Search PubMed⌕ Search

Biomedical subjects

C Kawai

Publications and source records attributed to C Kawai.

At least 361 records · Page 20Linked to original sources
PubMed1985

The reliability of the tracing-method of fine cardiac fibrosis at a magnification of x10--preliminary study for quantitative analysis of fibrosis in large tissue sections of hearts with cardiomyopathy.

to define the reliability of the tracing method of fine fibrosis at low magnification (x10), the percentage area of fine fibrosis was compared between the traced pictures at magnifications of x10 and x250, using an image analyzer (Olympus VIP-21). A total of 25 tissue areas, each approximately 4 x 7 mm, from the inner and middle thirds of the left ventricular free wall and ventricular septum were selected from ten hearts with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) and were stained with Masson trichrome. The percentage areas of fine fibrosis traced at a magnification of x10 correlated well with those traced at a magnification of x250 (Y = 1.08X - 1.1, r = 0.95, P less than 0.01). It is concluded that the overall percentage area of fibrosis is the same at magnifications of x10 and x250, despite the fact that at x10 one is unable to detect individual fibers which can be detected at x250. The tracing method of fine cardiac fibrosis at a magnification of x10 is reliable. Therefore, fine fibrosis in large tissue sections of hearts with cardiomyopathy, such as entire transverse sections of the left ventricular wall, can be quantitatively analyzed by this method.

Cardiomyopathies↗
PubMed1985

Adaptations of the left ventricle to chronic volume overload induced by mitral regurgitation in conscious dogs.

To assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, enddiastolic (ED) D had increased by 9% from 34.2 +/- 2.4 mm (SEM) (P less than 0.001), with significant thinning of the wall thickness (from 8.2 to 7.7 mm, P less than 0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control, P less than 0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1985

Modification of pacing-induced alterations in diastolic properties of the regional myocardium by nifedipine in patients with coronary artery disease.

The effects of nifedipine on regional dysfunction during pacing-induced ischemia were studied in eight 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 both before and after pretreatment with nifedipine. All patients developed typical anginal pain during pacing tachycardia before but not after pretreatment with nifedipine. After pacing, left ventricular end-diastolic pressure (EDP) increased from 10 +/- 5 (SD) mmHg to 23 +/- 9 mmHg (P less than 0.01) with enlargement of the end-diastolic volume (EDV). The ejection fraction (EF) was reduced from 66 +/- 10% to 54 +/- 13% (P less than 0.05). With nifedipine, a post-pacing increase in EDP was markedly attenuated together with a 17% reduction in left ventricular systolic pressure (P less than 0.05). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length (EDL) was augmented by 14% (from 26.1 +/- 5.2 mm to 29.7 +/- 6.1 mm, P less than 0.01) associated with a 23% increase in stroke excursion (P less than 0.05) with pacing stress. In the ischemic segments, EDL remained unchanged in the post-pacing beat but stroke excursion was significantly reduced (from 11.4 +/- 5.2 mm to 4.3 +/- 1.8 mm, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Improved evaluation of hypertrophic cardiomyopathy by biventriculography with axial projection.

To delineate the precise anatomic abnormalities of the interventricular septum (IVS), mitral valve (MV), and left ventricular posterior wall (LVPW) in patients with hypertrophic cardiomyopathy (HCM), we used axial biventriculography (BVG) (hepato-clavicular projection: angled BVG) to examine 17 patients with HCM and four with concentric hypertrophy due to systemic hypertension. We also examined 9 of these 21 patients with conventional left anterior oblique (LAO) BVG (non-angled BVG). The IVS and along axis of the LV cavity when measured by angled BVG were significantly longer than when measured by non-angled BVG. The IVS, MV, and LVPW were better seen in profile in angled than in non-angled BVG. In two patients with HCM with obstruction (HOCM), systolic anterior motion of the anterior leaflet of the MV was readily identifiable with angled BVG, which is usually not the case with non-angled BVG. Thus, angled BVG is superior to conventional LAO BVG in the angiographic assessment of patients with HCM.

Adult↗
PubMed1985

Lactate metabolism in acute myocardial infarction and its relation to regional ventricular performance.

