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Biomedical subjects

H Katsume

Publications and source records attributed to H Katsume.

At least 91 records · Page 5Linked to original sources
PubMed1983

The restorative action of coenzyme Q10 in 2,4-dinitrophenol-depressed electrical and contractile activities of guinea-pig heart.

With electrophysiological methods, mechanisms of the restorative action of coenzyme Q10 (CoQ10) in 2,4-dinitrophenol-depressed electrical and mechanical activities of isolated guinea-pig hearts were studied. Isoproterenol (3 X 10(-8) M)-induced action potential and contraction of the heart in 27 mM KCl Tyrode solution were abolished by 6 X 10(-6) M 2,4-dinitrophenol, while the additional application of CoQ10 (50 micrograms/ml) restored both these activities of the heart. This restorative action of CoQ10 was dose related (2 to 50 micrograms/ml) and was inhibited by 10 micrograms/ml 15-hydroperoxyarachidonic acid (15-HPAA) or pretreatment of the animals with indomethacin (5 mg/kg i.v.). When exogenously applied, 200 ng/ml prostacyclin also restored the 2,4-dinitrophenol-depressed electrical and contractile activities of the heart, but this restorative action of prostacyclin was affected neither by 15-HPAA nor by indomethacin pretreatment. These results suggest the possible participation of prostacyclin in the restorative action of CoQ10 in 2,4-dinitrophenol-depressed electrical and mechanical activities of the heart.

2,4-Dinitrophenol↗
PubMed1983

Left ventricular size and performance during graded supine exercise in normal subjects.

To investigate left ventricular size and performance during graded submaximal exercise, 14 normal subjects with a mean age of 21 years exercised in a supine position to achieve the target heart rate. Using two-dimensional echocardiography, we recorded and analysed the left ventricular (LV) cross-sectional area and internal dimension at the level of the tips of the mitral valve at rest and during mild, moderate and severe exercise. The heart rate and systolic blood pressure increased substantially from rest to peak exercise (71 +/- 11 to 162 +/- 10 beats/min, 122 +/- 10 to 204 +/- 22 mmHg). The end-diastolic cross-sectional area and internal dimension (EDA & EDD) increased by 1.1-2.2 cm2 (7-13%) and 0.2-0.3 cm (4-7%), respectively, from mild to moderate exercise, (p less than 0.05-0.001). At peak exercise, however, these decreased and showed no statistically significant difference from the values at rest. The end-systolic cross-sectional area and internal dimension (ESA & ESD) decreased by 1.1 to 1.6 cm2 (14-20%) and 0.2-0.3 cm (7-10%), respectively, from moderate to severe exercise (p less than 0.01-0.001). However, the end-systolic values during mild exercise were not significantly different from those at rest. The stroke area (EDA-ESA) and dimension (EDD-ESD) increased by 1.6-2.6 cm2 (19-31%) and 0.2-0.6 cm (25-38%), respectively, during all levels of graded exercise (p less than 0.05-0.001). The percent change of LV cross-sectional area and internal dimension during systole increased gradually from rest to moderate exercise (51.0 +/- 7.1 to 61.9 +/- 4.4%, 35.4 +/- 3.9 to 45.0 +/- 3.7%), respectively, and showed no further increase during peak exercise. The mean circumferential fiber shortening velocity increased sharply from rest to peak exercise (1.27 +/- 0.14 to 2.25 +/- 0.21 circ/sec). These results suggest that the Frank-Starling mechanism operates during mild to moderate exercise, and contractility increases markedly at moderate to severe exercise levels as cardiac performance is augmented during graded submaximal exercise.

Adolescent↗
PubMed1983

[Analysis of coronary hemodynamics in exercise by T1-201 scintigraphy: examination of rates of change of cardiac output, myocardial blood flow distribution, coronary blood flow and coronary vascular resistance].

