The role of local disparity in conduction and recovery time on ventricular vulnerability to fibrillation.
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Biomedical subjects
Publications and source records attributed to J Han.
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The effects of electrical stimulation of the vagus nerves and the administration of atropine on ventricular fibrillation threshold (VFT) were studied in open-chest hearts of 15 dogs anesthetized by alpha-chloralose. These studies were made in both normal and ischemic ventricles, i.e., before and during acute coronary occlusion. The ventricles were paces at a constant rate to eliminate rate-dependent changes and the minimal current required to induce ventricular fibrillation (or VFT) was determined by delivering a train of rapid rectanglular pulses (100 per second) to the venticle actoss the vulnerable period. In normal ventricles, VFT's were significantly increased by vagal stimulation (P less than 0.01) and decreased by atropine (P less than 0.05). Coronary occlusion markedly decreased VFT's (P less than 0.01), and vagal stimulation or atropine failed to alter VFT's significantly in these ischemic ventricles (P greater than 0.8). In additional 14 dogs, the effects of vagal stimulation and atropine were studied after the administration of propranolol. Propranolol alone increased VFT's significantly in boetreatment with propranolol, vagal stimulation and atropine failed to change VFT's significantly in both normal and ischemic ventricles (P greater than 0.8). These results indicate that the vagus nerves exert their effect on VFT by modifying the sympathetic nerve activity in normal ventricles, but such an effect is not significant enough to alter VFT in ischemic ventricles.
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The present experiments were conducted on isolated dog hearts to demonstrate that conduction disturbances can be induced in the bundle branches by transection of about 50 per cent of the cross-sectional area of the His bundle on the right or left side. The His bundle, the posterior and anterior divisions of left bundle, and the right bundle were exposed by careful dissection, and microelectrode techniques were used to record action potentials from the three bundle branches. Pacing stimuli were applied to the nonbranching portion of His bundle proximal and then distal to the site of transection to study the effect of such lesions on impulse conduction to the bundle branches. It was demonstrated that conduction to the bundle branches was not affected by such lesions in the His bundle at pacing rates slower than 100 per minute; however, conduction disturbances were rate-dependent and manifested at faster pacing rates. In nine out of all 16 experiments, partial or complete block occurred in all three bundle branches regardless of the side of the lesion. In the remaining seven experiments, they were observed in the bundle branch on the same side as the lesion. It was assumed that conduction disturbances of the bilateral bundle branches resulted from decremental conduction in the uncut portion of His at the level of lesion, and those of the ipsilateral branch from the functional failure of transverse crossover connections between the longitudinal His bundle fibers. The results indicate that localized lesions in the nonbranching portion of His bundle can indeed produce the pattern of bundle branch block under certain conditions.
Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.
The effect of acetylcholine on automaticity of Purkinje fibers was studied in isolated canine false tendon preparations with conventional microelectrode techniques. Of 15 preparations with the control spontaneous rate of 12-60 beats/min, acetylcholine in a concentration of 0.5 mug/ml decreased the spontaneous rate by 20-87% in 13 preparations. This decrease in automaticity was due to a decrease in the slope of phase 4 depolarization and an increase in the maximum diastolic potential. The inhibitory effect of acetylcholine could be reversed by atropine in a concentration of 3 mug/ml in six preparations and prevented by pretreatment with atropine in another six preparations. Atropine per se did not have any appreciable effect on automaticity of Purkinje fibers. The results indicate that acetylcholine significantly suppresses automaticity of canine Purkinje fibers through its muscarinic action.
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VFT's were determined in 12 open-chest dogs at epicardial sites in the right and left ventricles (RV and LV) following normally or aberrantly conducted beats. The normal beats were produced by right atrial pacing, and the aberrant beats by surgical RBBB or ventricular pacing at an RV or LV site. The mean VFT following normal beats was 21.2 plus or minus 1.8 ma. in RV and 23.0 plus or minus 2.7 ma. in LV. The mean VFT following aberrant beats of RBBB was 21.3 plus or minus 2.6 ma. in RV and 25.0 plus or minus 2.8 ma. in LV. The difference between the mean VFT of normal beats and that of aberrant beats was not statistically significant. The mean values of VFT's determined in RV or LV following aberrant beats produced by pacing of the contralateral ventricle were not significantly different from those of the normal beats. The mean VFT was 22.9 plus or minus 3.1 ma. in RV and 20.1 plus or minus 2.1 ma. in LV. These results indicate that the aberrancy of ventricular beats per se is not associated with decreased VFT or increased ventricular vulnerability to fibrillation. The most predictable observation was that the mean VFT's were significantly lower in both ventricles when they were determined at the site of application of pacing stimuli. The mean values were 12.4 plus or minus 1.2 ma. in RV and 13.6 plus or minus 1.6 ma. in LV. This decrease in VFT may be due to slow conduction and increased asynchrony of recovery of excitability at or near the site of application of pacing stimuli.
The effects of unipolar and bipolar stimulation on ventricular fibrillation threshold were studied during acute occlusion of the left anterior descending coronary artery in 13 anesthetized dogs. Values for ventricular fibrillation threshold were determined by delivering trains of rapid bipolar or unipolar pulses (100/sec) during the vulnerable period. The mean threshold value was found to be 13.0 ma for bipolar, 13.9 ma for unipolar anodal and 21.0 ma for unipolar cathodal stimulation. Ventricular fibrillation threshold was significantly lower (P less than 0.01) with both unipolar anodal and bipolar stimulation than with unipolar cathodal stimulation. In these animals, the first premature beats induced by the rapid stimuli occurred significantly earlier with unipolar anodal and bipolar stimulation than with unipolar cathodal stimulation. The effect of competition of unipolar or bipolar pacing stimuli with normally conducted ventricular beats was also studied in a group of 16 dogs. Repeated trials of competitive pacing during coronary occlusion showed that the incidence of ventricular fibrillation was significantly greater (P less 0.05) with bipolar pacing (36 percent) than with unipolar cathodal pacing (15 percent). These results indicate that bipolar pacing is potentially more dangerous than unipolar cathodal pacing and suggest that the incidence of pacemaker-induced ventricular fibrillation might be further reduced by the use of unipolar cathodal stimulation during acute myocardial infarction.
The effects of manganese chloride (MnCl2) and verapamil on automaticity of digitlazied Purkinje fibers were studied using conventional microelectrode techniques. The stduied wer made in isolated, spontaneously beating Purkinje prearations. Quabain alone consistently increased the automatic rate, whereas no such increase was observed when the preparations were superfused with a mixture of ouabain adn MnCl2. MnCl2 was also shown to be effective is suppressing the enhanced automaticity induced by ouabain. Mncl2 alone did not have a significant effect on the spontaneous rate of Purkinje fibers. The effect of verapamil was similar to that of MnCl2 in preventing and suppressing the ouabain-induced increase in automaticity. MnCl2 and verapamil have been shown to inhibt tha slow inward calcium current of cardiac fibers. The results therefore suggest that an inward calcium ion current may play a role in the development of digitalis-induced increase in the stope of phase 4 depolarization in Purkinje fibers.
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