To assess the appropriateness of hippocampal low-frequency kindling as an experimental model of epilepsy, we stimulated, bipolarly, left ventral hippocampus of 8 cats with 2 mA biphasic square wave pulses (1 msec duration) once a day. The pulse-interval was set at 300 msec. Recording electrodes were inserted in right ventral hippocampus, bilateral amygdaloid and bilateral globus pallidus. EEG was monitored before, during and after the delivery of stimulation. If the triggering of epileptic afterdischarge was observed on EEG monitoring, the delivery of stimulation was stopped immediately. Generalized convulsive seizures developed in all subjects within a mean of 26.2 days. In all seizures self-sustained epileptic afterdischarge, defined as epileptiform spikes three times the base line amplitude with a frequency greater than the stimulating pulse-interval (300 msec) in the stimulated hippocampus lead, was triggered abruptly. Therefore we could measure the number of stimulating pulses required for the triggering of epileptic afterdischarge, defined as pulse-number threshold, definitely in all cases. At the completion of kindling the pulse-number threshold was measured at 12.3 +/- 0.9 (+/- SE). After five generalized convulsions were induced we tested the stability of the pulse-number threshold and the duration of triggered epileptic afterdischarge. Both the two measures did not change statistically at the interstimulation interval from 24 hrs to 96 hrs. In addition we carried out testing with antiepileptic and antipsychotic drugs. Phenobarbital (10 mg/kg, i.p.) increased the pulse-number threshold and the after discharge duration simultaneously. Haloperidol (3 mg/kg, i.p.), oppositely, decreased the pulse number threshold and the after discharge duration.

Animals↗

PubMed1987

ST segment changes in exercise body surface mapping after myocardial infarction in patients with isolated left anterior descending coronary artery disease.

To investigate the clinical significance of exercise-induced ST segment elevation and ST segment depression after myocardial infarction (MI), we performed 87-lead ECG mapping after previous anterior infarction in 24 patients with isolated left anterior descending coronary artery disease before and 1.5 minutes after treadmill exercise. Thirteen patients showed ST segment elevation only, seven patients showed both ST segment elevation and depression, and four patients showed ST segment depression only. ST segment elevation most frequently occurred in the left anterior chest leads corresponding to the QS area, and ST segment depression developed in the left lower chest and left lower back leads. There was good correlation between the number of lead points showing ST segment elevation (nSTe) after exercise and the number of lead points showing QS waves (nQS) before exercise (r = 0.65). nSTe was also correlated with the asynergy index (r = 0.43). These findings suggest that ST segment elevation is mainly the result of aggravation of wall motion abnormalities of the infarcted myocardium. Body surface distribution of ST segment depression was similar to that in effort angina pectoris without MI. We conclude that exercise-induced ST segment depression in MI mainly reflects the ischemia of the surviving myocardium of small infarcts or the peripheral area of large infarcts.

Adult↗

PubMed1987

Segmental wall motion abnormalities in dilated cardiomyopathy: hemodynamic characteristics and comparison with thallium-201 myocardial scintigraphy.

This study assessed the hemodynamic characteristics of segmental wall motion abnormality of the left ventricle in patients with dilated cardiomyopathy (DCM) and its relation to the thallium-201 (TI-201) myocardial scintigraphy (MPI). Left ventriculograms and MPI in 23 patients were analyzed by the use of quantitative indexes of regional wall motion and TI-201 uptake based on a mean and a standard deviation of 13 normal subjects. Relative normokinesis in our definition was more frequently seen in the inferior wall than in the anterior wall (p less than 0.01). In contrast, severe asynergy was more often seen in the anterior wall than in the inferior wall (p less than 0.01). There were 11 patients who had relative normokinesis and asynergy together. By means of the index of wall motion, the DCM patients were divided into two groups, one with segmental wall motion abnormality (SWMA) and another with diffuse wall motion abnormality (DWMA). The DWMA group had higher left ventricular end-diastolic pressures (p less than 0.05) and the tendency of large left ventricular end-diastolic volumes than the SWMA group. There was a rough correlation (r = 0.58) between the quantitative indexes of TI-201 uptake and wall motion at the same region of the left ventricle. Thus, the nonuniformity of the left ventricular wall motion was recognized in the patients with DCM and more increased preload was shown in the patients with DWMA than in the group with SWMA. Further, the regional asynergy may be related to the localized fibrosis within the left ventricle in DCM, considering the result that the worse TI-201 uptake was roughly accompanied by the more severe asynergy.

Adult↗

PubMed1987

Ca and Na homeostasis in horizontal cells of the cyprinid fish retina: evidence for Na-Ca exchanger and Na-K pump.

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Animals↗

PubMed1987

Temporal changes in body surface peak R isochrone maps and left ventricular function in patients with myocardial infarction.

