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Biomedical subjects

C Kawai

Publications and source records attributed to C Kawai.

At least 289 records · Page 16Linked to original sources
PubMed1987

Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.

The effect of pacing-induced ischemia on early left ventricular filling and regional myocardial lengthening was studied in 11 patients with coronary artery disease (CAD) and six control patients with normal coronary arteriograms. All of the 11 patients with CAD developed typical anginal pain during pacing tachycardia, and in the postpacing beat, the left ventricular end-diastolic pressure (LVEDP) rose from 13 +/- 4 to 26 +/- 4 mm Hg (mean +/- SD, p less than .01), the relaxation time constant increased from 43 +/- 9 to 59 +/- 7 msec (p less than .01), and the ejection fraction diminished from 62.1 +/- 6.7 to 51.6 +/- 10.6% (p less than .01). However, the peak rate of early left ventricular filling (LVPF) obtained from frame-by-frame analysis of left ventriculograms and the LVPF normalized for the stroke volume and for the end-diastolic volume did not change significantly. In the ischemic segment, the peak rate of lengthening (PL) decreased by 45% with ischemia, and the PL normalized for the end-diastolic segment length decreased by 42%. However, the PL normalized for the extent of systolic shortening did not change. In the control segment there was a tendency for these three variables to increase, but the changes were not statistically significant. The time difference from the PL to the LVPF increased significantly in the ischemic segment (31 +/- 28 vs 75 +/- 48 msec, p less than .05). Although the LVEDP rose slightly but significantly from 9 +/- 3 to 12 +/- 5 mm Hg (p less than .05) in the control patients in the postpacing beat, the other global hemodynamic variables and the variables of regional myocardial dynamics did not change. The administration of nifedipine in six patients with CAD resulted in the disappearance or diminution of anginal pain even with the same duration and rate of pacing and was associated with restoration of global systolic function and regional myocardial shortening and lengthening in the ischemic segment. In the control segment, the three variables of segmental lengthening increased with administration of nifedipine. Thus, the segmental myocardial lengthening rate decreased with ischemia due to a decrease in segmental shortening and impairment of myocardial distensibility. The LVPF did not decrease with ischemia despite impairment in isovolumetric relaxation, accentuation of asynchrony in left ventricular filling, and a decrease in the PL in the ischemic segment because of an increase in the PL in the nonischemic segment secondary to an increase in left ventricular filling pressure.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Immunologic identification of lymphocyte subsets in experimental murine myocarditis with encephalomyocarditis virus. Different kinetics of lymphocyte subsets between the heart and the peripheral blood, and significance of Thy 1.2+ (pan T) and Lyt 1+, 23+ (immature T) subsets in the development of myocarditis.

To clarify the immune mechanism in myocarditis, immunofluorescence techniques with laser flow cytometry were used to examine serial changes in lymphocyte subsets in the heart, spleen, and peripheral blood of DBA/2 and BALB/c mice inoculated with encephalomyocarditis virus (Experiment I). B cells were identified by staining with fluorescein isothiocyanate-labelled rabbit anti-mouse immunoglobulin. T-cell subsets were identified with rat anti-Thy 1.2, and nonpolymorphic Lyt 1 and Lyt 2 monoclonal antibodies plus fluorescein isothiocyanate-labelled anti-mouse immunoglobulin. On days 7 and 14 postinfection, the percentage of Thy 1.2+ (pan T) cells in both strains had decreased in the peripheral blood; B cells showed no significant changes throughout the entire period. On the other hand, Thy 1.2+ (pan T) and Lyt 1+, 23+ (precursor and immature) T cells appeared to occupy the major portion of the myocardium on days 7 and 14 when congestive heart failure developed. To confirm this, serial immunohistologic studies (immunoperoxidase staining) of the hearts of DBA/2 and BALB/c mice with encephalomyocarditis virus-induced myocarditis were performed (Experiment II). In Experiment II, most of the stained cells in the hearts of both strains were Thy 1.2 positive and Lyt 1 and Lyt 2 positive on days 7 and 14. Thus, Experiments I and II demonstrated that lymphocytes at the site of inflammation in acute viral myocarditis carried antigenic markers that differed from those of peripheral lymphocytes and suggested that Thy 1.2+ (pan T) cells, especially the Lyt 1+, 23+ subset (immature T cells and T-cell subset precursors) were involved in the development of myocarditis in these animals.

