PROPAGATION OF ELECTRIC ACTIVITY IN MOTOR NERVE TERMINALS.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Multiple supraventricular tachycardias were induced in a patient with two left posterior accessory pathways and dual atrioventricular nodal conduction. One of the accessory pathways conducts slowly and exhibits decremental conduction. A "double retrograde response" (2:1 ventriculoatrial conduction) due to simultaneous retrograde propagation of a single ventricular depolarization over two longitudinally dissociated pathways plays a role not only in tachycardia initiation, but in the maintenance of a unique, irregular tachycardia.
1. Electrical stimulation of spinal sensory nerves evoked discharges in inferior cardiac and renal nerves. In the anaesthetized cat both an early and a late response could be recorded in each nerve.2. For any one afferent input the central delay of the late cardiac nerve response was significantly less than that of the late renal nerve response. The central delay of the early responses was similar for both nerves. In the spinal cat only the early response was present.3. Cooling the floor of the 4th ventricle abolished the late responses in renal nerves, but left reflex volleys in white rami and intercostal nerves unchanged.4. Stimulation in the brain stem evoked responses in both cardiac and renal nerves which had a shorter latency than the reflexes evoked in these nerves by stimulating dorsal roots.5. The late responses could be abolished by lesions in the cervical spinal cord.6. Such evidence led to the conclusion that there are two pathways for reflex discharge into inferior cardiac and renal nerves, one involving a supraspinal relay and the other confined to the spinal cord.
The unilaterally induced patterns of prominent excitatory post-synaptic activity within Areas 17 and 18 were investigated in normal and monocularly deprived cats. They were elicited by electrical stimulation of the optic nerves and evaluated with the one-dimensional current source-density method. 1. In Area 18 of normal cats the unilaterally and bilaterally induced current source-density patterns closely resemble each other. None of the mono-, di- or tri-synaptic activities is potentiated by binocular convergence. 2. In Area 18 of monocularly deprived cats the synaptic currents elicited by stimulating the nerve on the deprived side lead to approximately the same spatial and temporal distribution of sinks and sources as those induced from the normal eye; but the amplitudes are considerably smaller. This reduction is similar for mono-, di- and trisynaptic responses which indicates (a) that the imbalance between activity from the deprived and non-deprived eye is mainly due to reduced input to the cortical target cells from the deprived eye and (b) that the activity from the deprived eye still relayed to these cells is passed on to supra- and infragranular layers without diminution and in the same way as activity from the normal eye. 3. The imbalance of afferent activity from the deprived and non-deprived eye is apparent in the evoked potentials recorded from the white matter. This indicates that activity from the deprived eye is already strongly reduced in the thalamo-cortical fibres. 4. In monocularly deprived, but not in normal cats the monosynaptic activities from the two eyes are often segregated in depth within layer IV. 5. In Area 17 of both normal and deprived cats only a small fraction of the potential monosynaptic activity can be elicited by electrical stimulation of the optic nerves because of transmission failure in the lateral geniculate nucleus. Comparison of the current source-density patterns elicited from the normal and deprived nerve in monocularly deprived cats indicates that activity produced by fast conducting afferents is more affected (reduced) by deprivation that that conveyed by slower afferents.
We used close bipolar intramural electrodes and catheter electrodes to study the characteristics of conduction in the bundle of His and proximal bundle branches during premature atrial beats in 17 open-chest anesthetized dogs. The electrophysiological properties of the proximal conducting system were heterogenous. The shortest interval between a normal His bundle response and a premature response that was not accompanied by changes in conduction time (the total recovery time) was 258.8 +/- 23.9 (SD) ms for the proximal His and 310.7 +/- 30.6 ms for the distal His and proximal bundle branches. A period of supernormal conduction, in which the conduction times of premature beats were faster than during earlier or later beats, was localized to the distal portion of the bundle of His and proximal bundle branches. The minimal conduction time during the supernormal period was decreased by 9.6 +/- 4.6% below control diastolic conduction times, and the supernormal period was 61.0 +/- 25.7 ms in duration. The characteristics of the period of supernormal conduction in the distal bundle of His and proximal bundle branches were very similar to those previously found in the peripheral bundle branch-Purkinje system. The mechanism of supernormal conduction in the bundle of His is most probably due to a period of supernormal excitability.
The effects of strophanthidin on electrical and mechanical events in canine cardiac Purkinje fibers were studied in vitro in the absence and presence of tetrodotoxin (TTX), norepinephrine, and high calcium. In Tyrode solution, strophanthidin (1-3 X 10(-7) M), norepinephrine (3-5 X 10(-7) M), and high calcium 8.1 mM) increased the force of contraction, and TTX markedly reduced it. In the presence of TTX, strophanthidin had little or no inotropic effect, whereas that of norepinephrine and high calcium was less than in Tyrode solution. In the presence of TTX, strophanthidin increased force markedly if (and as long as) either norepinephrine or high calcium were also present. A higher dose of strophanthidin (10(-6) M) induced a markedly delayed increase in force in presence of TTX. The results suggest that, in the presence of TTX, in a low concentration strophanthidin has little effect on force, because cellular calcium is low; however, it becomes effective when the calcium is increased by norepinephrine or high calcium. In toxic doses, strophanthidin increases force even in the presence of TTX as the inhibition of the pump should increase intracellular sodium and therefore calcium.
