Local Depolarization Research Articles

Simulated dendritic spines influence reciprocal synaptic strengths and lateral inhibition in the olfactory bulb

Whereas many theories have been proposed for the function of dendritic spines in axodendritic processing, the influence of spines on reciprocal dendrodendritic processing has received relatively little attention. Mitral cells in the olfactory bulb, for example, synapse on granule cell spines (gemmules) which are in turn presynaptic to reciprocal inhibitory synapses back onto the same mitral cells. The postulate that these synapses respond with synaptic strengths graded by presynaptic depolarization results in a sensitivity of the reciprocal response to the local depolarization in the spine head. A biophysical computer simulation was performed to study this effect and the effect of changing the spine neck diameter and cytoplasmic resistance on the reciprocal and lateral inhibitory responses given graded dendrodendritic synapses. Since spine head local potentials are larger than similar inputs on dendritic shafts, spines facilitate the graded reciprocal response even for low levels of activity. Spine heads also reduce the synaptic current, lowering the contribution to the rest of the granule dendritic tree and thus reducing lateral inhibition. In addition, an increase in the effective spine neck axial resistance further increases the reciprocal synaptic response and decreases the lateral inhibitory response. Short-term, reversible, and long-term methods of implementing this resistance-based dendrodendritic plasticity are discussed as well as the partial dependence of the reciprocal increase/lateral decrease effect on a broad synaptic gradation. Candidate memory operations by the bulb are also discussed, including a possible recognition memory pass/block function.

Presynaptic alterations associated with enhancement of evoked release and synthesis of norepinephrine in hippocampus of chronically cold-stressed rats

We have previously demonstrated that prior exposure to chronic cold stress does not alter basal levels of norepinephrine (NE) release or synthesis in hippocampus of rat. However, in response to a subsequent novel stressor, an enhancement of both of these noradrenergic parameters is observed in the chronically stressed animals relative to naive controls. In the present experiments, we have examined whether the biochemical sensitization of NE release and synthesis produced by chronic stress can be demonstrated by local depolarization of the noradrenergic nerve terminals with elevated K +. The local application of elevated K + in dorsal hippocampus resulted in a greater increase in extracellular NE and 3,4-dihydroxyphenylacetic acid (DOPAC) in chronically stressed rats than in naive controls. It is proposed that in dorsal hippocampus, extracellular NE and DOPAC provide measures of NE release and biosynthesis, respectively. Therefore, these data suggest that local depolarization, similar to novel stress, elicits both enhanced NE release and synthesis in chronically stressed rats. One factor that is known to modulate both of these processes is the presynaptic α-2 adrenergic receptor. Therefore, we examined whether a change in the sensitivity of these receptors might contribute to the altered noradrenergic responsivity observed in chronically stressed rats. Local administration of clonidine, an α-2 receptor agonist, produced a decrease in extracellular NE and DOPAC in both naive and chronically stressed rats. The dose-response curve for the effect of clonidine on NE was shifted to the left in the latter group. In addition, local administration of idazoxan, an α-2 receptor antagonist, produced a greater increase in extracellular NE and DOPAC in the chronically stressed rats than in naive controls. These data suggest that an increase in the α-2 receptor modulation of NE release and synthesis is operative in the chronically stressed animals. Although this apparent supersensitivity of the α-2 receptors cannot readily explain the enhancement of evoked noradrenergic responses observed in chronically stressed rats, it may underlie the unaltered basal levels of NE release and synthesis observed in these animals.

Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias.