Animals↗
PubMed1987

Randomized double-blind trial of intracoronary urokinase for acute myocardial infarction: multicenter study.

The efficacy of intracoronary urokinase (UK) in an acute myocardial infarction has not been firmly established in a randomized fashion. Two hundred and ten patients were randomized to UK therapy (107 patients) and placebo (103 patients). Successful recanalization was achieved in 74% of the UK group vs 17% in the placebo group (p less than 0.01). The success rate was dose dependent up to 960,000 I.U. Clinical course was favorable and left ventricular enddiastolic pressure was reduced significantly in the UK group compared with the placebo group (p less than 0.05). Ejection fraction one month after the study was better in the reopened group than in the occluded group. Thus, early administration of UK can establish coronary reflow in a high proportion of patients and appears to favor the clinical course.

Aged↗
PubMed1987

Limitation of coronary thrombolysis: experimental study of reperfusion after ischemia.

Contraction band necrosis (CBN), coagulation necrosis (CN) and infarct size, expressed as CBN + CN, were quantitatively analyzed in 15 pig hearts without collateral circulation. The left anterior descending coronary artery was ligated for 60 and 120 minutes and then reperfused for eight hours (group 1 and 2, respectively). Five hearts were not reperfused (group 3). There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent infarct area of the perfused area in group 1, 2 and 3 were 80 +/- 9, 96 +/- 2% and 95 +/- 3%, respectively. The percent area of CBN was 68 +/- 11% in group 1, 2 +/- 1% in group 2 and 2 +/- 2% in group 3. We conclude that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even in reperfusion following one-hour occlusion. Therefore, in patients with acute myocardial infarction, coronary thrombolysis should be performed within one hour after the onset of the infarction to reduce the infarct size.

Animals↗
PubMed1987

Virus vaccine and passive immunization for the prevention of viral myocarditis in mice.

The effect of an inactivated virus vaccine and passive immunization was studied in an animal model of viral myocarditis. Encephalomyocarditis (EMC) virus was inactivated by 1:4000 formalin. Four-week-old CD-1 mice were injected subcutaneously and after 7 days intravenously with 0.1 ml vaccine. Seven days after the second vaccine, live EMC virus was inoculated intraperitoneally. None of ten mice with vaccine treatment died or showed myocardial lesions after challenge with EMC virus, whereas all ten mice without vaccine died 5-7 days after EMC virus inoculation and showed severe myocardial lesions. Hyperimmune rabbit serum, made by inactivated EMC virus, had a neutralizing antibody titer of 1:3000. Four-week-old BALB/c mice were injected intramuscularly with 1:10 dilution of hyperimmune rabbit serum in 6 groups (each, n = 10) on day -2, -1, 0, 1, 2, or 3, respectively, after inoculation with 10 plaque-forming units of EMC virus, and observed for 14 days. Eight mice infected with the virus without immune serum died and all ten mice showed severe myocardial lesions. No death or myocardial lesion was seen in mice with hyperimmune rabbit serum given on days -2 to 2. In this model, the virus vaccine prevented development of myocarditis, and passive immunization had a protective effect if given early after infection.

Animals↗
PubMed1987

Heparin requirement in tissue-type plasminogen activator-induced experimental coronary thrombolysis: comparison with urokinase-induced coronary thrombolysis.

The requirement of heparin in experimental coronary thrombolysis induced by tissue-type plasminogen activator (t-PA) was studied in closed-chest dogs with one hour old coronary thrombi and compared with that in urokinase (UK)-induced coronary thrombolysis. Animals were divided into 5 treatment groups as follows: group 1 received intracoronary t-PA alone (1,000 IU/kg/min; n = 5), and if thrombolysis was not induced within 40 to 50 min, dogs then received an intravenous injection of heparin (300 U/kg) plus intracoronary t-PA; group 2 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary t-PA (n = 5); group 3 also received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received t-PA but intravenously, as compared with the groups administered by the intracoronary route (n = 6); group 4 received intracoronary UK alone (1,000 IU/kg/min; n = 6); group 5 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary UK (n = 5). Thrombolysis was confirmed angiographically. In group I, coronary thrombolysis could not be induced within 44 +/- 4 min by intracoronary t-PA alone, but it occurred in 8 +/- 4 min when administered in combination with heparin in all dogs. Heparin alone failed to elicit reperfusion within 10 min in group 2, 3 and 5. t-PA, however, induced successful reperfusion in 16 +/- 5 min (group 2) and in 23 +/- 6 min (group 3), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Serum PGI2-regulating factors in acute myocardial infarction.

