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Biomedical subjects

S Mashima

Publications and source records attributed to S Mashima.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effects of early coronary reperfusion on the time course of signal-averaged electrocardiogram after myocardial infarction and its relation to late arrhythmic events, effects of early coronary reperfusion on signal-averaged ECGs.

The effect of early reperfusion on the time course of signal-averaged ECG was examined in 90 patients with myocardial infarction. Abnormal signal-averaged ECG disappeared more frequently (p < 0.05) and earlier in cases with early reperfusion than in those without. Serious arrhythmic events in the late phase (> 7 days) occurred in patients with abnormal signal-averaged ECG, but not in cases with early reperfusion. These results indicate that dynamic changes in tissue structure and the physiological state of viable muscles after early reperfusion produce different time courses for signal-averaged ECG. The risk of arrhythmic events among patients with abnormal signal-averaged ECG seems to be lower in cases with early reperfusion than in those without.

Aged↗
PubMed1995

Transient prolongation of ventricular action potential duration after metabolic inhibition.

Transient prolongation of the action potential duration was observed in canine ventricular muscle during the reoxygenation period following metabolic inhibition. We investigated the effects of verapamil, lanthanum (La3+), and hexamethyleneamiloride (HMA) on the recovery time course of the action potential and its rebound prolongation. The time course of the intracellular resistivity was estimated from the conduction velocity and electrograms. The action potentials of canine left ventricular trabeculae were recorded by the conventional microelectrode technique. After a control tracing was obtained, the preparation was perfused with a hypoxic, acidic solution for 20 min and then reoxygenated with regular Tyrode's solution. After reoxygenation, action potential prolongation exceeding the control value by 21.0 +/- 7.3% was observed depending on the degree of metabolic inhibition. Verapamil depressed the rebound prolongation when it was added before the start of metabolic inhibition, but not when added after reoxygenation was started. La3+ and HMA depressed the rebound phenomenon. Intracellular resistivity was increased during metabolic inhibition, but showed no significant changes during the period of action potential prolongation. It was concluded that the rebound action potential prolongation was related to the accumulation of intracellular Ca2+ during metabolic inhibition. Other ions, such as Na+ and H+ may also contribute to the phenomenon by modulating outward currents.

Action Potentials↗
PubMed1995

[Spectro-temporal mapping (STM)].

In recent years, various kinds of time-varying spectral analysis which estimate the frequency content of a signal as a function of time have been proposed. Spectro-temporal mapping (STM) is one of such methods with elaborate modification of a simple fixed period analysis. Merits and demerits of this method in clinical application are described in this chapter. Certain technical aspects pertinent to the interpretation of STM were also discussed. In conclusion, STM in present form is inferior to time domain analysis for the prediction of serious ventricular arrhythmias. But it has some usefulness to supplement time domain analysis in noise detection and application to patients with broad QRS complex.

Body Surface Potential Mapping↗
PubMed1995

[Dipole analysis of data base for body surface potential maps of normal population].

The dipolarity of the body surface potential distribution and locus of the main dipole were estimated by means of the least square method in data base for body surface potential maps of normal population. The main dipole moved smoothly within the actual cardiac region and was inscribed in a clockwise direction during the QRS. The nondipolar content (residue) showed time-dependent fluctuation the QRS. The main dipole during the T wave moved near the center of the heart. The nondipolar content during the ST-T period was less fluctuation than that during the QRS. These results indicated that a large percentage of the body surface potential maps of normal population could be represented by a single moving dipole.

Aging↗
PubMed1994

Advantageous effect of low-molecular-weight heparin administration on hepatic mitochondrial redox state.

The effect of low-molecular-weight heparin (LMWH) on hepatic mithocondrial metabolism was compared with that of unfractionated heparin (UH) after the intravenous administration of these two kinds of heparin to normal rabbits. The magnitude of decrease in blood triglyceride levels 5 min after administration of UH (200 U/kg) was significantly greater than after LMWH (200 U/kg). Free fatty acid levels in the blood were significantly higher after this dose of UH than after LMWH. Blood total ketone body levels (acetoacetate + 3-hydroxybutyrate) 15 min after injection of 50 U/kg of UH were significantly higher than those after a dose of 50 U/kg of LMWH, and levels after 200 U/kg of UH were significantly higher than those after 200 U/kg of LMWH at 15, 30, 45 and 60 min. Enhanced ketogenesis was not noted after LMWH at any of the doses, or after UH at 3 U/kg. Arterial ketone body ratio (AKBR; acetoacetate/3-hydroxybutyrate), which reflects the hepatic mitochondrial oxidation-reduction state (NAD+/NADH), was maintained above 1.0 in all groups except in the U-200 group, while AKBR in that group was significantly decreased to 0.99 +/- 0.14 at 30 min, and further decreased to 0.80 +/- 0.08 at 60 min. These results indicate that LMWH has less effect on lipolysis than UH and does not enhance ketogenesis, resulting in less deterioration of mitochondrial redox state.

Animals↗
PubMed1994

A new experimental model of specific liver hypoxia using membrane oxygenator.

