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Biomedical subjects

S Mashima

Publications and source records attributed to S Mashima.

At least 73 records · Page 4Linked 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↗
PubMed1988

ST-T isointegral analysis of exercise stress body surface mapping for identifying ischemic areas in patients with angina pectoris.

ST-T isointegral analysis of body surface mapping was used in an attempt to localize ischemic areas on exercise tests. In 28 patients with angina pectoris and 10 healthy subjects, body surface potential was recorded with 87 leads, and ST isopotential and ST-T isointegral maps were constructed. In all 10 healthy subjects, the basic pattern of the ST-T isointegral map showed no significant change after exercise. In 23 of 28 patients with angina pectoris (82%), alterations in the ST-T isointegral map after exercise were observed. They were divided into four types (anterior, inferoposterior, lateral, and global) according to the distribution of negative values, which were well correlated with the extent of ischemic area determined by thallium myocardial scintigraphy and coronary angiography. The postexercise ST-T isointegral map was normalized after administration of nitroglycerin in four of five patients. In five patients (18%) who did not show abnormalities on the postexercise ST-T isointegral map, the magnitude of maximal ST depression was significantly smaller than that observed in the other 23 patients with angina pectoris (0.14 vs 0.23 mV on the average, p less than 0.05). It was concluded that the exercise test with ST-T isointegral mapping is a new method for noninvasive detection of location and severity of ischemic regions.

Adult↗
PubMed1986

Epicardial activation patterns of torsade de pointes in canine hearts with quinidine-induced long QT interval but without myocardial infarction.

We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained polymorphic ventricular tachycardia and six episodes of monomorphic ventricular tachycardia were induced. Of 22 episodes of nonsustained polymorphic ventricular tachycardia, 12 episodes showed typical torsion of the spikes of the QRS complex around the isoelectric line (torsade de pointes). Isochronal maps were made from 38 simultaneously recorded bipolar electrograms and showed that each change in QRS morphology was associated with a change in the earliest epicardial activation site and/or a change of epicardial activation sequence. During episodes of torsade de pointes, the earliest epicardial activation site migrated gradually from one site to another site. The transitional QRS complexes had their earliest epicardial activation sites between the new and old site of the earliest epicardial activation. The changes in the earliest epicardial activation site during polymorphic ventricular tachycardia without torsade de pointes pattern was not as great as that noted during torsade de pointes. This study suggests that in a noninfarcted canine model torsade de pointes is produced by alteration in the earliest site of activation rather than by competition from two or more competing foci.

Animals↗
PubMed1986

Ventricular fibrillation threshold in canine hearts with quinidine induced prolonged QT interval: effects of atrial pacing, isoproterenol, and lignocaine.

Ventricular fibrillation threshold was determined using a train of pulses, 4 ms in duration, delivered at 10 ms intervals, in 20 anaesthetised dogs receiving toxic doses of quinidine sulphate (30 mg X kg-1) injected intravenously over 5 min to prolong the QT interval. The effects of atrial pacing, isoproterenol, and lignocaine on ventricular fibrillation threshold were investigated. Quinidine administration lowered the mean(SD) threshold from 14.7(5.1) to 8.8(3.6) mA (n = 20, p less than 0.001). Atrial pacing shortened the mean(SD) basic cycle length from 652 to 400 ms and the QT interval (378(28) vs 334(19) ms, n = 8, p less than 0.01) but did not alter the mean(SD) threshold (7.0(2.3) vs 7.5(1.5) mA). Isoproterenol infusion to maintain basic cycle length at 421(23) ms shortened the mean(SD) QT interval to 291(14) ms (p less than 0.001) and increased the mean(SD) threshold to 13.6(5.9) mA (n = 8, p less than 0.01). Lignocaine (plasma concentration 1.36 micrograms X ml-1) increased the mean(SD) threshold from 10.9(3.4) to 16.7(6.7) mA (n = 7, p less than 0.02) without affecting basic cycle length and QT interval. Thus atrial pacing shortened the QT interval slightly but did not make the canine heart with a quinidine induced prolonged QT interval less vulnerable to electrically induced ventricular fibrillation, whereas both isoproterenol and lignocaine did, although they affected basic cycle length and QT interval differently.

Animals↗
PubMed1985

Inhomogeneity of ventricular refractory period in canine heart with quinidine-induced long QT interval: a comparative study on effects of heart rate, isoprenaline, and lignocaine.

