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Biomedical subjects

C Kawai

Publications and source records attributed to C Kawai.

At least 199 records · Page 11Linked to original sources
PubMed1989

Alterations in left ventricular relaxation, early diastolic filling and passive viscoelastic properties during postpacing ischemia.

Alterations in left ventricular relaxation, early diastolic filling, regional myocardial dynamics and passive viscoelastic properties during postpacing ischemia were studied in 9 patients with coronary artery disease. In all patients typical anginal pain developed during pacing tachycardia, and in the postpacing beat, left ventricular end-diastolic pressure increased from 14 +/- 4 to 26 +/- 5 mm Hg (mean +/- standard deviation, p less than 0.01), relaxation time constant increased from 44 +/- 9 to 59 +/- 7 ms (p less than 0.01) and ejection fraction diminished from 63.1 +/- 9.1 to 52.8 +/- 10.8% (p less than 0.01). However, peak rate of early left ventricular filling obtained from frame-by-frame analysis of left ventriculograms did not change significantly. The time difference from segmental peak lengthening to left ventricular peak filling increased significantly in the ischemic segment (32 +/- 30 vs 77 +/- 49 ms, p less than 0.05). Chamber stiffness constant of a viscoelastic model increased significantly from 0.0177 +/- 0.01 to 0.0354 +/- 0.015 (p less than 0.01) without change in chamber viscosity constant. In the ischemic segment, peak rate of lengthening decreased by 45% with ischemia, and peak rate of lengthening normalized for the end-diastolic segment length by 36%. However, peak rate of lengthening normalized for the extent of systolic shortening did not change. The control segment showed a tendency to increase in these 3 parameters, but the changes were not statistically significant. Thus, peak rate of segmental myocardial lengthening decreased with ischemia because of a decrease in segmental shortening.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of nifedipine on left ventricular distensibility, relaxation and filling dynamics during pacing-induced myocardial ischemia.

Diastolic left ventricular properties were assessed in 8 patients with coronary artery disease at rest and during postpacing states before and after nifedipine (10 mg sublingually). Typical anginal pain developed in all patients during pacing tachycardia before but not after nifedipine. Postpacing increases in end-diastolic pressure (10 +/- 5 [mean +/- standard deviation] to 23 +/- 9 mm Hg) and volume (99 +/- 29 to 113 +/- 27 ml) were greatly attenuated with nifedipine (13 +/- 7 and 97 +/- 22 ml, respectively). These responses were associated with normalization of postpacing shifts of the ventricular diastolic pressure-volume curve upward or more to the right. The time constant of ventricular relaxation was prolonged by pacing tachycardia (44 +/- 10 to 62 +/- 5 ms) and was reduced to the control level in postpacing beats after nifedipine. The peak rate of early ventricular filling was affected neither by pacing stress nor by nifedipine. When regional myocardial function was expressed by a radial coordinate system, the nonischemic segment responded to the control pacing with an increase in end-diastolic length and comparable augmentation of the stroke excursion, while the ischemic segment showed a marked reduction in stroke excursion with end-diastolic length unchanged. Thus, the diastolic pressure-length relation moved up to the higher portion of the single curve in the nonischemic segment, while it shifted directly upward in the ischemic segment. These responses were markedly attenuated with nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1989

Can new inodilators displace digitalis in the therapy of congestive heart failure?

New inodilators that possess both positive inotropic and vasodilator actions have many favorable effects in patients with congestive heart failure, even in those with refractory heart failure. These effects are expected to prevent myocardial injury, improve peripheral circulation, depress the excessive endogenous neurohumoral activation, and, finally, improve the quality of life, and increase lifespan. However, experience with new inodilators has only begun. Several questions remain to be answered before these drugs can be widely used with safety, including whether life-threatening adverse effects appear, mortality rate is lessened, and drug tolerance occurs. The therapeutic level of the dose and the relation between the effectiveness of the drug and the degree of the severity of heart failure should also be established. Therefore, long-term, randomized, double-blind, placebo-controlled clinical trials will be necessary before the new inodilators can take the place of digitalis and thus become the mainstay of the therapy of congestive heart failure.