The present study introduces a new experimental canine model of hepatic arterial deoxygenation using a membrane oxygenator to investigate the influence of hepatic arterial hypoxia on hepatic hemodynamics and energy metabolism. Eighteen mongrel dogs weighing 10 kg each were randomly divided into three groups: group A served as a control (118.0 +/- 9.0 mmHg of hepatic arterial O2 content), group B as a moderately deoxygenated group (40 mmHg of hepatic arterial O2 content), and group C as a severely deoxygenated group (25 mmHg of hepatic arterial O2 content). Deoxygenation was achieved by perfusion of a gas mixture of O2 and N2 through the membrane oxygenator, which was interposed between the femoral artery and the proper hepatic artery, for 60 min. In group C, hypoxia decreased the mean systemic arterial blood pressure and hepatic arterial blood flow. Arterial blood ketone body ratio (AKBR = acetoacetate/3-hydroxybutyrate), which reflects the hepatic mitochondrial redox state, rapidly decreased prior to the significant increase of glutamate oxaloacetate transminase, glutamate pyruvate transminase, and lactate dehydrogenase after the initiation of hypoxia. Hepatic arterial deoxygenation to 25 mmHg for 60 min induced injury to hepatic hemodynamics, resulting in the deterioration of systemic hemodynamics even after the termination of liver hypoxia. This in vivo temporal hepatic arterial hypoxic model without alteration of inflow volume might be useful for investigating the mechanism of hypoxic injury and the critical point of liver hypoxia on hepatic and/or systemic hemodynamics and liver viability.

Alanine Transaminase↗
PubMed1994

Hemodynamics and hepatic energy metabolism in canine model of acute hepatic venous occlusion with mesocaval shunt.

The relationship between portal hemodynamics and the energy metabolism of the liver with acute hepatic venous occlusion (HVO) was investigated by assessing the changes in the hepatic blood flow, arterial blood ketone body ratio (AKBR) and adenylate energy charge potential (ECP) of the liver tissue in canine model. Acute HVO was induced by the ligation of both the supra- and infrahepatic inferior vena cava (IVC) over the protruding ends of a heparin-coated polyethylene cannula inserted into the IVC. All dogs with only HVO (n = 5) died within 30 min. HVO dogs with additional mesocaval (MC) shunt (n = 10) survived longer than 7 days, during which time their AKBR were maintained in the normal range (over 1.0). ECP was also maintained above the normal level (over 0.850) during the 28-day period. Along with increasing portal pressure caused by the narrowing of the shunt anastomosis, the hepatic blood flow decrease gradually, resulting in a sudden decrease in AKBR and ECP when the portal pressure increased over 11 mm Hg. It is suggested that the normalization of portal pressure is one of the most important factors for maintaining the hepatic energy metabolism and that MC shunt is an effective therapy for maintaining the function of the liver with HVO, as long as portal pressure can be kept within normal range.

Animals↗
PubMed1994

Correlation of diagnostic accuracy of dipyridamole thallium-201 myocardial scintigraphy and clinical findings during stress.

The relationship between dipyridamole thallium-201 myocardial single-photon emission computed tomography and clinical findings during stress testing was investigated in 57 patients (mean age 72 years), including 11 patients with normal coronary arteries. Systolic blood pressure decreased from 138.2 +/- 19.7 to 119.8 +/- 20.1 mmHg (mean: -13.8 +/- 6.6%) after dipyridamole infusion (0.568 mg/kg/4 min). Scintigraphic sensitivity for the diagnosis of coronary artery disease was higher in 30 patients with a systolic blood pressure decrease above the average value than in 27 patients with a blood pressure reduction of less than 14% (88% vs. 60%, p < 0.005). Reversible perfusion defects among stenosed coronary arteries were more frequent in the former group (73% vs. 27%, p < 0.001) with no difference in other clinical findings. In conclusion, systolic blood pressure change during stress testing was significantly correlated with dipyridamole-induced perfusion defects and detectability of coronary stenosis.

Aged↗
PubMed1994

A quantitative estimation of electric current due to myocardial injury.

Myocardial injury causes electric current at the border of injured muscle and the surrounding intact region. In order to determine the magnitude of the injury current, experiments were performed with the isolated canine heart perfused with Tyrode's solution. The anterior descending branch of the left coronary artery was perfused selectively with high potassium (K+) solution and the resulting injury current was reflected in the ST shift of the orthogonal electrocardiogram, derived from the surface of a cubic container in which the heart was placed. After measurement of the ST vector with different K+ concentrations, the heart has fixed with formalin and the injury zone was delineated with serial sections. The boundaries of the selectively perfused region were reconstructed. The algebraic sum of orthogonal components of boundary surfaces determined the average direction normal to the boundary, which was found to be parallel with the ST vector. With increasing K+ concentrations, the ST shift became more marked. However, it was saturated at about 30 mEq/L K+. The maximum injury current, calculated from the saturated value of the ST magnitude, amounted to 0.10 mA.cm per unit area of the boundary surface. Additional experiments were performed with right ventricular papillary muscle preparations. Injuries were caused by a cotton pad containing high K+ solution placed in two directions to make the border along and across the long axis of the papillary muscle. The results indicate that the injury current in an anisotropic structure was essentially directed along the fiber orientation.

Aged↗
PubMed1993

[Electrocardiogram in heart failure].

Heart failure is basically a manifestation of mechanical disturbances of the heart, but not of electrical abnormalities and is not associated with specific ECG patterns. Several ECG findings are, however, experienced in cases with heart failure as a result of cardiac chamber enlargement and other related changes. Left atrial enlargement is known to cause characteristic P wave changes, which sometimes show parallel course with the clinical state. ECG criteria for atrial enlargement are critically reviewed. In cases with cardiac enlargement, which was improved in a relatively short period of time, R wave height often showed first increase and then decrease. Tissue edema was thought to be the major reason for the initial increase and the distance between the recording electrode and the heart for the later decrease, although other factors can contribute and modify the findings. Minor conduction disturbances due to myocardial stretch and other reasons may also contribute to changes of QRS complex. Analysis of RR intervals offers another possibility to characterise heart failure. A decrease in variability of the RR intervals and in high frequency components on frequency spectrum has been reported in cases with heart failure.

Electrocardiography↗