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Biomedical subjects

M Murayama

Publications and source records attributed to M Murayama.

At least 289 records · Page 16Linked to original sources
PubMed1978

Changes in ventricular recovery properties during and after temporary coronary artery occlusion.

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.

Animals↗
PubMed1977

Prolongation of ventricular action potential due to sympathetic stimulation.

The changes of monophasic action potential durations due to stellate stimulation for the period of 3 sec were studied in dogs with suction electrodes from the anterior surface of the right ventricle and the posterior surface of the left ventricle. Prolongation of monophasic action potential duration was observed from the period of 2 to 3 sec during stimulation to that of 10 to 20 sec after the termination of stimulation. Prolongation of monophasic action potential duration due to right stellate stimulation was predominant in the right ventricle and that due to left stellate stimulation was predominant in the left ventricle. The transient T wave change in the surface electrocardiogram occurring immediately after the beginning of stellate stimulation could be explained by this local difference in prolongation of ventricle repolarization. Since the onset of prolongation of monophasic action potential duration preceded increase in blood pressure following stellate stimulation, this prolongation of monophasic action potential duration did not result from the hemodynamic changes and could be a primary effect of the sympathetic nerve stimulation.

Action Potentials↗
PubMed1976

The significance of T-loop change in Frank's lead exercise electrocardiography.

Thirty-one patients with angina pectoris and 15 patients with myocardial infarction who performed exercise test by Master's double two-step test have been longitudinally followed up for 4-10 years. Exercise electrocardiogram was taken by Frank's lead and T loop was constructed in frontal and horizontal planes from 3 scalar tracings recorded at a paper speed of 100 mm/sec. ST vector was determined at 100 msec from the beginning of Q wave and the line connecting 2 ST vectors before exercise and at the point of the maximal ST change after exercise was determined as ST exercise vector. To indicate width of the T loop, the length to width ratio (L/W) was used and the change of width of the T loop induced by exercise was expressed by a ratio of L/W between before exercise and at the maximal change in frontal and horizontal planes. In cases having ST exercise vector of 0.1 mV or more the magnitude or the direction of the ST exercise vector alone has little prognostic value and widening of the T loop in addition to the ST exercise vector of 0.1 mV or more occurring after exercise was a predictive sign of poor prognosis and no widening of the T loop was a predictive sign of good prognosis.

Aged↗
PubMed1976

Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle. Echocardiographic and ultrasono-cardiotomographic study.

Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).

Adult↗