Although the existence of myocardial mechanoelectrical feedback is well established, the mechanism of arrhythmia induction by ventricular dilatation or stretch remains insufficiently defined. In particular, controversy exists when comparing the arrhythmogenic potential of chronic versus acute myocardial stretch. Also, assessment of cellular electrophysiological effects of myocardial stretch has been incomplete. To evaluate the electrophysiological and arrhythmogenic effects of slow versus rapid ventricular wall stretch, we developed an isolated Langendorff-perfused rabbit heart model in which left ventricular (LV) volume can be changed by a computer-controlled servopump. Cellular electrophysiological effects and premature ventricular excitations (PVEs) and their origin produced by the volume increases were assessed by a multiple-site monophasic action potential (MAP) recording system and by volume-conducted ECGs obtained by immersing the entire preparation in a saline-filled tank. Volume was increased either gradually with slow volume ramps (0.1 ml/sec) or suddenly by volume pulses of varying pulse waveforms (three different amplitudes and five different rise velocities) applied randomly 250-350 times to each of eight hearts. Gradual LV volume loading caused gradual decreases in MAP resting and action potential amplitude, whereas rapid, transient volume pulses caused transient depolarizations. Despite similar membrane potential effects of stretch, gradual volume increases rarely (11%) produced PVEs, even with large volume loads, whereas rapid volume pulses of moderate amplitudes regularly triggered PVEs (45-100% of interventions). Logistic regression analysis showed that the probability of PVE occurrence increased independently with both the amplitude and the velocity of the volume increase, with the greatest sensitivity to stretch velocity exhibited at low and intermediate pulse amplitudes. Faster volume pulse rise velocities triggered PVEs at a lower instantaneous pulse amplitude than lower rise velocities, further corroborating the dependence of stretch-activated arrhythmias on the velocity of stretch. In contrast, an increase in the basic ventricular volume had no effect on the probability of PVE occurrence during the volume pulses. The MAP recordings demonstrated spatial variability in the extent of local depolarizations and site of PVE origin; transient depolarizations occurred, and PVEs originated most often in the posterolateral region of the left ventricle. Membrane depolarization is caused by both gradual and rapid ventricular stretch, but PVEs are more easily elicited by rapid stretch. Regions of greater myocardial compliance that experience greater relative stretch may act as "foci" for stretch-activated arrhythmias during dynamic ventricular loading. These whole-heart data corroborate the existence of stretch-activated membrane channels in ventricular myocardium and may help explain ventricular ectopy under conditions of differential ventricular loading, as in ventricular dyskinesia, or regional muscle traction, as in mitral valve prolapse syndrome.

Analysis of local electrogram characteristics correlated with successful radiofrequency catheter ablation of accessory atrioventricular pathways.

Due to the limited myocardial lesions produced by radiofrequency current, the ablation of accessory pathways (AP) requires precise localization of such connections. The purpose of this study was to ascertain which characteristic(s) of the local bipolar electrogram, recorded from the ablation and adjacent electrode immediately prior to the application of radiofrequency current, correlated with precision in localization adequate to permit AP ablation. Signal analysis was performed for 326 sets of electrograms preceding the attempted ablation of 107 APs in 100 consecutive patients. For 80 antegrade APs, the following variables were evaluated: (1) the presence or absence of an AP potential; (2) the local atrial-AP interval; (3) the local atrioventricular (AV) interval; and (4) the relationship between the onset of local ventricular depolarization and onset of delta wave of the surface electrocardiogram. For the 27 concealed APs, the following characteristics were evaluated: (1) the presence or absence of an AP potential; and (2) the local VA interval during reciprocating tachycardia or ventricular pacing. Antegrade APs: By statistical analysis, the best correlate of successful ablation of an antegrade AP was a local AV interval less than or equal to 40 msec (positive predictive value = 94%; 95% confidence intervals [CI] = 81%-100%). Local AV intervals less than or equal to 50 msec preceded 88% of successful AP ablations, compared to only 8% of failed radiofrequency current applications. The positive predictive value of the other variables were: presence of an AP potential: 35% (95% CI = 27%-40%); local atrial-AP intervals less than or equal to 40 msec: 54% (95% CI = 43%-66%); and local ventricular depolarization preceding onset of the delta wave 43% (95% CI = 34%-52%). For concealed APs, the positive predictive value of a VA interval less than 60 msec was 71% (95% CI = 48%-88%); the positive predictive value for the presence of an AP potential was 58% (95% CI = 32%-81%). No single electrogram characteristic had a positive predictive value and a sensitivity greater than 90% for AP localization adequate for radiofrequency current ablation. For antegrade APs, the best correlate of adequate localization was a local AV interval less than or equal to 40 msec; as a corollary, radiofrequency current applications at sites where the local AV was greater than 60 msec, were unlikely to be effective. Objective criteria for the localization of concealed APs were less certain. Electrogram analysis, as a guide to AP localization and ablation, requires careful analysis of multiple variables, with analysis of the local AV interval a salient objective factor.

