inhibitor of VSMC proliferation as well as a vasodilator.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Metabolic activity in the areas of new fill-in after thallium-201 reinjection: comparison with positron emission tomography using fluorine-18-deoxyglucose.

Reinjection of thallium-201 after recording the 3-hr delayed scan often demonstrates improvement in areas of persistent abnormalities. To determine the metabolic activity of these areas, the changes seen on stress/redistribution/reinjection thallium SPECT were compared with PET using fluorine-18-fluorodeoxyglucose (FDG) in 18 patients with coronary artery disease. Of 48 segments showing no redistribution on the delayed scan, the reinjection scan identified new fill-in in 20 segments (42%), all of which demonstrated FDG uptake. In contrast, only 7 of the 28 segments (25%) showing no fill-in after reinjection were PET viable (p less than 0.01). Eleven patients had coronary bypass graft surgery after the radionuclide study. The majority of the segments showing redistribution (87%) and new fill-in after reinjection (65%) improved in wall motion, whereas only eight segments (25%) without new fill-in improved after surgery. Of those without new fill-in, two segments showing PET ischemia improved in wall motion, whereas the remaining six segments showing PET scar did not improve after surgery. Thus, the segments showing new fill-in after reinjection are PET viable myocardium. However, reinjection thallium imaging still underestimates the extent of tissue viability compared to PET imaging.

Coronary Circulation↗
PubMed1991

Regional wall thickening of left ventricle evaluated by gated positron emission tomography in relation to myocardial perfusion and glucose metabolism.

Regional wall thickening was assessed by electrocardiographically gated positron emission tomography (ECG-gated PET) in 26 patients with coronary artery disease. The standardized percent count increase from end-diastole to end-systole (S-percent Cl) was calculated as an index of wall thickening. The S-percent Cl was 77.8% +/- 28.9% in the segments with normal perfusion at rest, 51.9% +/- 29.5% in those with mild hypoperfusion, and 32.8% +/- 30.9% in those with severe hypoperfusion (p less than 0.001, each). Among the segments with resting hypoperfusion, the S-percent Cl was 38.9% +/- 31.5% in those without stress-induced ischemia and 48.7% +/- 30.9% in those with ischemia (p less than 0.05). Furthermore, among resting severe hypoperfusion, the S-percent Cl was 23.0% +/- 23.9% in the segments without fluorine-18-fluorodeoxyglucose (FDG) uptake and 37.8 +/- 32.9% in those with FDG uptake (p less than 0.05). These results suggest that stress-induced ischemia and FDG accumulation correlated with wall thickening. Thus, quantitative analysis of regional wall thickening seems to be useful for combined analysis of regional function, perfusion and metabolism in coronary patients.

Adult↗
PubMed1991

Pathogenic role of polyclonal and polymeric IgA in a murine model of mesangial proliferative glomerulonephritis with IgA deposition.

Molecular size and charge distribution of IgA of sera and glomerular eluates were investigated in ddY mice, spontaneously developing mesangial proliferative glomerulonephritis (GN) with IgA deposition after 40 weeks of age. Serum IgA levels were increased in aged ddY mice more than 40 weeks old with a significant increase (P less than 0.01) at the age of 60 weeks, comparing with those of BALB/c mice. The isoelectric focusing (IEF) spectrotype of pooled serum IgA in 60-week-old mice ranged from 4.2 to 5.5, being similar to those in younger ddY (16 weeks old) and control BALB/c mice (12 weeks old) without enhanced expression of specific IgA peaks. However, IgA in the glomerular eluate from the 60-week-old mice showed limited anionic spectrotypes from pH 4.2 to 4.8. HPLC of IgA in pooled sera and glomerular eluates of 16-, 40- and 60-week-old ddY mice, revealed markedly increased ratios of the dimeric IgA (dIgA) and polymeric IgA (pIgA) in the total IgA with age. In the contrast to serum profiles, monomeric IgA (mIgA) was always detected as the smallest peak of the IgA fractions in glomerular eluates. Furthermore, aged mice with severe GN showed a higher percentage of dIgA and pIgA in total IgA (80%) in the sera than that of the mice with mild GN (64%). HPLC analysis under acid condition of glomerular IgA from 40-week-old ddY mice showed a similar pattern of dIgA and pIgA peaks in neutral buffer without the appearance of mIgA. These findings suggest that there is a selective mechanism for glomerular accumulation of more acid IgA among the polyclonally expanded IgA in old ddY mice, and that the polymeric form of IgA plays a pathogenic role in the development of mesangial proliferative GN in these mice.

