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Biomedical subjects

M Fukunami

Publications and source records attributed to M Fukunami.

47 records · Page 3Linked to original sources
PubMed1985

Loading sequence is a major determinant of afterload-dependent relaxation in intact canine heart.

To elucidate the role of loading sequence in afterload-dependent slowed relaxation in hearts in situ, the time constants (Texp from best exponential fitting method and TL from semilogarithmic method) of isovolumetric left ventricular (LV) pressure decay were studied in nine anesthetized open-chest dogs under the pharmacological blockade of autonomic nerve activity. An afterload change was imposed by clamping the ascending or descending aorta to make the peak LV pressure early or late in systole. During afterload interventions, in contractions with the peak LV pressure in late systole Texp and TL were significantly (P less than 0.05) larger than in those with the peak LV pressure in early systole in any comparable peak LV pressure range. Moreover, both time constants were directly correlated (P less than 0.01) with the time of peak LV pressure irrespective of peak LV pressure and clamp mode of aorta. In another protocol, marked differences both in Texp and TL were also observed between each of 25 pairs of contractions with different loading sequence but with comparable peak LV pressure and LV dimension (segment length). Thus afterload-dependent slowed relaxation in hearts in situ could not be attributed to an increased total load but to the altered loading sequence associated with an increase in afterload.

Animals↗
PubMed1984

Computer-assisted education system for arrhythmia (CAESAR).

A computer-assisted education system for arrhythmia (CAESAR) was developed for students to acquire the ability to logically diagnose complicated arrhythmias. This system has a logical simulator of cardiac rhythm using a mathematical model of the impulse formation and conduction system of the heart. A simulated arrhythmia (ECG pattern) is given on a graphic display unit with simulated series of the action potential of five pacemaker centers and the "ladder diagram" of impulse formation and conduction, which show the mechanism of that arrhythmia. For the purpose of the evaluation of this system, 13 medical students were given two types of tests concerning arrhythmias before and after 2-hr learning with this system. The scores they obtained after learning increased significantly from 73.3 +/- 11.9 to 93.2 +/- 3.0 (P less than 0.001) in one test and from 47.2 +/- 17.9 to 64.9 +/- 19.6 (P less than 0.001) in another one. These results proved that this CAI system is useful and effective for training ECG interpretation of arrhythmias.

Arrhythmias, Cardiac↗
PubMed1984

Ejection timing as a major determinant of left ventricular relaxation rate in isolated perfused canine heart.

In the present study, we attempted to test the hypothesis that ejection timing rather than peak left ventricular pressure is a primary determinant of ventricular relaxation rate. In cross-circulated isolated canine hearts instantaneous left ventricular volume was controlled by a servo-pump system. To eliminate the effects of end-systolic and end-diastolic volumes and ejection velocity on left ventricular relaxation rate, these parameters were clamped, and only the ejection timing (onset and end of ejection) was altered, keeping the duration of ejection unchanged. Left ventricular relaxation rate was assessed by time constants of left ventricular pressure decline during the isovolumic relaxation phase calculated by both a semilogarithmic method, assuming that the asymptote is zero, and a best exponential fitting method. In 25 runs, a pair of contractions with ejection timings which differed by 53.1 +/- 2.1 (SE) msec were imposed, while end-systolic and end-diastolic left ventricular volumes and ejection duration were unchanged. All pairs of contractions demonstrated early ejection resulted in significantly (P less than 0.001) slowed relaxation as indicated by a prolongation of the time constants of isovolumic left ventricular pressure decay (delta 4.2 +/- 0.7, sec and delta 15.4 +/- 2.1 msec by semilogarithmic plot and the best exponential fit respectively), although peak left ventricular pressures (104.6 +/- 2.4 mm Hg) were even lower than those (116.6 +/- 2.8 mm Hg) in contractions with later ejection timing. Furthermore, in seven experiments, the heart was allowed to eject at five different timings; onset and end of ejection were progressively delayed in steps of 20 or 30 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl] -2(1H)-quinolinone (OPC-8212), a new inotropic agent, on cardiotonic activity and coronary hemodynamics.