Increased dispersion of “refractoriness” in patients with idiopathic paroxysmal atrial fibrillation

The average interval between local depolarizations during atrial fibrillation, the so-called atrial fibrillation interval, was used as an index for local “refractoriness.” This was based on the assumption that during fibrillation, cells are reexcited as soon as their refractory period ends. A very good correlation was found between refractory periods determined with the extrastimulus technique at a basic cycle length of 400 ms and atrial fibrillation intervals measured at the same epicardial sites of the right atrium.This new technique was used to assess dispersion in atrial fibrillation intervals in 10 patients with idiopathic paroxysmal atrial fibrillation and in a control group of 6 patients who were undergoing cardiac surgery. After a routine median sternotomy a multiterminal grid with up to 40 electrodes was placed over the right atrium, and atrial fibrillation was induced by premature stimulation. The average fibrillation interval in the test group, recorded at 247 sites, was 152 ± 3 ms and that is the control group, recorded at 118 sites, was 176 ± 8.1 ms (p < 0.05). Dispersion in atrial fibrillation intervals, defined as the variance of the fibrillation intervals at all the recording sites, was three times larger in the group with paroxysmal atrial fibrillation than in the control group.This study suggests that both a shorter refractory period and a larger dispersion in refractoriness are responsible for the recurrence of atrial fibrilation.

Electrophysiologic Changes and Ventricular Fibrillation in Acute Regional Ischemia in the Porcine Heart: The Concept of Wavelength

Early Electrophysiologic Changes in Acute Ischemia. Introduction: The purpose of this study was to match changes in conduction velocity, refractoriness, and wavelength during acute regional ischemia with initiation of ventricular fibrillation. Methods and Results: In 30 isolated, Langendorff‐perfused pig hearts we measured refractory period duration and conduction velocity in ventricular myocardium during the first minutes of regional ischemia in an attempt to determine the minimal changes in these parameters related to the occurrence of ventricular fibrillation (VF). In addition, we wanted to evaluate whether wavelength, i.e., the product of conduction velocity and refractory period, was a useful parameter to predict the occurrence of arrhythmias, as has been shown to be the case for atrial arrhythmias.1 The refractory period increased significantly after 1 minute of ischemia at basic cycle length and after one and two premature beats. Longitudinal and transverse conduction velocities varied with ischemic time. Compared to the preocclusion value, the longitudinal conduction velocity decreased significantly, but only after 2 minutes of ischemia and at basic cycle length. Wavelength was the least sensitive parameter for ischemia: neither in the longitudinal nor in the transverse direction did it change significantly even during 5 minutes of ischemia. VF was never induced by applying a single premature stimulus within the ischemic area. It occurred in 33% of the occlusions when three successive premature stimuli were delivered from within the ischemic zone, and in 100% when they were applied to the nonischemic myocardium. Whenever fibrillation was induced, it occurred within 3 minutes following coronary occlusions. Wavelength, neither before nor after coronary occlusion, could predict whether VF would occur. The only difference between hearts that fibrillated by stimulation of the ischemic myocardium and those that did not was that, in the first group, the refractory period at the site of stimulation prolonged significantly less than in the no‐VF group. Since electrophysiologic changes within the ischemic zone are inhomogeneous,2 an attempt was made to measure simultaneously at 52 sites the onset of inhomogeneity by determining the average interval between local depolarization during VF. This so‐called VF interval is an index of local refractoriness.3 The coefficient of variation of the VF interval, taken as an index of spatial dispersion in refractoriness, increased significantly 1 minute after occlusion in the border zone and 2 minutes after occlusion in the central ischemic area. Conclusion: In conclusion, wavelength is not a useful parameter to predict the occurrence of VF in hearts with regional ischemia because of the inhomogeneity in refractoriness, which develops within 2 minutes of ischemia. VF occurs when hearts are stimulated from sites with relatively short refractory periods, either within or outside the ischemic zone. (J Cardiovasc Electrophysiol, Vol. 3, pp. 128–140, April 1992)

MEMBRANE POTENTIAL RESPONSES TO THERMAL STIMULATION AND THE CONTROL OF THERMOACCUMULATION IN PARAMECIUM CAUDATUM.