Animals↗
PubMed1990

Stabilizing factor(s) of nitric oxide (NO) synthetase.

We found that the cytosol of rat peritoneal polymorphonuclear neutrophils contains factor(s) that can stabilize an unstable enzyme, nitric oxide synthetase, in the cytosol. This enzyme has been purified to a single protein from the cytosol. Its half-life was 3 hours at 4 degrees C and was prolonged to greater than 24 hours by the stabilizing factor in the cytosol. The molecular weight of the stabilizing factor was greater than 100,000. Its activity was lost by the treatment with heating or alkali for 1 min or with acid for 5 min. It did not adhere to the carboxymethyl or diethylaminoethyl column at neutral pH. This stabilizing factor(s) may play a role in the regulation of the nitric oxide synthetase.

Amino Acid Oxidoreductases↗
PubMed1990

Atrial natriuretic peptide reduces the basal level of cytosolic free Ca2+ in guinea pig cardiac myocytes.

The cytosolic free Ca2+ concentration ([Ca2+]i) was monitored in quiescent atrial and ventricular myocytes isolated from guinea-pig hearts by the fura-2 fluorescence ratio technique. Recombinant human atrial natriuretic peptide (ANP) was found to reduce their basal [Ca2+]i level in a dose-dependent manner. Dibutyryl-cGMP mimicked the effect of ANP. Neither the prior application of caffeine nor removal of extracellular Na+ impaired the ANP effect. ANP had no inhibitory effect on voltage-gated Ca2+ currents measured by a whole-cell patch clamp technique. The ANP-induced [Ca2+]i decrease was abolished by orthovanadate. Thus, it is concluded that ANP reduces the basal [Ca2+]i presumably through the cGMP-mediated activation of the plasma membrane Ca2(+)-pump in cardiac myocytes.

Animals↗
PubMed1990

A case of biopsy-proven myocarditis progressing to autopsy-proven dilated cardiomyopathy.

A 22-year-old man presented with congestive heart failure following flulike symptoms. The diagnosis of acute myocarditis was confirmed by endomyocardial biopsy, which revealed mild infiltration of inflammatory cells. A favorable response to beta-adrenergic receptor blockade was seen, and the patient was discharged without symptoms. Five months later, however, congestive heart failure recurred, and intracardiac thrombi were demonstrated. The patient died after two months. Postmortem examination revealed left ventricular dilatation with slight interstitial fibrosis; the diagnosis was dilated cardiomyopathy. Thus, progression of biopsy-proven myocarditis to dilated cardiomyopathy 10 months after the onset of disease was documented.

Adrenergic beta-Antagonists↗
PubMed1990

Identification and distribution of atrial natriuretic polypeptide in ventricular myocardium of humans with myocardial infarction.

The expression of atrial natriuretic polypeptide (ANP) in the ventricles of human hearts with myocardial infarction (MI) was studied immunohistochemically. Immunoreactive myocytes were identified in the ventricular tissues of all of 16 hearts with old MI (both with and without heart failure) and in all five hearts with subacute MI, but not in any of the eight hearts without MI nor in the five with acute MI. In the nonfailing hearts with MI, ANP positive myocytes surrounded the areas of infarction, and were also seen in the subendocardium of the infarcted segment. In the failing hearts with MI, ANP expression was noted in the whole ventricular subendocardial region, in addition to the border of infarcts. The sites of ANP expression corresponded well to those of marked stress attributable to tissue shrinkage or fibrosis due to MI, haemodynamic overload, or both. It thus appears that ANP expression is augmented in human hearts with MI regardless of the presence or absence of heart failure, and it is suggested that regional mechanical stress on the ventricular myocardium, as well as haemodynamic overload, may be very closely associated with ventricular ANP expression.

Aged↗
PubMed1990

Effects of nifedipine on cardiac function in patients with coronary artery disease evaluated with ambulatory radionuclide monitoring.

The effects of nifedipine on left ventricular function were evaluated in 17 patients with coronary artery disease with an ambulatory radionuclide detector (VEST). Hemodynamic data were recorded continuously at rest and during upright bicycle ergometer exercise before and 30 minutes after 10 mg of oral nifedipine administration. The heart rate increased and the resting systolic blood pressure decreased significantly with nifedipine. The end-diastolic and end-systolic volumes during exercise were significantly reduced and EF increased during exercise after nifedipine administration. These salutary hemodynamic responses of nifedipine appear to be beneficial for patients with effort angina pectoris.

Aged↗
PubMed1990

Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.

In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 +/- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 +/- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