Body surface peak R isochrone mapping and radionuclide ventriculography were performed twice in 22 patients with myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, the time from the onset of QRS to the peak of the R wave was measured. From this data for 87 leads an isochrone map was constructed. The lead points where R waves were not observed were designated the no R-wave area (No-R area), which was postulated to correspond to the unexcited regional myocardium. Other abnormal findings, i.e., delay of peak R time near the No-R area (peri-No-R area delay), crowding of isochrone lines, and an island-like zone of delayed peak R times were postulated to indicate slow conduction in the partially excited regional myocardium. In three patients, abnormal patterns in the peak R isochrone maps during the acute phase (within a month from the onset of myocardial infarction) improved in the chronic phase with a significant increase in left ventricular ejection fraction. In two patients, the No-R area decreased after the left ventricular aneurysmectomy. In other patients, abnormal patterns of the isochrone maps and the ejection fraction remained unchanged during the chronic phase of myocardial infarction. We conclude that the comparison of peak R isochrone map patterns between the acute and chronic phase may be useful in evaluating the balance of reversible and irreversible regional damage in myocardial infarction.

Electrocardiography↗

PubMed1987

Using body surface mapping to detect vulnerability to ventricular arrhythmias in patients with coronary artery disease.

In order to examine the clinical usefulness of the vulnerability map, body surface mapping was performed in ten normal subjects and 32 patients with CAD using dipyridamole infusion to induce ventricular arrhythmias. A vulnerability map and the vulnerability index (VI) proposed by Urie et al. were constructed from QRS and T isointegral maps in the control state and QRST isointegral map after dipyridamole infusion. Premature ventricular complexes (PVCs) did not occur in normal subjects but occurred in 13 patients after dipyridamole infusion. The vulnerability index in normal subjects was significantly lower than that in patients without PVCs (8.3 +/- 1.7 vs 10.4 +/- 1.7, P less than 0.01). Patients with PVCs showed increased density of contour lines in the vulnerability map and significantly higher VI than those without PVCs (12.6 +/- 2.1 vs 10.4 +/- 1.7, P less than 0.01). This result suggests that a higher vulnerability index indicates that the condition of the cardiac muscle is at high risk of ventricular arrhythmias. It is concluded that the vulnerability map is useful for assessing whether or not the cardiac state is at high risk of ventricular arrhythmias in CAD.

Adult↗

PubMed1987

Inhibition of dipyridamole-induced myocardial ischemia by diltiazem in patients with coronary artery disease.

We investigated the effect of diltiazem on dipyridamole-induced myocardial ischemia in eight patients with coronary artery disease. Dipyridamole was infused at a rate of 0.142 mg/kg/min for 4 min, and 87-lead mapping was performed to determine the number of leads with ischemic ST-segment depression greater than or equal to 0.05 mV (nST). The range of nST was 8-24 (mean, 13.8) in the control study. Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5). It was concluded that diltiazem could suppress the myocardial ischemia following dipyridamole infusion.

Aged↗

PubMed1987

Sodium-dependent suppression of gamma-aminobutyric-acid-gated chloride currents in internally perfused frog sensory neurones.

1. The effects of the Na+ electrochemical potential gradient on gamma-aminobutyric acid (GABA)-induced Cl- currents (ICl) in frog sensory neurones were studied, using a suction pipette technique with which internal perfusion can be accomplished under current- and voltage-clamp conditions. 2. Under current clamp, the depolarizing response to GABA decreased in the presence of external Na+. A similar external Na+-dependent reduction in the GABA-induced inward ICl was observed under voltage clamp. The reversal potential of GABA-induced ICl (EGABA) was nearly equal to the Cl- equilibrium potential (ECl), irrespective of the presence or absence of external Na+. 3. Varying the Na+ influx by changing the holding membrane potential (VH) altered the GABA response: the GABA-induced ICl decreased progressively as VH became more negative. 4. The effects of changing the external and internal Na+ concentrations ([Na+]o and [Na+]i) on the GABA-induced ICl were also studied. Increasing [Na+]o at a constant [Na+]i reduced this current while increasing [Na+]i at a fixed [Na+]o facilitated it. 5. A high temperature coefficient of about 3 was estimated with respect to the percentage reduction in GABA-induced ICl due to [Na+]o. 6. These results indicate that the [Na+]o-dependent suppression of GABA-induced ICl was mediated chiefly by the uptake of GABA subserved by a Na-GABA co-transport mechanism. 7. GABA dose-response measurements were made with and without external Na+. The [Na+]o-induced suppression was more pronounced in relative amount at lower concentrations and in absolute amount at intermediate concentrations. Analysis of these data indicates, however, that the Na+-coupled GABA influx kept increasing at GABA concentrations high enough to nearly saturate GABA-induced ICl, and the same saturating level was observed as in the Na+-free case. This indicates that the electrogenic co-transport current was much smaller so that our measurements of GABA-induced ICl' were contaminated very little. Thus, the present method based on recording of GABA-induced ICl was legitimate for the analysis of the Na-GABA co-transport. 8. By analysing the [Na+]o-dependent suppression of GABA-induced ICl, the stoichiometric ratio of the underlying co-transport was estimated to be one: one Na+ ion per GABA molecule. 9. The ICl induced by GABA agonists such as beta-alanine, taurine, l-GABOB (l-gamma-amino-beta-hydroxybutyric acid) and muscimol was not affected by the amount of external Na+ present, suggesting difference in the affinity between receptor and transport carrier.