1. The overall membrane potential response of the ciliate Paramecium caudatum to a rise in the temperature of its environment was depolarizing when the ambient temperature before stimulation (Te) was equal to or higher than the culture temperature (Tc), but hyperpolarizing when Te was lower than Tc. 2. The anterior region of the cell responded to a rise in temperature with a localized membrane depolarization. The posterior region was depolarized when Te was equal to or higher than Tc but hyperpolarized when Te was lower than Tc. The Te-dependent polarity reversal of the posterior response was responsible for the comparable reversal of the overall response. 3. The temperature at which the polarity reversal of the posterior response took place shifted according to Tc. This shift caused a comparable shift in the temperature at which polarity reversal occurred for the overall response. 4. The Te-dependent polarity reversal of the posterior response and its Tc-dependence are major causes of thermoaccumulation mediated by ciliary activity of Paramecium in regions with temperatures close to Tc.

Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction.

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.

The Atrial Electrogram During Clinical Electrophysiologic Studies: Onset versus the Local/Intrinsic Deflection

The Local Atrial Deflection. Introduction: As a wave front passes unfiltered bipolar recording electrodes, the point of local depolarization is marked by a maximal change in voltage, i.e., the intrinsic deflection. However, during electrophysiologic studies, the depolarization (A) on the lead recording the His‐bundle potential traditionally has been measured at the first rapid reproducible deflection on a filtered electrogram. This methodology permits considerable latitude for subjective interpretation. The purpose of this study was to assess the timing of the atrial electrogram using the intrinsic deflection of relatively unfiltered electrograms (0.1‐4.0 to 1,250 Hz) or the equivalent on filtered recordings. Methods and Results: To do this we studied 70 patients without evidence of atrial or atrioventricular (AV) nodal disease, documenting the difference in timing between the A wave as traditionally measured and as measured at its peak local deflection (AL) determined from simultaneously recorded filtered and relatively unfiltered electrograms. New ranges based on the AL were established for timing of intra‐atrial and AV nodal conduction intervals. The P‐A (41 ± 11 msec) was significantly shorter than the P‐AL (55 ± 12) and the A‐H (80 ± 20) was longer than the AL‐H (66 ± 21 msec), both P &lt;0.001. Interobserver differences in measurements were smaller when using the local (AL) rather than traditional criteria. Conclusions: Conventional measurement of the A deflection provides only a rough estimate of local depolarization of the atrium near the AV node. The criteria proposed in the present article may (1) provide a better estimate of the timing of local depolarization; (2) have application in computerized timing of intervals; and (3) decrease technical problems and subjective error.

Fluctuation of Local Field and Depolarization Ratio of the ν1 Raman Line of Carbon Tetrachloride in Carbon Disulfide Solution

Abstract The depolarization ratio of a molecule having Td symmetry has been expressed in terms of the mean-square fluctuation of the local field which is felt by a molecule in the condensed phase. The fluctuation of the polarizability at each position in the scattering volume was found to dominantly affect local-field fluctuation. The concentration dependence of the depolarization ratio for the ν1 Raman line of carbon tetrachloride in a carbon disulfide solution could be well described by this expression.

Termination of Ventricular Tachycardia by Nonpropagated Local Depolarization: Further Observations on Entrainment of Ventricular Tachycardia from an Area of Slow Conduction

A 60-year-old woman with a large left ventricular apical aneurysm underwent preoperative catheter mapping of ventricular tachycardia. A zone of slow conduction with marked decremental conductive properties was identified between the left ventricular aneurysmal pouch and the right ventricular septum. Pacing from the right ventricular septum produced a QRS on the surface electrocardiogram of the same morphology as that of spontaneous ventricular tachycardia, while pacing from the left ventricular aneurysm caused tachycardia entrainment without fusion. Termination of ventricular tachycardia invariably occurred in association with an unpropagated left ventricular capture, followed by a change in ventricular activation to an opposite direction. This case provides a direct demonstration of reentrant ventricular tachycardia termination by orthodromic block in a zone of slow conduction.

The effects of nerve terminal activity on non‐quantal release of acetylcholine at the mouse neuromuscular junction.