Human serum or plasma contains two factors which regulate PGI2 metabolism. The one is "PGI2-synthesis stimulating factor" which stimulates PGI2 synthesis in the vessel wall. The other is "PGI2-stabilizing factor" which stabilizes PGI2 in the blood. In the very early phase of acute myocardial infarction, the serum levels of these two factors were significantly reduced, which may be related to the thrombus formation in the coronary artery in acute myocardial infarction.

Blood Proteins↗
PubMed1987

Hemodynamic effect of oral TA-064 after dobutamine in congestive heart failure.

The hemodynamic effect of oral TA-064 (20 mg), a newly synthesized inotropic agent, was compared with that of intravenous dobutamine (5 micrograms/kg/min) in eight patients with congestive heart failure who had been treated with intravenous dobutamine, digitalis, diuretics, and prazosin. Hemodynamics was measured using a Swan-Ganz catheter during the pre-dobutamine control period, during dobutamine infusion period, during the pre-TA-064 control period and at 90 minutes after oral administration of TA-064. Stroke work index was increased and mean pulmonary capillary wedge pressure was decreased with TA-064 or dobutamine. Cardiac index and stroke index was increased by each drug, and pulmonary and systemic vascular resistances were decreased. Mean systemic arterial pressure, heart rate and pressure-rate product did not significantly change in comparison with the control level. In conclusion, TA-064 has a hemodynamic effect similar to that of dobutamine and may be useful as an oral substitute for dobutamine in patients with congestive heart failure after temporary management with dobutamine.

Administration, Oral↗
PubMed1987

Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different (p less than 0.01) among hearts with hypertrophic cardiomyopathy (12.6 +/- 4.0 and 8.2 +/- 3.3%), hypertensive hearts (6.6 +/- 3.6 and 2.5 +/- 1.4%) and normal hearts (2.8 +/- 1.2 and 1.0 +/- 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 +/- 4.2 in hypertrophic cardiomyopathy 2.5 +/- 1.7 in hypertensive hearts and 2.5 +/- 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.

Cardiomegaly↗
PubMed1987

Morphological features of hypertrophic cardiomyopathy with congestive heart failure and a small left ventricular cavity.

To clarify the morphologic basis of marked congestive heart failure in cases of hypertrophic cardiomyopathy with a small left ventricular cavity, the size of myocytes, the extent of myocardial fiber disarray and fibrosis were quantitatively evaluated in two autopsied cases. Compared with the control hypertrophic cardiomyopathy, both cases had larger myocytes and less fibrosis, and one of them had markedly extensive myocardial fiber disarray. Probably, the hypertrophy of the myocytes or myocardial fiber disarray or both rather than myocardial fibrosis are important in the pathogenesis of severe congestive heart failure in these cases.

Adult↗
PubMed1987

Pathogenesis and preventive and therapeutic trials in an animal model of dilated cardiomyopathy induced by a virus.

An animal model of dilated cardiomyopathy following encephalomyocarditis (EMC) virus has been developed. Virus was isolated from mouse hearts and viral antigens were detected in the myocardium until the second week of infection, but neither was found thereafter. Differences were found among different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathologic lesions. Thus, genetic factors may play an important role in the pathogenesis. Autoantibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Virus, vaccine, maternal vaccination, recombinant interferon alpha A/D and ribavirin were effective in protecting the mice from developing myocarditis. This animal model is suitable for studying the pathogenesis of viral myocarditis and evaluating preventive and therapeutic interventions of the condition.

Animals↗
PubMed1987

An analysis of regional left ventricular function utilizing pressure-length relationship in patients with coronary artery disease.