Action Potentials↗

PubMed1987

Antiallergic substance from Asarum sagittarioides and synthesis of some analogues.

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Animals↗

PubMed1987

The body surface distribution of the QT interval in patients with previous myocardial infarction and normal subjects.

In spite of the clinical importance of the QT interval, its body surface distribution is still unclear. To determine the spatial distribution of the QT interval, we studied 20 normal subjects and 45 patients with previous myocardial infarction (25, anterior; 20, infero-posterior). Unipolar electrocardiograms were recorded from 87 torso sites. The QT interval in each lead was determined semi-automatically. In normal subjects, the longer QT intervals were located on the left anterior chest and the right shoulder portion. And, the relatively shorter QT intervals were shown on the right inferior chest. In the anterior MI group, the remarkably longer QT intervals were located on the left anterior chest. In the infero-posterior MI group, the longer QT intervals were found on the left lateral and back. In both MI groups, the sites of longer QT intervals corresponded to the sites of infarcted area. In the aneurysm (+) subgroup of the anterior MI group, the remarkably longer QT intervals could be found on the left anterior chest, while in the aneurysm (-) subgroup, these characteristic patterns could not be recognized. Our data suggest that QT intervals are not equal on a torso. In patients with myocardial infarction, the sites of prolonged QT intervals corresponded to the sites of infarcted area. The QT interval was thought to have some bearing on the abnormal repolarization of the residual myocardium in the infarcted area.

Aneurysm↗

PubMed1987

Body surface mapping for the assessment of left ventricular hypertrophy in patients with essential hypertension.

To investigate the electrocardiographic abnormalities of left ventricular hypertrophy (LVH), body surface potential maps were acquired from 42 patients with essential hypertension. We adopted the time integral technique for analyzing body surface mapping data and used echocardiographic left ventricular muscle mass (LV mass) as the index of advance of LVH. The QRS, ST-T and QRST isointegral maps in normal volunteers all demonstrated smooth bipolar surface distribution patterns, with positive values located over the precordium and negative values over the right upper chest and back. In patients with essential hypertension, changes in the isointegral maps were observed as LVH advanced; A QRS increased on the upper left lateral chest and decreased (became more negative) on the right chest, A ST-T decreased on the lower left lateral chest and increased on the right upper chest, and areas of significant difference in A QRS and A ST-T were expanded as LVH advanced. A QRST decreased on the lower left lateral chest and increased on the right upper chest only in patients with severe LVH. We conclude that the changes of QRS and ST-T isointegral maps depend on the degree of advance of LVH and the severe grade of LVH causes the alterations in intrinsic repolarization properties.

Adult↗

PubMed1987

Determination of the site of myocardial infarction by QRST isointegral mapping in patients with abnormal ventricular activation sequence.

QRST isointegral maps were constructed from 87-lead ECGs in 37 patients with abnormal ventricular activation, such as ventricular premature beats, WPW syndrome, left bundle branch block and right bundle branch block. Patients were divided into 2 groups, the old myocardial infarction (OMI) group (n = 18) and the non-infarction group (n = 19). In the latter group, QRST isointegral maps showed smooth bipolar surface distributions, with positive values located over the precordium and negative values over the right upper anterior chest and the back, independent of the ventricular activation sequence. In the OMI group, for individual patients, the distribution patterns of QRST isointegral maps were similar between normal sinus rhythm and VPB or WPW conduction. Including the patients with BBB, a decrease of the time-integral value was consistently found in leads which corresponded to an asynergic site indicated by left ventriculography. To evaluate the abnormalities of QRST isointegral maps, particular attention was given to the area where the QRST time-integral value was less than the lower limit determined by 40 normal subjects; this area was designated as the negative departure area. Characteristic distribution patterns of the negative departure area seem to indicate the asynergic site, independent of the activation sequence. Thus, the QRST isointegral map may be useful for identifying the asynergic site in patients with abnormal ventricular activation sequence, that is hardly detected with conventional electrocardiograms.

Adolescent↗

PubMed1987

Determination of the hypertrophic site of the left ventricle by body surface mapping in patients with hypertension.

To estimate the hypertrophic sites of the left ventricle by body surface mapping (MAP), we performed MAP in 55 patients with hypertension and compared the MAP data with echocardiographic findings. MAP data were analyzed using the departure map technique reported by Flowers et al. The mean and standard deviation (SD) of the normal control were obtained from 40 normal volunteers. We constructed departure maps at 20, 30, 40, 50 and 60 msec from the onset of the QRS. Each map indicates the area of abnormally increased potential outside the normal range at the time. Subjects were classified into 5 groups according to the appearance time of the abnormal positive area. Septal thickness was significantly increased in groups that had an abnormal positive area at 20 msec, and left ventricular posterior wall thickness was significantly increased in the groups that had an abnormal positive area at 60 msec. We postulate that the increased electrical potential due to hypertrophy of the interventricular septum is represented by the abnormal positive area at 20 msec, and the increased potential of the left ventricular posterior wall by the abnormal positive area at 60 msec. MAP, especially the departure map technique, is a useful method to detect the abnormal electrical potential distribution in patients with left ventricular hypertrophy.

Adult↗