Cardiotonic Agents↗
PubMed1989

Response of large and small coronary arteries of pigs to intracoronary injection of acetylcholine: angiographic and histologic analysis.

With coronary arteriography we examined the effect of acetylcholine (ACh) on large and small coronary arteries. ACh (12.5 to 200 micrograms) was injected into the right coronary arteries of 10 pigs during left ventricular pacing. The percentage of narrowing of the epicardial major coronary artery was used as an indicator of the constriction of the large coronary arteries, and the time required for the contrast medium to reach the posterior descending coronary artery from the ostium of the right coronary artery (blood-flow delay) was used as an indicator of the constriction of the same coronary arteries. A small dose of ACh (12.5 to 100 micrograms) induced mild narrowing (14 to 41%) of the epicardial major coronary artery and a marked blood-flow delay of over 7.0 sec (control: less than or equal to 1.8 sec) in all 10 pigs. A large dose of ACh (100 to 200 micrograms) caused over 75% narrowing of the epicardial major coronary artery and a marked blood-flow delay in 4 of the 10 pigs. When the marked blood-flow delay appeared, the perfused right ventricular myocardium became macroscopically anemic (ischemic). The constriction of large and small coronary arteries was not prevented by diphenhydramine (H1 blocker: 100 mg i.v.), but was prevented by pretreatment with atropine (1.0 mg i.v.). The intracoronary injection of histamine (1.5 mg) in 5 pigs constricted the epicardial major coronary artery over 75% in 2 pigs, 50 to 75% in 1 pig, and 25 to 50% in 2 pigs, but there was no evidence of blood-flow delay. Neither methoxamine nor norepinephrine caused any significant coronary artery narrowing. The histology of the large and small coronary arteries was examined quantitatively with an image analyzer. The coronary artery showed no intimal thickening, and the endothelium was intact on light microscopic examination. The % area of the smooth muscle layer (media) to the calculated total vascular area, and the ratio of the calculated medial thickness to the calculated inner radius (h/Ri) were 64 +/- 7% (mean +/- SD) and 0.69 +/- 0.16, respectively, in the small coronary arteries less than 100 microns in external diameter, 47 +/- 9% and 0.39 +/- 0.12 in the small coronary arteries 100 to 2000 microns in external diameter, and 34 +/- 4% and 0.24 +/- 0.03 in the large right coronary arteries over 2000 microns in external diameter; the % area of the media and the h/Ri showed a negative correlation with the size of the coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1989

Influence of propranolol on high energy phosphate and tissue acidosis in regional ischemic myocardium of pigs: assessment with arterial pressure and respiration gated in vivo 31-phosphorus magnetic resonance spectroscopy.

In an attempt to define the metabolic abnormalities of the ischemic myocardium, the changes in high energy phosphates, inorganic phosphate and intracellular pH were serially and quantitatively evaluated in ischemic porcine hearts having no collateral circulation, using arterial pressure and respiration gated in vivo 31P magnetic resonance spectroscopy. The protocol was also modified for propranolol pretreatment (0.6 mg/kg intravenously) to define its effect on the metabolism of ischemic myocardium. In the non-treated group, creatine phosphate was rapidly depleted by 10 minutes after ischemia; by 40 minutes, ATP and intracellular pH gradually decreased to 10 +/- 11% of control and to 5.90 +/- 0.26, respectively, and inorganic phosphate rose to 303 +/- 43% of control. In the propranolol treated group, the concentrations of creatine phosphate and ATP were higher, and those of inorganic phosphate and tissue pH were similar compared with controls during 40 minutes of ischemia. This suggests that the beneficial effect of propranolol on the ischemic myocardium is due to the preservation of ATP, an essential energy resource for numerous enzymatic reactions in viable myocardium.