Myocardial metabolism was assessed in 20 patients with acute anterior myocardial infarction using lactate uptake (defined as (aortic lactate - great cardiac venous lactate)/aortic lactate X 100) as an index. The regional ejection fraction of the anterior wall was obtained from left ventriculography. There was a linear relation between lactate uptake and regional ejection fraction (r = 0.79, p less than 0.001). Four patients without total occlusion in the infarct vessel had a higher lactate uptake (19.6 +/- 6.7 versus 4.2 +/- 13.4%, p less than 0.05) and regional ejection fraction (26.3 +/- 7.9 versus 14.9 +/- 7.0%, p less than 0.05) than did 16 patients with total occlusion. The latter group of patients underwent intracoronary infusion of urokinase, which resulted in reperfusion in 13 patients. Lactate uptake before urokinase infusion (sample I), just after reperfusion (sample II), 30 minutes after reperfusion (sample III) and 4 weeks after reperfusion (sample IV) was 5.7 +/- 13.2, -13.9 +/- 14.7, 2.9 +/- 15.2 and 20.2 +/- 11.0%, respectively (sample I versus II and II versus III, p less than 0.01; sample I versus IV and III versus IV, p less than 0.05). The decrease in lactate uptake immediately after reperfusion, which was accompanied by an increase in creatine kinase-MB isoenzyme release into the blood, was considered to be the result of a "washout" effect. Lactate uptake was ameliorated 4 weeks later, accompanied by an improvement (from 15.1 +/- 7.1 to 23.4 +/- 7.2%, p less than 0.01) in the regional ejection fraction. It is concluded that the degree of asynergy was closely related to the extent of metabolic deterioration in myocardial infarction.

Acute Disease↗
PubMed1985

Changes in diastolic properties of the regional myocardium during pacing-induced ischemia in human subjects.

Mechanisms related to alterations in the diastolic properties of the left ventricle during angina were studied in seven patients with coronary artery disease. Single plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in both the resting state and immediately after rapid cardiac pacing. In all patients, typical anginal pain developed with pacing stress. After atrial pacing, the left ventricular end-diastolic pressure increased from 10 +/- 3 to 21 +/- 7 mm Hg (+/- standard deviation) (p less than 0.005) regardless of the changes in the end-diastolic volume. The ejection fraction was reduced from 59 +/- 10 to 48 +/- 13% (p less than 0.05). The diastolic pressure-volume curves shifted upward in post-pacing beats in four patients, while in three the curves shifted more to the right. The regional myocardial function was expressed in quantitative terms by a radial coordinate system with the origin at the center of gravity of the end-diastolic silhouette. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length was augmented by 15% (p less than 0.005) and was associated with a 24% increase in stroke excursion with pacing stress (p less than 0.05). The increase in diastolic pressure was accompanied by comparable increases in end-diastolic length, and the diastolic pressure-length relation moved up to the higher portion of the single curve. In the ischemic segment, the end-diastolic length remained unchanged in the post-pacing beat, but segment shortening was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Improvement in recovery of left ventricular function during reperfusion with coenzyme Q10 in isolated working rat heart.

To investigate the protective effect of coenzyme Q10 on left ventricular function during ischaemia and reperfusion, we studied isolated working rat hearts contracting 300 times per min perfused with Krebs-Henseleit solution at 37 degrees C. There was no significant difference in left ventricular end-diastolic pressure and left ventricular dP/dt between the coenzyme Q10-treated group (intravenous injection of 0.0115 mmol per kg of body weight, n = 7) and the vehicle-treated control group (n = 7) throughout 45 min of ischaemia and 30 min of reperfusion. The left ventricular peak systolic pressure in the coenzyme Q10-treated group was higher than in the vehicle-treated control group (48.7 +/- 10.9 versus 29.7 +/- 10.0 mmHg, p less than 0.05) after 30 min of reperfusion, although there was no significant difference between the two groups before and during ischaemia (45 min). During 5 to 30 min of the recovery period, the coronary sinus flow in the coenzyme Q10-treated group was greater than in the control group (5.4 +/- 1.8 versus 3.1 +/- 0.5 ml X min-1 after 30 min of recovery, p less than 0.05). It was concluded that coenzyme Q10 improved recovery of the left ventricular peak systolic pressure and the coronary sinus flow. Although it is possible that coenzyme Q10 facilitated ATP production and improved recovery, it is more likely that coenzyme Q10, which is an antioxidant, protected the myocardium against free radical damage during reperfusion.