1. Local endplate depolarization induced by anticholinesterase application to mouse nerve-diaphragm preparations was taken as a measure of non-quantal release of acetylcholine. 2. Non-quantal acetylcholine release occurred within 20-60 s after anticholinesterase application, either spontaneously or evoked by nerve stimulation. Non-quantal release declined with time and disappeared after 3-5 min. 3. The amplitude of stimulation-evoked non-quantal release increased with the frequency of stimulation and was maximal at frequencies above 50 Hz. Two stimuli were sufficient to evoke the maximal effect. 4. Micromolar concentrations of atropine, pirenzepine and vesamicol reduced the amplitude and shortened the duration of non-quantal release. Oxotremorine (10(-8) M) enhanced the amplitude and ouabain (10(-4) M) prolonged the duration of non-quantal release. 5. Our results support the idea that the non-quantal release is due to the vesicular acetylcholine transport system which becomes transiently a part of the nerve terminal during exocytotic release of quantal acetylcholine.

The Precision of Electrophysiological Mapping: Localizing Depolarization Wave Fronts from Digitized Extracellular Eleetrograms and the Role of Data Sampling Rate

The Precision of Electrophysiological Mapping: Localizing Depolarization Wave Fronts from Digitized Extracellular Electrograms and the Role of Data Sampling Rate. Electrophysiological mapping uses extracellular electrograms to estimate the timing of local cellular depolarization. To measure the precision of localizing propagating wave fronts with this technique and determine its dependence on data sampling rate, extracellular electrograms were recorded with a laboratory computer from 61 bipolar epicardial and endocardial electrodes during 10 morphologically distinct episodes of ventricular tachycardia (VT) in 10 chronically infarcted dogs. Four investigators assigned local activation times to 610 computer displayed local electrograms (61 from each of 10 VTs) sampled at 1,000 Hz (trial 1). With the investigators blinded to the result of the first trial, activation mapping was again repeated in serial independent trials using identical eleetrograms displayed at the data acquisition rate (1,000 Hz), in addition to sampling rates of 500 Hz, 250 Hz, and 125 Hz. The temporal precision of activation mapping (± 10 msec, 95% confidence) was derived from the reproducibility of measuring local activation time from maximally sampled (1,000 Hz) extracellular electrograms. Multivariate analysis revealed decreased precision at epicardial (P &lt;0,02) and infarcted sites, which was attributed to fractionated eleetrograms observed in these regions. Nonetheless, map guided localization of the anatomic breakthrough site of each tachycardia varied by only 1.0 ± 1.2 cm between trials. This value was consistent with the spatial resolution (± 0.5 to + 1.0 cm) that was predicted from the measured temporal precision. Extracellular electrograms contained minimal frequency content above 150 Hz resulting in negligible distortion of waveform morphology at sampling rates as low as 250 Hz. Moreover, the accuracy of activation mapping was not significantly impaired until sampling rate was slowed to 125 Hz.

Excitatory synaptic responses in turtle cerebellar Purkinje cells.

1. Climbing fibre responses (CFRs) and parallel fibre responses (PFRs) in Purkinje cells have been analysed in intracellular recordings obtained at various levels from cell body to terminal dendrites in the turtle cerebellum in vitro. 2. With increasing stimulus intensity, the PFR recorded in distal dendrites displayed an early regenerative component which was graded at rest and at hyperpolarized membrane potentials, but was all-or-none at depolarized membrane potentials. 3. The all-or-none component had the same characteristics as Ca2+ spikes triggered by passing depolarizing current through the recording electrode. 4. The repolarizing phase of the PFR had a fast component enhanced by depolarization and diminished by hyperpolarization. 5. In the mid-molecular layer the PFR also included a plateau component which was increasingly prolonged by depolarization and abolished by hyperpolarization. 6. CFRs recorded in the soma had a plateau component, prolonged by local depolarization and abolished by local hyperpolarization. 7. The CFR in distal dendrites included a regenerative component. In some cells this component appeared in an all-or-none manner with local depolarization. In other cells it was smoothly graded with local polarization. 8. In mid-molecular records the CFR was prolonged by local depolarization and presumably electrotonically affected by the configuration of the response more distally and proximally in the cell. 9. It is concluded that excitatory synaptic responses in Purkinje cells include a regenerative Ca2+-mediated spike component in the spiny dendrites and a plateau component located in the proximal dendrites and/or the cell body. It is shown that both responses are modulated in configuration by the local membrane potential. In the spiny dendrites activation and inactivation of the transient hyperpolarizing potential appear to govern the Ca2+ influx during the CFR.

Calcium and neuronal function.