Acid-Base Equilibrium↗
PubMed1989

Cineangiographic and pathological features of the infarct related vessel in successful and unsuccessful thrombolysis.

The postmortem histology and the results of cineangiography after selective intracoronary thrombolysis in vessels that were recanalized and in those that were not were compared in 21 patients who died within seven days (mean 2 days) of selective intracoronary thrombolysis. There was a persistent intraluminal thrombus in the infarct related coronary artery in five of six segments in which recanalisation was unsuccessful and in one of 15 segments in which recanalisation was successful. Rupture and haemorrhage of the atheromatous plaque were seen in most of the infarct related segments, both in those in which recanalisation was achieved and in those in which it was not. Irregular narrowing and filling defects on the coronary cineangiograms were associated with rupture and haemorrhage of the atheromatous plaque. These results suggest that failure of coronary thrombolysis to recanalize the infarct related artery does not indicate that the occlusion was not caused by thrombus.

Aged↗
PubMed1989

Immunoelectron microscopic localization of fibrin-related antigen in human glomerular diseases.

The distribution of fibrin-related antigen (FRA) in glomeruli was examined by immunoelectron microscopy in 9 patients with idiopathic membranous nephropathy (MN), 8 patients with minimal-change nephrotic syndrome, and 10 patients with IgA nephropathy (IgA-N), using antisera against human gamma--chain, alpha-chain, mu-chain, and fibrinogen. Electron-dense reaction products of FRA were observed in the endothelium, subendothelium, and/or in electron-dense deposits (EDD). Among the three glomerular diseases, the amount of electron-dense reaction products of FRA in the endothelium was highest in MN. This suggests that coagulation occurs on the endothelium in MN. Although the mesangial EDD of IgA-N were intensely stained with reaction products of FRA, the staining was weak in the subepithelial EDD of MN. This suggests that FRA hardly penetrates into the subepithelial EDD in MN.

Antigens↗
PubMed1989

Ultrastructural distribution of von Willebrand factor in human glomerular diseases.

The distribution of the von Willebrand factor (vWF) as the factor-VIII-related antigen in glomeruli was examined by immunoelectron microscopy in 10 patients with idiopathic membranous nephropathy (MN), 8 patients with minimal-change nephrotic syndrome (MCNS), and 11 patients with IgA nephropathy (IgA-N). Electron-dense reaction products of vWF were observed in the endothelium and mesangium in all specimens examined. However, they were not detected in subepithelial electron-dense deposits of MN. The amount of electron-dense reaction products of vWF in the endothelium was significantly higher in MN than that in MCNS or IgA-N. This finding suggests that the glomerular endothelium in MN is the site of the local activation of coagulation and platelet aggregation system in glomerular capillary wall lesions.

Glomerulonephritis, IGA↗
PubMed1989

Myocardial uptake of antimyosin monoclonal antibody in a murine model of viral myocarditis.

The myocardial uptake of 125I- and 131I-antimyosin monoclonal antibody Fab in experimental myocarditis in BALB/c mice induced by encephalomyocarditis virus was studied. The biodistribution of 125I-antimyosin demonstrated that the highest ratio of radioactivity appears in the heart of infected mice on day 14 (the ratio of percent dose per gram for the organ to percent dose per milliliter for blood; 9.75 +/- 2.79 vs. 1.27 +/- 0.78 at 24 hours in inoculated mice vs. control mice). There was no statistically significant difference between the mean activity ratios of tissues other than the heart in control and inoculated mice. The uptake ratio for the heart increased significantly 3 days after virus inoculation and reached a maximum on day 14 when myocardial lesions were most extensive and prominent. The uptake ratio decreased significantly, but it still remained high compared with controls on day 28 when cellular infiltration had decreased and fibrosis was evident. The scintigraphic images obtained with 131I-antimyosin monoclonal antibody clearly demonstrated that visualization of the heart in experimental myocarditis was possible 24 hours after administration of radiotracer, and localized activity was still observed in the 48-hour image. We conclude that antimyosin monoclonal antibodies localize selectively in the heart from the acute to subacute stage of viral myocarditis. These findings indicate that antimyosin scintigraphy is a reliable noninvasive method for the evaluation of patients suspected of having myocarditis.

