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Biomedical subjects

S Mashima

Publications and source records attributed to S Mashima.

16 recordsLinked to original sources
PubMed1992

Preserved mitochondrial function by allopurinol despite deteriorated hemodynamics in warm ischemia-damaged canine liver.

To investigate the pathophysiology of warm ischemia (WI) of the liver, the changes in hemodynamics and energy metabolism were studied during and after 60-min complete WI induced by total hepatic vascular exclusion (HVE) in the canine model. Hepatic arterial blood flow after WI was maintained at 76% of the pre-ischemic level, while portal blood flow was only 27% of the pre-ischemic level associated with increased portal vein pressure, which was twice the pre-ischemic level, resulting in a decrease of total hepatic blood flow to 46% of the pre-ischemic level. Concentration of tissue lipid peroxide increased after WI. Arterial blood ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, could not recover to the pre-ischemic level after termination of WI. However, when 100 mg/kg of allopurinol (xanthine oxidase inhibitor) was administered intravenously 10 min prior to initiating WI, AKBR was restored to the pre-ischemic level at 30 min after WI in spite of the fact that allopurinol administration to one group produced no remarkable changes in the hepatic hemodynamics compared with the group without allopurinol treatment. Concentration of adenine nucleotides was significantly higher for the treated group at the end of and after WI than for the group without allopurinol treatment and was maintained at a higher level even after WI. Lipid peroxide production was suppressed. Electron microscopic examination revealed that allopurinol treatment could not prevent mitochondrial swelling. It is suggested that WI causes injury primarily to the portal sinusoidal circulation, resulting in portal congestion concomitant with high portal pressure after the release of WI. Allopurinol could prevent the deterioration of mitochondrial ATP metabolism, and was able to inhibit lipid peroxide production, resulting in the rapid recovery of mitochondrial redox state in spite of the fact that it produced no amelioration of hepatic hemodynamics and morphological alterations.

Adenosine Triphosphate↗
PubMed1992

A possible mechanism for pacemaker-induced T-wave changes.

The genesis and the significance of pacemaker-induced T-wave changes remain unclear. Changes in body surface potential mapping (BSM) were observed and compared with resting thallium-201 myocardial scintigraphy (T1-SC) findings before, during and after ventricular pacing (VP) in 10 patients with various bradyarrhythmias. All studies were performed with the patients taking no medication. In all patients, isoarea QRST maps showed a characteristic abnormal dipolar pattern with positive values distributed over the upper chest and negative values over the lower chest during VP at a physiological rate for 14 days or more. These abnormalities were preserved almost completely after pacing was terminated; and coincided with deep T-wave inversions in leads II, III, aVF and V4-6. In three patients, BSM performed before VP showed normal QRST isoarea maps with positive values distributed over the left lower chest. All patients in whom resting T1-SC was performed during chronic VP showed transient perfusion defects in the posteroinferior (seven cases) or inferolateral (one case) left ventricular wall. In three patients, T1-SC was performed before VP and showed a normal distribution. Both the pacing-induced perfusion defects and the T-wave abnormalities remained unchanged 2 h after ceasing VP, were attenuated 7 days later and disappeared within a month. These findings suggest that chronic ventricular pacing may produce myocardial ischaemia, and that it persists for a certain period after the cessation of pacing, resulting in post-pacing T-wave inversion.

Adult↗
PubMed1992

A case of right atrial mobile thrombus complicating multiple pulmonary emboli.

Right atrial thrombi are usually immobile. However, a mobile type mimicking a cardiac tumor, especially myxoma, has been described on rare occasions. We report here a case of atrial thrombus which was mobile in the cardiac chambers. A 29-year-old male was admitted because of exertional dyspnea. On admission, his echocardiogram showed an abnormal mass in the right atrium with a stalk attached to the interatrial septum. It decreased in size on the next day. On the fourth day of admission, it moved to the right ventricle. Multiple pulmonary emboli were revealed by the lung perfusion scintigram. Two days after the administration of intravenous urokinase, the abnormal mass in the cardiac chambers was no longer seen on the echocardiogram. This was a rare case of mobile atrial thrombus associated with multiple pulmonary emboli. Thrombolytic therapy appeared to be effective in this case.

Adult↗
PubMed1991

Study on the genesis of giant negative T wave in apical hypertrophic cardiomyopathy using a three-dimensional computer model.