In anaesthetised open chest dogs, 30 mg . kg-1 of quinidine sulphate was injected intravenously over 5 min to produce QT prolongation. The sinus node was crushed. Effective refractory period (ERP) was determined at eight test points of the right ventricle using extra-stimuli after every seven basic ventricular pacings. Stimuli were of 2 ms duration and 1.5 times diastolic threshold. Temporal dispersion was estimated as the difference between the maximum and the minimum ERP of eight test points. Cycle lengths of basic ventricular drive were 700, 600, 500, and 400 ms. Time course of changes in ERP and its temporal dispersion was tested in five dogs. The effect of a 2 mg . kg-1 bolus injection followed by 70 micrograms . kg-1 . min-1 drip infusion lignocaine, on quinidine-induced changes in ERP was studied in eight dogs, and that of a 0.06 microgram . kg-1 . min-1 infusion of isoprenaline, was tested in six dogs. ERP was significantly prolonged after quinidine injection (220 +/- 20 vs 258 +/- 25 ms n = 19, basic cycle length = 500 ms, p less than 0.001). Temporal dispersion was also increased after quinidine (18 +/- 9 vs 33 +/- 12 ms n = 19, basic cycle length = 500 ms, p less than 0.001). With shortening of basic cycle length (BCL), ERPs were shortened significantly. Temporal dispersion, however, did not change. Lignocaine prolonged ERP even further (250 +/- 25 vs 273 +/- 16 ms BCL = 500 ms, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The electromotive force of the ventricular free wall and papillary muscle preparations.

The electromotive force of the ventricular tissues with different anatomy and activation patterns was studied. The left ventricular wall was perfused with Tyrode's solution from the circumflex branch of the left coronary artery and was stimulated first at an epicardial and then endocardial site to induce ectopic beats. The early QRS voltage was compared with the activated area at the same instant. In other experiments, the whole heart was perfused from the aorta, and the anterior papillary muscle of the right ventricle was introduced into a small separate chamber. Different locations were stimulated to induce longitudinal and transverse activation, and the remote potential was measured with leads in both directions. By means of a calibration system with artificial dipoles, the strength of the double layer was expressed in terms of mA X cm per unit area of the activation wave front. The results indicated that epicardial stimulation of the left ventricular wall produced voltage proportional to the activated area; the average moment was found to be 0.11 mA X cm per unit area. The potential curve produced by endocardial stimulation of the same preparation was characterized by an initial low-voltage phase, followed by a sharp upstroke. The right ventricular papillary muscle produced a larger double layer moment during activation in the longitudinal direction, but voltage due to transverse activation was several times smaller.

Animals↗
PubMed1985

[Secondary pauses following high frequency atrial stimulation: incidence and possible underlying mechanisms].

Atrial pacing up to 250 bpm was performed in 88 patients with suspected sick sinus syndrome or syncopes of unknown origin. Measurements were done on the first five return cycles. According to cSNRTmax they were divided in 3 groups (group 1 less than 525 ms, group 2 greater than or equal to 525 ms less than 1000 ms, group 3 greater than or equal to 1000 ms). The return cycle pattern (PSM) was calculated (mean + standard deviation of PSI 1-PS15 at each pacing rate). A "normal" PSM with long PSI1 and gradual shortening of the subsequent cycles was found only at low pacing rates in group 1 and group 2. At higher rates, the PSI1 shortened and PSI2 lengthened, resulting in frequent secondary pauses (SP). Atrial pacing up to 400 bpm was performed in 20 open chest dogs. SP were frequently obtained at pacing rates above 300 bpm. Intravenous application of propranolol and atropine did not diminish SP, neither did bilateral vagotomy. Additional subthreshold stimuli, as well as stimulation with large interpolar distance did not influence the PSM of SP at high frequencies. Simultaneous stimulation of right atrium and right ventricle had no significant effects on SP. Pacemaker shifts occurring frequently after high rate pacing were not necessarily accompanied by SP. The velocity of activation spread over the sinoatrial region was significantly slower in cases of postpacing beats preceding a SP. It was concluded that the PSM of SP provoked by high rate atrial pacing is neither caused by local release of neurotransmitters nor by pacing induced changes of the autonomic tone nor by pacemaker shifts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Studies on the mechanisms of secondary pause after high rate atrial pacing.

Atrial pacing up to 400 beats per minute (bpm) was performed in 20 open chest dogs. Measurements were made on the first five return cycles. Instances with the first cycle shorter than the basic cycle length were excluded. Secondary pauses (SP) were frequently observed at pacing rates equal to or faster than 280 bpm. Intravenous application of propranolol and atropine did not diminish SP, nor did bilateral vagotomy. Additional subthreshold stimuli, as well as stimulation with electrodes with large interpolar distance influenced neither the length of sinus node recovery time (SNRT) nor the SP phenomenon. Simultaneous pacing of the right atrium and right ventricle had no significant effects on SNRT and SP. Pacemaker shifts occurring frequently after high rate pacing were not necessarily accompanied by SP. The velocity of activation spread over the sinoatrial region was significantly slower (46.9 +/- 7.3 cm/s) in cases with SP than in those with primary pauses (PP) (72.5 +/- 8.1 cm/s). It was concluded that high rate induced SP was a feature indicating suppression of sinoatrial conduction.

Animals↗
PubMed1984

Effects of atrial pacing, isoprenaline and lignocaine on experimental polymorphous ventricular tachycardia.