Animals↗
PubMed1985

Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Mural thrombi in mice with acute viral myocarditis.

In an investigation of the relationship between mural thrombosis and congestive heart failure (CHF) in acute viral myocarditis, inbred BALB/c mice were inoculated intraperitoneally with the M variant of encephalomyocarditis (EMC) virus and sacrificed on days 7 (n = 33), 10 (n = 35) and 14 (n = 39). Myocarditis was found in 105 of 107 sacrificed mice (98.1%). Myocardial necrosis with cellular infiltration was evident after day 7 and was extensive in the ventricles and atria. In the 105 mice with myocarditis, 17 mice (16.2%) developed CHF after day 10, and 15 mice (14.3%) had thrombi as early as day 7. All thrombi were in the left and/or right atrium. The incidence of thrombi in mice with CHF was higher, but not significantly so, than that in mice without CHF (23.5% vs 12.5%). All 50 control mice had no myocardial lesions or thrombi. This study demonstrates that thrombus formation was not rare in the absence of CHF in the acute stage of viral myocarditis and suggests that clinically acute viral myocarditis has a risk of systemic and/or pulmonary embolism even when resting cardiac function is normal.

Acute Disease↗
PubMed1985

Number and size of myocytes, amount of interstitial space and extent of disarray of the hearts in patients with systemic hypertension and asymmetric septal hypertrophy.

Wall thickness, the extent of disarray, the number and the size of myocytes and the amount of interstitial space were measured in the ventricular septum (VS) and left ventricular (LV) free wall in hearts of 6 patients with chronic systemic hypertension and asymmetric septal hypertrophy (ASH). Twenty-five subjects (15 with no cardiac disease, and 10 with systemic hypertension) without ASH served as the controls. In the six patients with ASH, the degree of ASH ranged from 1.3 to 1.6. The extent of disarray in VS was 20% in one heart and within normal limits (mean +/- SD = 3 +/- 3%) in the other 5. The size of myocytes increased both in the VS and LV free wall and the VS/LV ratio ranged from 0.9 to 1.0. There was no significant difference in the % area of interstitial space between hearts with ASH and controls, and the VS/LV ratio ranged from 0.9 to 1.1. The number of transmural muscle layers (number of myocytes) was 680 +/- 90 in the VS and 440 +/- 40 in the LV free wall of these with ASH, and 500 +/- 60 in the VS and 490 +/- 60 in the LV free wall of control subjects. The VS/LV ratio of the number of myocytes ranged from 1.3 to 1.7 and was correlated with the VS/LV ratio of wall thickness. Although the sample is small, our findings suggest that most hearts from patients with chronic systemic hypertension and ASH have no diffuse disarray in the VS and that ASH probably occurs secondary to pressure overload.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

A new stable prostacyclin analogue OP41483 (15-cyclopentyl-omega-pentanor-5(E)-carbacyclin).

Effects of a new stable prostacyclin analogue OP41483 (15-cyclopentyl-omega-pentanor-5(E)-carbacyclin) on platelet aggregation, plasma thromboxane B2 levels, hemodynamic parameters, and clinical safety were studied. Normal volunteers received intravenous infusions of OP41483 at doses of 2.5 (n = 3), 5.0 (n = 3), 10 (n = 3), and 20 (n = 5) ng/kg/min for one hour. During infusion, ADP (adenosine diphosphate)-induced platelet aggregation decreased significantly, and blood pressure decreased slightly, but plasma thromboxane B2 levels did not change significantly. The intravenous infusion of OP41483 at the dose of 10 ng/kg/min for one hour over three successive days was performed. During the each infusion, platelet aggregation and mean blood pressure decreased significantly.

Adult↗
PubMed1985

Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations.

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.

Adult↗
PubMed1985

Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction.

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.

Aged↗
PubMed1985

Left ventricular responses to supine bicycle exercise assessed by radionuclide angiocardiography and a Swan-Ganz catheter.