Stimulation of abdominal sympathetic visceral afferents reflexly excites the cardiovascular system. The present study examined the role of summation of afferent input in this reflex. Single-unit activity of A delta- and C-fiber afferents was recorded from the right thoracic sympathetic chain in anesthetized cats to determine the relationship between intensities of electrical stimulation and the types of nerve fibers within the right greater splanchnic nerve. The differential effect of cooling on A delta- and C-fiber axons in the sympathetic chain also was examined by recording single-unit afferent activity. Reflex cardiovascular responses were induced by electrical stimulation of the central cut end of the right greater splanchnic nerve. We observed that the numbers of A delta and C fibers activated by electrical stimulation were proportional to the intensity of stimulation. However, neither local cooling nor intensity of stimulation provided a means to separate A delta and C fibers contained in the sympathetic chain. The results demonstrate that the magnitude of excitatory cardiovascular reflexes is frequency dependent and is related directly to intensity of electrical stimulation, suggesting that both adequate discharge frequency of the afferent and sufficient numbers of afferents recruited are crucial factors for full expression of reflex cardiovascular responses.
Explore the source record for details and available documents.
BACKGROUND: The effect of verapamil on long-term tachycardia-induced atrial electrical remodeling has not been reported. METHODS AND RESULTS: Forty-eight dogs were randomly divided into verapamil and control groups. The dogs in the verapamil group received verapamil 120 mg every day, those in the control group did not receive verapamil. Atrial effective refractory period (AERP), inducibility of atrial fibrillation (AF), and duration of AF were assessed before and after complete atrioventricular junction ablation with 1-day, 1-week, or 6-week rapid atrial pacing (780 bpm). AERP shortening, AERP dispersion, AERP maladaptation, and inducibility of AF after 1-day pacing was significantly attenuated by verapamil. However, verapamil did not have any significant effect on these parameters in the dogs with 1-week or 6-week pacing. Verapamil did not have any significant effect on the conduction velocity in the dogs with 1-day, 1-week, or 6-week pacing. Before rapid atrial pacing, verapamil significantly prolonged the duration of AF. In the dogs with 1-day pacing, the duration of AF measured immediately after termination of pacing was similar between the control and verapamil groups. However, in the dogs with 1-week or 6-week pacing, the duration of AF after pacing was significantly longer in the verapamil group. CONCLUSIONS: Verapamil cannot prevent long-term (1 and 6 weeks, respectively) tachycardia-induced changes of atrial electrophysiological properties. Furthermore, verapamil increases the duration of AF in the dogs either before or after long-term rapid atrial pacing.
Explore the source record for details and available documents.
Electrophysiological studies in one patient with type B pre-excitation and dual A-V nodal pathway revealed several types of paroxysmal narrow QRS tachycardia (PSVT). One type of PSVT reflected antegrade fast A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retorgrade activation of right atrial appendage, P following QRS and cycle length of 290 to 350 msec. A second PSVT reflected antegrade slow A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retrograde activation of right atrial appendage, P following QRS, and cycle length of 440 msec. A third PSVT reflected A-V nodal re-entrance with antegrade slow pathway and retrograde fast pathway conduction. This PSVT was characterized by normal retrograde atrial activation sequences, P simultaneous with QRS, and cycle length of 320 msec. All PSVT inductions could be explained in terms of antegrade and retrograde properties of fast and slow A-V nodal and anomalous pathways.
The electrophysiologic determinants of conversion and the prevention of atrial flutter are poorly defined. This issue was therefore investigated by evaluating the effects of the new class III antiarrhythmic drug d-sotalol and the class I antiarrhythmic drugs quinidine and lidocaine. Atrial flutter was reproducibly induced in the open-chest anesthetized dog with intercaval crush and rapid atrial pacing. In this preparation, intravenous d-sotalol restored sinus rhythm in 14 of 15 (93%) dogs, whereas quinidine converted nine of 15 (60%) and lidocaine two of 10 (20%). d-Sotalol prevented reinduction in eight (53%), whereas quinidine was effective in four (27%) and lidocaine in none (0%). In the atria, d-sotalol induced significant increases in effective refractory period (+32%; p less than .01), functional refractory period (+30%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+9%; p less than .05), and atrial flutter cycle length (+8%; p less than .01). Quinidine increased effective refractory period (+40%; p less than .01), functional refractory period (+27%; p less than .01), conduction time at sinus cycle length (+13%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+18%; p less than .01), and atrial flutter cycle length (+31%; p less than .01). Lidocaine decreased functional refractory period (-6%; p less than .05) while lengthening the atrial flutter cycle length (+13%; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to examine the effects of ablation of the superficial endocardium and Purkinje network on left ventricular fibrillation threshold. Lugol's solution was applied through small ventriculotomies to the left and right ventricular endocardium of 10 dogs on cardiopulmonary bypass. Two control groups of five animals each underwent either endocardial application of saline or epicardial application of Lugol's solution. Ventricular fibrillation threshold was measured before and after each intervention by the single-stimulus technique. Application of Lugol's solution to the endocardium resulted in a 102 +/- 15% increase in ventricular fibrillation threshold from a control value of 26 +/- 2 to 53 +/- 6 mA (p less than .005). In two animals, ventricular fibrillation could not be initiated postoperatively. In the control groups, there were no significant changes in ventricular fibrillation threshold. Histologic examination revealed that Lugol's solution obliterated less than 0.5 mm of superficial endocardium while sparing the adjacent myocardium. Electrophysiologic and rheologic data confirmed the discrete nature of the chemical injury. Thus ablation of the superficial ventricular endocardium with Lugol's solution results in a profound increase in the ventricular fibrillation threshold with only minimal tissue destruction.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.