In 22 anaesthetised dogs, iv, administration of quinidine sulphate (30 mg X kg-1) over 5 min produced bradycardia and marked prolongation of the QT interval. Right ventricular extrastimulations, four times diastolic threshold, provoked polymorphous ventricular tachycardia in 18 dogs, and typical torsade de pointes was observed in four of these 18 dogs. Ventricular flutter was induced in another four dogs. In one of these 22 dogs, double stimuli were required to induce ventricular tachyarrhythmias, in 19 dogs triple stimuli, and in two dogs quadruple stimuli. Using this experimental model, effects of interventions including atrial pacing, isoprenaline, and lignocaine on the QT interval and induction of polymorphous ventricular tachycardia by extrastimuli were studied. Atrial pacing shortened QT interval only slightly and did not prevent induction of polymorphous ventricular tachycardia in nine dogs studied. Isoprenaline infusion definitely shortened QT interval, and in four out of nine dogs triple stimuli could not elicit polymorphous ventricular tachycardia. By contrast, although the QT interval was not shortened, lignocaine was effective in preventing induction of polymorphous ventricular tachycardia by triple stimuli in three out of nine dogs. These results indicate atrial pacing is an ineffective means of preventing induction of polymorphous ventricular tachycardia by extrastimuli in dogs with a long QT interval, but that isoprenaline and lignocaine are effective in some dogs.

Animals↗
PubMed1983

Exercise test in variant form of angina pectoris. Comparison of the results with spontaneous attacks.

Exercise tests were performed in 14 patients with untreated variant angina with frequent spontaneous attacks and in 15 patients after treatment abolished the attacks. (1) Anginal attacks associated with ST elevation were induced by exercise in 79% of untreated patients. By contrast, ST elevation was not observed in treated patients and ST depression was induced in 53% of the cases. (2) Exercise-induced ST elevation in untreated patients was shown in the same leads as the spontaneous attacks. (3) Exercise-induced ST elevation appeared initially during the recovery phase after exercise in 36% of untreated patients. Exercise-induced ST depression appeared during or immediately after exercise. (4) The reproducibility of exercise-induced ST elevation was low with repeated tests at different stages, but exercise-induced ST depression was consistently observed. (5) The exercise-induced ST depression and lack of ST changes in treated patients were highly suggestive of the presence and absence of organic coronary artery disease, respectively. However, the exercise-induced ST elevation in untreated patients did not differentiate between the presence or absence of organic stenosis of the coronary arteries. The results of exercise tests vary with the stage of variant angina. It is suggested that a coronary arterial spasm is a trigger mechanism for exercise-induced angina in cases of variant angina with frequent spontaneous attacks.

Adult↗
PubMed1983

On the absolute magnitude of the human lead vector.

Twelve cases with temporary artificial pacing were used to investigate on the efficacy of a bipolar current source within the heart to generate potential variations in Frank lead ECGs. A constant current, subthreshold square pulse was applied to the catheter electrodes and the artefact was recorded with the Frank system. Assuming that the Frank system was normalized and orthogonal, the lead vector magnitude was calculated as 0.58 ohm/cm on the average. The value of the lead vector was inversely related to the thorax size. The direction of the vector determined from the recorded potentials approximated the direction of the catheter tip on the X-ray film. In addition, similar measurements were made with a homogeneous torso model and the results were compared with those of clinical cases.

Adult↗
PubMed1982

Pacing echocardiography: regional wall motion, left ventricular dimension and R wave amplitude in patients with angina pectoris.

In view of the fact that stable echocardiograms are easily obtained during atrial pacing, pacing echocardiography was performed to evaluate the usefulness for detecting regional wall motion abnormalities during pacing-induced ischemia and to investigate the relationship between changes in the R wave and left ventricular dimension. The patients were 12 cases of angina pectoris (10 of coronary artery disease; CAD, and 2 of coronary patent aortic valvular disease; AVD) and 6 control cases. Simultaneous recording of two-dimensional and M-mode echocardiograms and electrocardiograms was done before, during and after the atrial pacing at increasing heart rate until angina appeared or the heart rate of at least 140/min was reached. In 12 angina cases, angina and ST depression were induced in 10 and 11, respectively. Excursion of the interventricular septum (IVS) decreased during pacing-induced ischemia in 6 of 7 CAD cases, in which the left anterior descending coronary artery was significantly stenosed (more than 75%). Excursion of the left ventricular posterior wall (LVPW) decreased during pacing-induced ischemia in 4 of 7 CAD cases, in which the vessels giving rise to posterior descending coronary artery were significantly stenosed (more than 75%). In 2 AVD cases, excursion of both IVS and LVPW decreased during ischemia. Left ventricular end-diastolic dimension (LVEDD) increased in only 2 angina cases, although R wave amplitude increased in 6 angina cases.

Adult↗
PubMed1982

"Entrainment" phenomenon during reciprocating tachycardia in the Wolff-Parkinson-White syndrome.

In a case with the Wolff-Parkinson-White syndrome, the phenomenon "entrainment without interruption" was observed during spontaneous tachycardia. Electrophysiologic study revealed that the tachycardia was due to reentry with the antegrade limb being the AV node-His axis and the retrograde limb being the accessory pathway. This report is the second report showing "entrainment" phenomenon which is consistent with macro reentry as the mechanism of tachycardia as shown in atrial flutter.

Adult↗