From our observation that initial distribution of 201T1 in tissue is mainly dependent on blood flow distribution, we designed the method to obtain the rates of change of coronary blood flow and coronary vascular resistance and applied it to the analysis of coronary hemodynamics in patients with ischemic heart disease during submaximal exercise. We measured the rates of change of cardiac output (delta CO) and myocardial blood flow distribution (delta Fract ) in two occasions by the sequential two injections of T1, and obtained the rate of change of coronary blood flow (delta Flow) from delta CO and delta Fract . Using the rate of change of mean blood pressure, we calculated also the rate of change of coronary vascular resistance (delta CVR). The initial components of histograms of the right ventricle by the first and second injections of T1 were fitted into gamma function curve. S1 and S2 were the areas bounded by the curve and baseline of the first and second injections, and then the cardiac output ratio was estimated by R X S1/S2, where R was the dose ratio measured by another camera system. The five min count rates on the myocardium by the first (H1) and second (H2) injections of T1 were calculated five min after the injection. H2 was approximately H1 X R in the same condition of T1 injection but H2 was not equal to H1 X R, when the T1 injection was done in the different loading condition. Therefore the rate of change of myocardial blood flow distribution was calculated as delta Fract = (H1 X R-H2)/H2.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1982

Comparative study of two methods of estimating sinoatrial conduction time in patients with abnormal sinus node function.

This study compared a new method to estimate sinoatrial conduction time (SACT) using continuous atrial pacing proposed by Narula et al with the widely used method using premature atrial stimulation originally proposed by Strauss et al. The estimated SACTs by the two methods were obtained in 19 patients with normal sinus node (SN) function (Group A) and 8 patients with abnormal SN function (Group B). Estimate of the SACT by the Narula method was taken as the difference between the first atrial return cycle after pacing and the basic sinus cycle length (BSCL). The Narula method was performed for a train of 8 consecutive beats at three different pacing cycle length (PCL); PCL (1) greater than or equal to BSCL--50, PCL (2) greater than or equal to BSCL--100 and PCL (3) greater than or equal to BSCL--150 msec. In group A, the estimated SACTs by the Strauss method was 185 +/- 49.3 msec, meanwhile the SACTs by the Narula method were 148 +/- 80.7 at PCL (1), 181 +/- 58.7 at PCL (2) and 212 +/- 84.5 msec at PCL (3) (mean +/- SD); the coefficient of correlation between the Strauss method and the Narula method were 0.58, 0.84, and 0.67, respectively. On the other hand, in group B, atrial return cycles by the Narula method were abnormally prolonged (over 215 msec) in 5 of 8 cases (63%) even at PCL (2) and in all of the cases (100%) at PCL (3). By the Strauss method, SACTs in 6 of 8 cases could not be defined; however it was possible to assess the type of SN dysfunction by the pattern of the atrial return cycles. In conclusion, the estimated SACT by the Narula method at PCL (2) corresponded well with the SACT by the Strauss method in patients with normal SN function. However, it was difficult to determine SACT in patients with Sick Sinus Syndrome by both methods.

Adult↗
PubMed1982

[Two-dimensional echocardiographic evaluation of the right ventricular wall in hypertension and hypertrophic cardiomyopathy].

The thickness and motion of the right ventricular wall (RVW) were studied with two-dimensional echocardiography from a subxiphoid approach in 20 normal subjects (N Group), 86 patients with hypertension (HT Group) and 20 patients with hypertrophic cardiomyopathy (HCM Group). Comparison was made between the patients with and without echocardiographic RVW hypertrophy in each patient group in regard to the thickness of the interventricular septum (IVS) and the left ventricular posterior wall (LVPW) as well as the motion of the RVW and cardiac catheterization data. 1. RVW hypertrophy was visualized in 39.5% of the HT Group and in 40% of the HCM Group. There was no difference in the thickness of RVW between the two groups. 2. A localized hypertrophy and an abnormal motion of RVW were obtained in the HCM Group, but not in the HT Group. 3. RVW hypertrophy in the HT Group was seen in patients with marked IVS hypertrophy, while that in the HCM Group was not related to IVS hypertrophy. 4. Pulmonary arterial pressure remained normal in each group. Therefore, RVW hypertrophy did not appear to be the result of pressure overload. 5. Right atrial mean pressure and right ventricular end-diastolic pressure were elevated only in HCM patients with RVW hypertrophy. We conclude that there is a different mechanism in the mode of production of RVW hypertrophy between patients with hypertension and those with hypertrophic cardiomyopathy.

Cardiac Volume↗
PubMed1982

[Cardiotoxicity of daunorubicin and aclacinomycin A in patients with acute leukemia].