Animals↗
PubMed1989

Induction of mRNA for low-density lipoprotein receptors in heterozygous Watanabe heritable hyperlipidemic rabbits treated with CS-514 (Pravastatin) and cholestyramine.

We administered CS-514, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, alone and in combination with cholestyramine to heterozygous Watanabe heritable hyperlipidemic rabbits. This rabbit model for heterozygous familial hypercholesterolemia has hepatic low-density lipoprotein receptors that are assumed to be half as many as in normal rabbits. CS-514 alone lowered plasma low-density lipoprotein cholesterol levels by 50%, and in combination with cholestyramine, it lowered levels by 80%. The membrane-binding assay showed these drugs caused 1.5- and 1.8-fold increases in the number of hepatic low-density lipoprotein receptors, respectively. We also measured the amount of mRNA for low-density lipoprotein receptor by S1 nuclease protection assay in the same livers as above. These drugs induced mutant mRNA for the low-density lipoprotein receptor, which has an in-flame deletion of 12 nucleotides, as well as normal receptor mRNA. CS-514 alone produced a 1.8-fold increase in the amount of mRNA for the normal receptor and a 2.3-fold increase for the mutant mRNA, whereas CS-514 in combination with cholestyramine produced 1.9- and 3.1-fold increases, respectively. We conclude that CS-514 induces mRNA for the low-density lipoprotein receptor, subsequently increasing the receptor protein in the liver, and then reduces the levels of plasma cholesterol, and that the induction is augmented when the drug is administered in combination with cholestyramine.

Animals↗
PubMed1989

Silent myocardial ischemia in patients with myocardial infarction: evaluation with positron emission computed tomography.

To evaluate myocardial blood flow and glucose utilization, N-13 ammonia and F-18 deoxyglucose positron emission tomography were performed in 33 patients with myocardial infarction. The N-13 ammonia study was performed at rest and during supine exercise, and the F-18 deoxyglucose was done at rest after greater than or equal to 5 hours of fasting. Based on angina, exercise-induced hypoperfusion, and deoxyglucose uptake, 3 groups of patients were classified; 10 patients in group I (neither angina nor exercise induced hypoperfusion), 8 patients in group II (painless exercise-induced hypoperfusion) and 15 patients in group III (anginal patients with/without exercise-induced hypoperfusion). The F-18 deoxyglucose positron study demonstrated accumulation of deoxyglucose in 6 patients in group I, 7 in group II, and 14 in group III. Thus, our results indicated that a significant number of patients with antecedent myocardial infarction had exercise-induced hypoperfusion and/or altered glucose metabolism without accompanying anginal pain.

Adult↗
PubMed1989

Liver function in congestive heart failure: abnormal elevation of serum hepatic enzyme and hepatic venous flow velocity.