Left ventricular responses to supine bicycle ergometer exercise were studied by gated radionuclide angiocardiography (RNA), in 12 normal subjects (group A), 11 coronary patients without effort angina (group B) and 17 coronary patients with effort angina (group C). In the serial measurement of global ejection fraction (EF) there was a significant increase during peak exercise (PEx) in group A and B. In group C, global EF during mild exercise (MEx) did not increase, but decreased significantly during PEx. These results suggest the necessity of achieving adequate exercise loading in the diagnosis of exercise-induced ischemia, and also, that the serial measurement of global EF during exercise appears to be highly valuable. In the assessment of regional wall motion on the basis of regional EF, abnormal responses to exercise were highly inducible in the anteroseptal region in coronary patients with left anterior descending artery involvement. Abnormal wall motion in the other regions was less indicative for right coronary or left circumflex artery dysfunction. We examined hemodynamic responses to exercise by a Swan-Ganz catheter during RNA study in 5 patients of group A, 5 of group B, and 9 of group C. There was a large increase in left ventricular stroke work index (LVSWI) with a small rise in pulmonary capillary wedge pressure (PCWP) in group A. In group B LVSWI increased with a moderate rise in PCWP during PEx. In group C there was a negligible increase of LVSWI despite a marked rise in PCWP. A similar relationship was present between the LVSWI and the end-diastolic count (EDC) in the left ventricular region of interest. In MEx, however, the rise in PCWP in group C was more prominent than the increase in EDC. Thus, the present data indicate that the left ventricle in group C operates on a steeper portion of the diastolic pressure-volume curve than that in group A or B.

Adult↗
PubMed1985

Acute myocardial infarction associated with systemic lupus erythematosus documented by coronary arteriograms.

A 19-year-old man with untreated systemic lupus erythematosus had an acute myocardial infarction. A coronary arteriogram five hours after the onset of symptoms revealed total occlusion of the left anterior descending coronary artery. Reperfusion was achieved by coronary thrombolytic therapy with urokinase. Four weeks later, a coronary arteriogram showed only minimal luminal irregularities at the original site of occlusion, where significant reduction in diameter could be induced by ergonovine maleate. This case suggests that coronary arterial involvement in systemic lupus erythematosus may be related to coronary arterial spasm.

Adult↗
PubMed1985

Effects of enalapril maleate (MK-421) on renovascular hypertension.

The effects of enalapril maleate (MK-421), a new angiotensin converting enzyme inhibitor, were studied on 5 patients with renovascular hypertension (RVH) due to unilateral renal artery stenosis. The therapeutic dosage was increased when the blood pressure (BP) was not controlled for more than 3 days. Blood sampling was performed before, and 5 hr and 24 hr after the first administration, and on the 3rd day with each dosage. The BP was normalized on 5 mg/day in 1 case, 10 mg in 1 case, 20 mg in 2 cases, and 40 mg plus mefruside in 1 case. Plasma renin activity (PRA) was significantly increased after 5 hr and recovered after 24 hr with 2.5 mg of the enalapril maleate, when the BP was not affected. This indicates that the increase in PRA is likely due to the reduced negative feedback of angiotensin II. When the blood pressure was lowered, PRA was increased and plasma aldosterone concentration (PAC) was decreased significantly. This rise of PRA may depend not only on the reduced negative feedback but also on the fall of BP. It is also considered that the PAC was decreased through the decrease in plasma angiotensin II. A fall of the glomerular filtration rate in one case and also a fall of the perfusion of the kidney of the stenotic side in another case were observed by radioisotope renograms. MK-421 administration was a useful treatment for RVH, and clearly normalized the BP of all the patients studied. However, there was a risk of a fall of renal function on the stenotic side due to the decrease in perfusion pressure.

Adolescent↗
PubMed1985

Production and release of inactive renin by human vascular smooth muscle cells.

Human arterial smooth muscle cells were obtained from surgically excised tissues and cultured by the explant method. The cultured cells had both active and inactive forms of an angiotensin I forming enzyme. About a five-fold increase in the activity was obtained by trypsin treatment. This renin-like enzyme was also found in abundance in the culture media, mostly in an inactive form. Most of the enzyme activity, either before or after the activation, was suppressed by an antibody specific to human renin. The inactive enzyme was activated to some extent also by acidification and by cold exposure. The molecular weight of the inactive enzyme was estimated to be approximately 49,000 by gel filtration. These results suggest that human vascular smooth muscle cells can produce renin and release an inactive form of renin, and can be a potential source of plasma inactive renin under certain conditions such as the anephric state.

Angiotensin I↗