Calcium is unique among metals because its ions have a very large concentration gradient across the plasma membrane of all cells, from 10(-3) M Ca2+ outside, to 10(-7) M Ca2+ inside. This gradient is maintained by the use of metabolic energy through ion pumping, and its existence allows cells to use transient increases in the intracellular Ca2+ concentration as signals, which regulate cell function. In neurones these Ca signals are initiated by electrical activity (action potentials) which open voltage-dependent Ca channels in the plasma membrane, allowing Ca to enter the cell. Intracellular Ca signals can also be produced by transmitters at synapses, which open Ca channels, either directly, or indirectly by causing local depolarization and the opening of voltage-dependent Ca channels. The main effects of Ca signals on neurones are to alter their electrical activity, by modifying the opening and closing of Na and K channels, and to stimulate the release of transmitter substance. Ca has a host of other effects, such as the regulation of metabolic activity, the regulation of cell growth, and the long-term modification of synaptic efficiency, and it is even implicated in the destruction of neurones.

Mechanism of depolarization in the ischaemic dog heart: discrepancy between T-Q potentials and potassium accumulation.

1. To study the origin of ischaemic myocardial depolarization, the diastolic surface potential - T-Q depression-was correlated with subepicardial extracellular K+ accumulation during serial episodes of widespread ischaemia in open-chest dogs, and in isolated, blood-perfused canine hearts. Placement of the reference electrode on a small island of non-ischaemic myocardium simplified the interpretation of the T-Q potentials. 2. In some experiments, changes in resting potential in the ischaemic zone were recorded using a 'contact' monophasic action potential (MAP) electrode. The change in MAP resting potential was linearly related to T-Q depression for a wide range of experimental conditions (R greater than 0.98). T-Q depression is therefore a linear index of depolarization in superficial myocardial cells. 3. The validity of T-Q depression as a 'measure' of local cellular depolarization was further tested by infiltration of isotonic KCl into the superficial myocardium subjacent to the ischaemic zone electrode. Resulting T-Q depression was 2- to 3-fold larger than the maximum values obtained in ischaemia; and the ratio of T-Q depression to the amplitude of the accompanying monophasic potential was consistent with the assumption that KCl had fully depolarized the underlying myocardium (delta Vm = 89 mV). KCl prevented (i.e. occluded) further changes in the T-Q potential during ischaemia. KCl did not have these effects if it was introduced at sites more remote from the electrode (greater than 4 mm). 4. Ischaemic T-Q depression was drastically accelerated by increasing the heart rate from 90 to 180 beats/min and was further accelerated by arterial infusion of CaCl2. These effects were most striking during the first minute of ischaemia. 5. In contrast, the above manoeuvres produced little acceleration of subepicardial K+ accumulation. After CaCl2 infusion, large ischaemic potentials, severe conduction impairment, and arrhythmias could be observed when K+ activity was almost normal (aK = 4.0-4.5 mM). 6. T-Q depression was larger in vivo than in isolated hearts, both absolutely and relative to K+ accumulation. 7. Based on the reproducible amplitude of ischaemic epicardial potential-estimates of cellular depolarization (delta Vm) could be obtained, which were compared with the concurrent change in K+ electrode potential (delta EK) for each experimental condition. 8. Estimated depolarization was nearly identical to delta EK in isolated hearts under basal conditions. However, depolarization significantly exceeded delta EK during rapid pacing, CaCl2 infusion, or during paced occlusions performed in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

The Local Depolarization Field of Two-Dimensional 180° Bloch-Type Boundaries

The approximate analytic solution of the constitutive micromagnetic equations yields a self-consistent expression for the inhomogeneous two-dimensional distribution of the depolarization field within 180° Bloch walls. As a consequence of the assumed constraints, the field distribution is symmetric with respect to the central wall plane and depends, apart from the lateral coordinate, critically upon the actual distance to the crystal surface. The derived results permit a check of the phenomenologic Neel approach as well as a closer discussion of the recently observed wall polarization-reversal process. Die analytische Naherungslosung der konstituierenden mikromagnetischen Gleichungen liefert einen selbstkonsistenten Ausdruck fur die inhomogene zweidimensionale Verteilung des Depolarisationsfeldes innerhalb von 180°-Blochwanden. Als Konsequenz der angenommenen Zwangsbedingungen ist die Feldverteilung symmetrisch in bezug auf die zentrale Wandebene und hangt, neben der lateralen Koordinate, kritisch vom aktuellen Abstand zur Kristalloberflache ab. Die abgeleiteten Resultate erlauben eine Uberprufung des phanomenologischen Neel-Ansatzes sowie eine eingehendere Diskussion des kurzlich beobachteten Wand-Polarisationsumkehrprozesses.