Fifty one patients (pts) with various heart diseases and 6 normal subjects (N) were studied. Four of the 51 pts showed unusually high GOT values (greater than 3000 IU) without preceding evidence of acute heart failure, myocardial infarction, or hepatitis. Of these 4 pts, either ventricular tachyarrhythmias, marked bradycardia, or rapid ventricular response with atrial fibrillation (af) were evident a few days prior to the GOT elevation. GOT values returned to below 100 IU within a few days, but hypotension and frequent arrhythmias were sustained in 3 of the 4 pts and these 3 pts died about one month later. The symptoms of the remaining one improved but he too died 9 months later of ventricular fibrillation. A postmortem histological examination revealed centrilobular necrosis of the liver cells. Thus, abnormal GOT elevation may result from hepatic cell necrosis, which is probably due to tissue hypoperfusion caused by severe arrhythmias. Hepatic venous flow velocity (HFV) was measured in the remaining 47 pts and 6N using a pulsed doppler echocardiogram. The HFV curve was biphasic, with the first curve corresponding to the forward flow velocity during ventricular systole (s-HFV) and the second corresponding to ventricular diastole (d-HFV). The ratio of the area under s-HFV curve to the sum of areas under s-HFV and d-HFV curves was defined as the VI ratio. In N, the VI ratio was 0.7 +/- 0.06 whereas the VI ratio in pts in sinus rhythm tended to be above 0.7. This indicated that s-HFV is greater than d-HFV in N while s-HFV is less than d-HFV in pts in sinus rhythm. There was a good negative correlation (n = 15: r = -0.70) between VI ratio and cardiac index (CI) in these pts, suggesting that the contribution of s-HFV to the venous return becomes greater as the cardiac function becomes more impaired. In pts with af, the VI ratio was below 0.5 and there was a good positive correlation (n = 14: r = 0.82) between the VI ratio and CI. This suggested that the s-HFV may be reduced due to a lack of atrial contribution in af so that contribution of d-HFV to venous return becomes greater as the cardiac function becomes more impaired. Thus, the HFV pattern may reflect the abnormality of the cardiac pump function in human beings.

Adult↗
PubMed1989

Viral myocarditis: immunopathogenesis and the effect of immunosuppressive treatment in a murine model.

Serial changes in lymphocyte subset were investigated in an animal model of encephalomyocarditis (EMC) virus myocarditis in mice. The lymphocyte subset in the peripheral blood was measured by flow cytometry and, T cell subset in the myocardium was stained by labeled avidin-biotin technique. Helper-inducer T cells (Lyt 1 cells) decreased significantly on day 7, but there was no change in cytotoxic-suppressor T cells in the peripheral blood. During the acute stage a significant number of T cells (Thy 1.2 cells) were seen in the heart with helper-inducer T cells predominating. The effect of prednisolone and cyclosporine on viral myocarditis was studied in our experimental model. Prednisolone or cyclosporine given in the early stage aggravated the course, and they did not have beneficial effects during the early recovery period.

Acute Disease↗
PubMed1989

Effects of co-culture with vascular endothelial cells on the renin-like enzyme production in vascular smooth muscle cells.

Cultured human vascular smooth muscle cells (VSMC) produced an immunologically specific renin-like enzyme. The production of the renin-like enzyme was increased by 1 mM N6-O2'-dibutyryladenosine 3',5' cyclic monophosphoric acid sodium salt (db-cAMP). When co-cultured with human vascular endothelial cells (EC) and human skin fibroblast (FB), the basal production of the renin-like enzyme was increased. And the extent of the increase by db-cAMP was amplified by co-culture with EC, but not by the co-culture with FB.

Cells, Cultured↗
PubMed1989

Increased synthesis and secretion of atrial natriuretic polypeptide during viral myocarditis.

To elucidate the pathophysiological role of atrial natriuretic polypeptide (ANP) in diseased hearts, ANP levels in atrial and ventricular tissues and plasma were investigated in mice with congestive heart failure after viral myocarditis. The study was performed on day 14 after encephalomyocarditis viral inoculation, when congestive heart failure developed. The atrial ANP level increased to a value two times higher than that of noninoculated age-matched mice (the control mice). The ventricles of the control mice contained an approximately 1,000-fold lower ANP level than the atrial ANP level. The ventricular ANP concentration of the infected mice showed about a 21 times higher level than the control value. The plasma ANP level was also elevated 20 times. On immunofluorescence studies, increase of immunostaining were found in the atrial of the infected mice, and positive staining appeared on the cardiocytes in almost all areas of the remaining ventricular tissues of the infected mice, whereas staining was not found on the ventricles of the control mice. The staining seemed particularly strong in the area surrounding the myocardial lesions. These results indicate that atrial and ventricular ANP synthesis and ANP secretion increase in the heart with viral myocarditis. The marked increase in the ventricular ANP level suggests that the ventricle is another important production site for circulating ANP.

Animals↗