Anthracycline antibiotics are principal agents in the treatment of acute non-lymphocytic leukemia, although the usefulness are limited by their adverse side effects, especially by the cardiotoxicity. Aclacinomycin A (ACM) is known to be a new anthracycline antibiotic which has been isolated from Streptomyces galilaeus, and its cardiotoxicity on the experimental animal systems was reported to be more than 10 times lower than that of adriamycin. We investigated the cardiotoxicity of ACM on 29 patients with acute leukemia and compared it with daunorubicin (DNR). The measurement of STI (PEP:LVET) has been recommended to be convenient method of assessing the anthracycline cardiotoxicity, but through out analytical study, QTC measurement was proved to be more valuable for the simple and rapid detection of the cardiotoxicity induced by the agents. In comparison with the QTCs in DNR and ACM, the cardiotoxicity of ACM was much lower than that of DNR, and the reversibility of ACM induced cardiotoxicity was much more rapid. Moreover, these effects were observed even in the patients treated with the maximum dose of DNR. Therefore, ACM was expected to be one of the agents of the first choice for the relapsed cases of acute leukemia, especially APL.

Aclarubicin↗
PubMed1982

[Analysis of end-systolic pressure-volume relation by gated radionuclide angiocardiography].

Left ventricular end-systolic pressure-volume relation has been proved experimentally to be an useful index of left ventricular contractility relatively independent of preload or afterload. But less clinical application has been reported because of its invasive nature, and we evaluated this relationship non-invasively using gated radionuclide angiocardiography as volume determination and cuff sphyngomanometer in the arm as pressure measurement. Gated equilibrium blood pool scintigrams were obtained at rest and during intravenous infusion of angiotensin or nitrate. Ventricular volumes were derived from ventricular activity and peripheral blood volume and activity. The peak systolic pressure (PSP) by cuff method to end-systolic volume index (ESVI) relations showed good linearity (r greater than .930 in 84% of consecutive 50 cases) and were gentler in the groups with more impaired left ventricular function. Emax was related exponentially to ejection fraction (EF) and hyperbolically to end-diastolic volume index. The dead volume (VoI) was unfixed and fell into positive or negative value, and was not related to EF under control condition. PSP/ESVI in each loading condition was less variable with the alteration of blood pressure than EF. The linear relation was found between PSP/ESVI under control condition and Emax (PSP/ESVI = 0.651 . Emax + 0.958, r = 0.841, p less than .001). Thus in measuring ventricular volume, gated radionuclide angiocardiography is a non-invasive method less affected by the geometry of the left ventricle. Non-invasive determination of end-systolic pressure-volume relation using the volume by radionuclide and the blood pressure by cuff method is clinically useful in the assessment of left ventricular contractility.

Angiocardiography↗
PubMed1981

[Analysis of left to right ventricular stroke count ratio by gated radionuclide angiocardiography: detection and quantitation of valvular regurgitation and shunts (author's transl)].

The stroke count ratio (SC ratio: SCL/SCR) for left to right ventricular enddiastolic-endsystolic count differences was obtained from LAO multi-gated cardiac blood pool scintigrams for quantitative assessment of valvular regurgitation and shunts. SC ratio, 1.48 +/- 0.24 (mean +/- S.D.) in 21 normal subjects, was decreased in 7 patients with atrial septal defects (ASD) and in one with isolated tricuspid regurgitation (TR), and increased in 15 patients with aortic regurgitation (AR) and in 6 with mitral regurgitation (MR). In post-surgical reassessment of 3 patients, the ratio was restored in normal range. Comparison between SC ratio and angiographic estimates of regurgitation revealed good agreement. Regurgitant fraction (RF) in AR or MR and shunt ratio (SR) in ASD were calculated by the formula: RF = 1-1.48/SC ratio, and SR = 1-SC ratio/1.48, respectively. These were derived by assuming that an excess of stroke counts was due to regurgitant or shunt flow and that the coefficient in counting ventricular radioactivity was 1.48. Agreement was found between RF or SR measured by this formula and by the invasive method. This method permits noninvasive quantitation in patients with valvular regurgitation and shunts without complicated computer procedures.

Aortic Valve Insufficiency↗