Mechanisms related to increased left ventricular filling pressure associated with myocardial ischemia were studied in 13 patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in the control and post-pacing periods. All patients developed typical anginal pain during pacing tachycardia. Seven patients (group I) demonstrated no significant changes in ejection fraction (EF) and peak systolic pressure-end-systolic volume ratio (P/Ves) after rapid pacing. End-diastolic pressure (EDP), however, increased significantly from 14.9 +/- 4.9 to 24.4 +/- 8.5 mmHg (p less than 0.01). Six patients (group II) exhibited significant decreases in EF and P/Ves. Here again, EDP increased significantly from 14.0 +/- 7.6 to 28.0 +/- 7.7 mmHg (p less than 0.01). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. In the normal segment, the end-diastolic length (EDL) was augmented by 13.6%, associated with a 22.4% increase in stroke excursion with pacing stress. In the ischemic segment, EDL remained unchanged, but stroke excursion was significantly reduced. The diastolic pressure-volume curve shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward in the ischemic segment, so that pressure was higher at any given segment length in the ischemic segment, indicating regional alteration of the diastolic properties. Thus, an ischemic response to pacing tachycardia involves both systolic and diastolic impairment, but the latter is more sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Diffuse triple-vessel coronary artery spasm complicated by idioventricular rhythm and syncope.

A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. Atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.

Aged↗
PubMed1987

Beneficial effects of nicorandil on cardiovascular hemodynamics and left ventricular function.

The effects of sublingual nicorandil (5 mg), an antianginal drug, were investigated in pacing-induced ischemia in 11 patients with coronary artery disease. Hemodynamic parameters were measured, and single-plane left ventriculograms were obtained in control and postpacing periods both before and after pretreatment with nicorandil. Regional wall motion of the left ventricle was assessed by measuring shortening of the radial axes originating from the center of the gravity of the end-diastolic silhouette. Heart rate, left ventricular (LV) systolic pressure, and end-diastolic volume index were not changed in immediate postpacing with or without medication. The LV end-diastolic pressure decreased from 22.0 +/- 1.8 (SEM) to 18.4 +/- 1.7 mm Hg (p less than 0.01) and LV systolic volume index from 48.5 +/- 7.1 to 37.4 +/- 7.7 ml/m2 (p less than 0.01). Ejection fraction increased from 42.2 +/- 3.7 to 56.7 +/- 3.7% (p less than 0.01), stroke index (SI) from 34.5 +/- 3.7 to 43.1 +/- 2.2 ml/beat/m2 (p less than 0.01), and cardiac index (calculated from heart rate and SI) from 2.49 +/- 0.30 to 3.09 +/- 0.19 L/min/m2 (p less than 0.01). With rapid right ventricular pacing, dyskinesis of the left ventricle increased in both area and degree, but was improved with premedication with nicorandil. Thus, nicorandil has salutary effects on ventricular contractile and hemodynamic responses to transient ischemia induced by pacing stress.

Angina Pectoris↗
PubMed1987

The effects of nifedipine and captopril on renal function in patients with essential hypertension: comparison with sodium nitroprusside.

In comparison with a nonspecific vasodilator, sodium nitroprusside (SNP), we intended to deduce the characteristics of nifedipine (NIF) and captopril (CAP) in the treatment of hypertension. Ten patients with essential hypertension were hospitalized and kept on a constant sodium diet (10 g NaCl/day). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured before and after the respective administration of SNP (0.9 +/- 0.5 mcg/kg/min), NIF (17 +/- 5 mg), and CAP (85 +/- 24 mg). SNP significantly reduced the mean blood pressure (MBP), the renal vascular resistance index (RVRI), urine volume (UV), urinary excretion of sodium (UNaV), and significantly raised active renin concentration (ARC), plasma norepinephrine (NE), and the heart rate (HR). RBF, GFR, and plasma epinephrine (E) were not changed. Compared with SNP, NIF significantly raised RBF, UV, UNaV, and fractional excretion of sodium (FENa) and significantly reduced RVRI. The differences between the increases in ARC, NE, and HR by NIF and those by SNP were not significant. GFR and E were not changed by NIF. Although CAP did not reduce MBP as much as SNP did, the increase in RBF by CAP was significantly greater than that by SNP. Changes in GFR, UV, UNaV, FENa, and E by CAP were not different than those by SNP. CAP increased ARC and did not raise E, NE, and HR. In conclusion, compared with SNP, NIF significantly raised RBF, UV, UNaV, and FENa and significantly reduced RVRI. On the other hand, the renal response to CAP was not very much different from the response to SNP. The characteristics of CAP were the suppressed sympathetic response to the decrease in blood pressure.

Adult↗