Spreading depression in the olfactory bulb of rats: Reliable initiation and boundaries of propagation

Spreading depression in the olfactory bulb of rats is an elusive phenomenon, the demonstration of which requires specific conditioning procedures. The present paper describes a simple technique for reliable initiation of bulbar spreading depression with microinjections of potassium acetate. Adult hooded rats were anesthetized with pentobarbital (50 mg/kg) and slow potential changes accompanying spreading depression were recorded with capillary microelectrodes stereotaxically inserted into the olfactory bulb and adjacent forebrain structures. KCl microinjection (0.5–1.0 μl, 0.134–0.670 mol/l) into the olfactory bulb elicited local depolarization which only exceptionally developed into a propagating spreading depression. Potassium acetate (0.5–1.0 μl, 0.15 mol/l) injected into the rostral olfactory bulb evoked a negative slow potential wave (amplitude of around 25 mV and duration 30–50 s) propagating at a rate of 3–4 mm/min through all the olfactory bulb layers. Low positive (5 mV) instead of negative waves were recorded in the superficial olfactory nerve layer with reversal in the glomerular layer (200–300 μm). The slow potential decreased in the rostrocaudal direction and expired at the caudal boundary of the olfactory bulb. Bulbar spreading depression never spread to neocortex, and cortical spreading depression never entered into the olfactory bulb but stopped in the anterior olfactory nucleus 7 mm rostral to bregma. Repeated potassium acetate injections into the olfactory bulb occasionally elicited a series of spreading depression waves recurring at regular intervals, probably reflecting reverberation of scroll-shaped waves around the rostrocaudal axis of the olfactory bulb. It is argued that the low susceptibility of the olfactory bulb to spreading depression is due to powerful GABAergic inhibition which can be weakened by (Cl −) e reduction after potassium acetate injections.

Mechanisms of ventricular tachycardia termination and acceleration during transvenous cardioversion as determined by cardiac mapping in man

We examined the EP mechanisms underlying efficacy and inefficacy of transvenous cardioversion shocks in 13 patients with coronary artery disease and sustained VT during preoperative and intraoperative cardiac mapping procedures. Shocks were delivered at the right ventricular apex with a Medtronic 6880 catheter and a Model 5350 external cardioverter/defibrillator with two or three electrode configurations, resulting in unidirectional or bidirectional shocks, respectively. Single transvenous shocks with incremental energies ranging from 0.03 to 25 J were delivered in sinus rhythm and VT, and simultaneous right and left ventricular electrograms were obtained.Transvenous cardioversion shocks of 0.03 J in sinus rhythm and VT produced immediate local right ventricular depolarization and subsequently conducted to distant right ventricular and left ventricular sites after 30 to 100 msec. Shocks of 0.05 to 0.5 J produced immediate depolarization of progressively larger right ventricular and left ventricular regions, with shocks ≥0.5 J producing immediate depolarization of distant left ventricular sites in sinus rhythm. High energy (>5 J) shocks produced instantaneous depolarization of multiple right ventricular and left ventricular sites in VT. VT termination occurred due to either delay or interruption of conduction in the tachycardia circuit, despite prior depolarization of the early sites of ventricular activation during the QRS complex. This could be due to instantaneous or paced depolarization of critical “excitable” components of the VT circuit, resulting either in immediate conduction block or in instability followed by termination. VT acceleration with transvenous cardioversion was due to modification of the “excitable,” slowly conducting components of the VT circuit with the development of new areas of conduction block, along with altered intra-ventricular conduction. Similar EP mechanisms were observed with unidirectional and bidirectional transvenous shock patterns. We conclude that transvenous shocks alter conduction in human ventricle, and clinical effects of QRS synchronized shocks are related to conduction changes induced in the excitable components of the VT circuit.

No evidence for local electromagnetic depolarization effects in SERS from coldly deposited silver films

We have studied the coverage dependence of the Raman intensities of various vibrational modes of pyridine, benzene and cyclohexane adsorbed on coldly deposited silver films (10 K < T s < 100 K). It cannot be described with a classical depolarization model. We offer a different explanation based on a model of electronic enhancement.