Apical hypertrophic cardiomyopathy is characterized by a spade-like left ventricular cavity and by both giant negative T waves and tall R waves in the electrocardiogram. However, the mechanisms of these ECG abnormalities have not been satisfactorily clarified. We have recently developed a three-dimensional computer model of ventricular depolarization and repolarization processes. This model has successfully simulated normal QRST waves and changes characterizing some abnormal conditions. A model of apical hypertrophic cardiomyopathy was constructed by adding model units to the endocardium of the left ventricular apex. The surface ECG was then calculated by assuming different gradients of action potential durations and different proportions of the hypertrophic cells in the apical segment. A negative T wave of -1.45 mV in lead V4, similar to the clinically reported ECG, was obtained by assuming: (1) diffusely distributed hypertrophic cells at the apex and (2) uniform, long action potential durations of hypertrophic cells. It is suggested that these properties may account for the distinctive ECG abnormalities in apical hypertrophic cardiomyopathy.

Cardiomyopathy, Hypertrophic↗
PubMed1990

Adenosine-5'-triphosphate-induced sinus tachycardia mediated by prostaglandin synthesis via phospholipase C in the rabbit heart.

Effects of adenosine 5'-triphosphate (ATP) and adenosine on cardiac sinus pacemaker activity were examined in the rabbit heart. Electrocardiograms of hearts were recorded while using the Langendorff perfusion method. Both adenosine and ATP, added to the perfusate, slowed the sinus pacemaker activity in a concentration-dependent manner. But in about 40% of the cases. ATP higher than 300 microM initially accelerated and then slowed the heart. The sinus slowing caused by adenosine and ATP was blocked by theophylline (a P1 receptor antagonist) and disappeared in the hearts pre-treated with islet-activating protein (1AP). In contrast, the ATP-induced sinus acceleration was not affected by either theophylline or IAP. In about 75% of the IAP-treated hearts. ATP persistently accelerated the sinus pacemaker. In the remaining 25% of the hearts, ATP caused junctional tachycardia, which may have masked the ATP-induced sinus acceleration. Apamin specifically blocked the ATP-induced sinus acceleration, suggesting that P2 receptors are involved. Among various adenine nucleotide analogues, the order of potency in inducing tachycardia in IAP-treated hearts is adenosine-5'-[gamma-thio]triphosphate greater than adenylyl imidodiphosphate greater than adenosine 5'-[alpha, beta-methylene]triphosphate = ATP greater than adenosine diphosphate = adenosine 5'-[beta, gamma-methylene]triphosphate. ATP-induced acceleration was partially blocked by indomethacin and aspirin (cyclooxygenase inhibitors), but not by nordihydroguaiaretic acid (a lipoxygenase inhibitor). These results suggest that cyclooxygenase and not lipoxygenase metabolites of arachidonic acid, e.g. prostaglandins, may be involved in the generation of tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1978

The magnitude of the electromotive force of canine ventricular myocardium.

The isolated and perfused dog heart was placed in a cubic container filled with Tyrode's solution. Ventricular ectopic beats were produced by electrical stimulation of the left ventricular wall, and initial QRS vectors of these beats were determined with orthogonal leads from the surface of the container. At the same instants, the activated area on the epicardial surface was measured by means of a large number of contiguous bipolar leads from the epicardial surface. The QRS vector and the activated epicardial area were found to be nearly porportional. By use of these results and a calibration system with artificial dipoles, the double layer moment of the ventricular activation wave was calculated as 0.13 mA.cm per unit area. This value corresponds to 60% of the maximal possible strength of the tissue electromotive force. Lowering the conductivity of the surrounding solution increased the QRS voltage but not as much as the potential caused by a constant-current dipole within the solution. The relationship between the QRS voltage and the conductivity of the medium was analyzed by a simplified model of the system and was found to correspond approximately to that of a constant-current source within a spherical heart with a resistivity 2 to 3 times that of Tyrode's solution.

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

Theoretical considerations on the electrocardiogram of ventricular hypertrophy.

The electrical effect of ventricular hypertrophy is evaluated with an idealized model. Perfectly symmetrical hypertrophy is expected to enlarge the QRS complex with a certain proportion of the amplitude and duration. If the conduction velocity is unaltered, the QRS area will be increased proportionally to the myocardial mass. 2) Based on the preservation of the ventricular gradient, the secondary T change is expressed as a function of the QRS and G vectors. A theoretically interesting parameter, G/QRS ratio, is defined as a measure of the "ventricular gradient density," which is important for the over-all recovery pattern. This ratio is decreased in ventricular hypertrophy and is closely related to the QRS-T angle. 3) From the viewpoint of the theory, clinical cases with left ventricular hypertrophy are examined. The theory describes the cases with uncompicated hypertension fairly well, although variations from case to case are not small. Underlying assumptions and causes of deviations in actual cases are discussed.

Aortic Valve Insufficiency↗