Cardiotonic activity and chronotropic effect of a new positive inotropic agent, 3,4-dihydro-6-[4-(3,4- dimethoxybenzoyl )-1-piperazinyl]-2(1H)- qu inolinone ( OPC -8212), were studied in isolated canine hearts eliminating the secondary effect due to neurohumoral alterations. Positive inotropic action of OPC -8212 was dose-dependent and its potency was equivalent to about 1/10(5) of isoprenaline (isoproterenol). However, the duration of action was two to three times longer than that of isoprenaline, and arrhythmogenic activity was not observed at any dose studied. An index of inotropic state, Emax, was increased by this agent even under the blockade of beta-adrenoceptors, indicating that the positive inotropic effect of this agent is not due to a stimulation of beta-adrenoceptors. the ventricular relaxation rate was enhanced dose-dependently in similar extent to the equivalent dose of isoprenaline. Effects of this agent on coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were also assessed in open chest dogs, eliminating secondary increases in these parameters due to an increase in mechanical load or heart rate. OPC -8212 increased MVO2 significantly even without significant alterations in heart rate and LV pressure. These increases both in CBF and MVO2 were similar to those of isoprenaline while arterio-venous difference in oxygen content was not affected by OPC -8212. Thus, we conclude that the efficiency of myocardial oxygenation of OPC -8212 is similar to that of isoprenaline and a direct coronary vasodilatory effect of this agent is minimal.

Animals↗
PubMed1981

Inverse solution of ST vector as a single unfixed location dipole in patients with acute myocardial infarction.

For the quantitative assessment of infarct site and size in patients with acute myocardial infarction, an attempt was made to solve the inverse problem, that is, to characterize ST vector in the infarcted myocardium from ST segment deviations in 29 precordial leads and their sterical positions A simple inverse model was employed, assuming that the source origin of ST segment displacement in surface electrocardiograms was a single unfixed dipole embedded in the homogeneous infinite medium. The magnitude, direction and position of ST vector were calculated as an inverse solution by computer. The direction of ST vector determined by this inverse problem was well in accord with infarct site assessed by left ventriculography or myocardial scintigraphy carried out later. However, the magnitude of ST vector was poorly correlated (r = 0.47, p less than 0.005, n = 17) with infarct size estimated from serum creatine phosphokinase, although a good correlation (r = 0.74) was obtained when 3 cases with extremely large infarction were excluded. These results suggest that our inverse solution of ST vector is useful for prediction of the site and size of acute myocardial infarction.

Aged↗
PubMed1981

The reappraisal fo ST segment elevation as an index of infarct size in patients with acute anterior myocardial infarction.

The clinical meaning or precordial ST segment mapping for assessment of infarct size was studied in 12 patients with acute anterior myocardial infarction. sigma ST39 (the sum of ST segment elevations in 39 precordial leads), sigma STV1--6 (the sum of ST segment elevations in the standard chest leads) and STMAX (the maximum of ST segment elevation in 39 precordial leads) were obtained serially after the onset from precordial electrocardiographic mapping records. The infarct size and the time (Tf) when the evolution of myocardial infarction finished were calculated by the total creatine phosphokinase released (sigma CPK) and serial changes in CPK releasing rate, respectively. sigma STV1--6 at Tf, as closely as sigma ST39 (r = 0.82, p less than 0.01), correlated with sigma CPK (r = 0.79, p less than 0.01). Even STMAX at the time of Tf significantly correlated with sigma CPK (r = 0.60, p less than 0.05), although the correlation coefficient was not so well as the former two. These results showed that sigma STV1--6 reflected infarct size as satisfactorily as sigma ST39 and could be useful for measuring infarct size.

Creatine Kinase↗
PubMed1979

Evaluation of praecordial ST segment mapping as an index of infarct size in patients with acute myocardial infarction.

We evaluated the usefulness and limitations of praecordial ST segment mapping as a clinical means of assessing the size of acute myocardial infarction in 14 patients with anterior myocardial infarction and 13 patients with inferior myocardial infarction. sigma ST, the sum of ST segment elevations, and nST, the number of leads showing ST segment elevation, were obtained from serial electrocardiograms recorded through 39 praecordial leads. The infarct size and period of the evolution of myocardial infarction were estimated respectively from the total creatine kinase (CK) released and the serial changes of the CK releasing rate. sigma ST and nST obtained at the time when the CK release had ceased correlated closely with the total CK released. Peak sigma ST and nST, and values 48 hours after the onset of myocardial infarction, also correlated well with the total CK released; but those on admission or 12 hours after the onset correlated poorly. These results suggest that sigma ST and nST at the end of evolution of myocardial infarction or 48 hours after the onset may be two useful indices for the assessment of infarct size in patients with either anterior or inferior myocardial infarction.

Adult↗