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Biomedical subjects

J Han

Publications and source records attributed to J Han.

At least 433 records · Page 24Linked to original sources
PubMed1984

Postextrasystolic T wave changes in normal canine hearts.

Premature ventricular beats were induced at variable coupling intervals and postextrasystolic T wave changes were observed following various postextrasystolic cycle lengths in 19 closed chest dogs with normal hearts. Following relatively longer postextrasystolic cycle lengths, reversal of the T wave polarity was seen in six dogs (31%), only T wave amplitude changes were seen in 6 dogs (31%), and no significant T wave changes were seen in seven dogs (38%). It was concluded that postextrasystolic T wave changes occur in normal hearts and have no useful diagnostic values.

Animals↗
PubMed1983

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction.

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.

Aged↗
PubMed1983

Uptake, initial effects, and chemotherapeutic efficacy of harringtonine in murine leukemic cells sensitive and resistant to vincristine and other chemotherapeutic agents.

[3H]Harringtonine was shown to be taken up rapidly by L1210/0 cells using a fast-mixing, fast-separating technique and was retained with a slow rate of limited release to the medium. Cells resistant to vincristine (L1210/VCR) showed impaired capability to take up the drug at 20 degrees. Its initial uptake in L1210 sublines in vitro was: L1210/0 greater than L1210/cyclophosphamide, L1210/1-beta-D-arabinofuranosylcytosine, L1210/6-mercaptopurine greater than L1210/5-fluorouracil, L1210/Adriamycin greater than L1210/VCR. In [3H]harringtonine-preloaded cells, L1210/0 retained significantly more radioactivity than did L1210/VCR cells after repeated washing with fresh medium at 37 degrees. The radioactivity appeared to be predominantly bound to the microsomal fractions. [3H]Leucine incorporation into protein in L1210/0 cells was inhibited 90% within 15 min by harringtonine (0.5 micrograms/ml); incorporation of [3H]thymidine into DNA and [3H]cytidine into RNA was much less inhibited and showed an apparent lag of onset for 5 and 10 min, respectively. The relative potency of harringtonine to inhibit [3H]leucine incorporation in the above sublines in vitro follows an order similar to their rates of uptake of harringtonine by these sublines of cells. The efficacy of harringtonine, 2.4 or 3.6 mg/kg i.p., in increasing the life span of C57BL/6 X DBA/2 F1 mice bearing the sublines of leukemic cells, on the average, was: L1210/0 greater than L1210/cyclophosphamide, L1210/6-mercaptopurine greater than L1210/1-beta-D-arabinofuranosylcytosine, L1210/5-fluorouracil greater than L1210/Adriamycin, L1210/VCR. These results suggest that: (a) protein synthesis is the major initial target for the effect of harringtonine; (b) harringtonine bound more tightly to the cellular components of VCR-sensitive leukemic cells than to VCR-resistant cells; and (c) cellular uptake of harringtonine and the relative potency of inhibiting protein synthesis in sublines have a rank order similar to the chemotherapeutic efficacy of harringtonine in these cells.

Alkaloids↗
PubMed1982

Effects of epinephrine on the electrophysiologic properties of Purkinje fibers surviving myocardial infarction.

The electrophysiologic effects of epinephrine on canine subendocardial Purkinje fibers were examined 24 hours after two-stage ligation of the left anterior descending coronary artery. Transmembrane action potential were monitored simultaneously in noninfarcted (NZ) and infarcted (IZ) zones during epinephrine superfusion at 37 degrees C. Epinephrine (10(-8) M to 10(-5) M) induced dose-dependent increases in maximum rate of phase O depolarization (Vmax), action potential amplitude (APA), and maximum diastolic potential (MDP) in both NZ and IZ. Epinephrine consistently shortened effective refractory period (ERP) in both regions No significant change in action potential duration (APD) was noted at either 50% or 90% repolarization. Impulse conduction through the NZ and into the IZ was significantly improved, as indicated by an increased maximum follow-rate in each region at 10(-6) and 10(-5) M epinephrine. The IZ fibers showed a marked hypersensitivity to this agent, in that responses were particularly pronounced in the IZ vs the NZ in terms of both absolute and percentage changes. The effects of epinephrine on Vmax, MDP, APA, and ERP were generally reversed by propranolol, while remaining relatively unaffected by phentolamine, suggesting a beta-adrenergic mechanism. Increased stimulation of ventricular beta-adrenoceptors in the period 16 to 72 hours after myocardial infarction may influence ventricular vulnerability to "late-phase" arrhythmias through nonuniform effects in Purkinje fibers.

Action Potentials↗
PubMed1982

Electrophysiologic effects of mexiletine on normal and ischemic ventricles.

The effects of mexiletine on ventricular electrophysiologic properties were studied in seven normal and ten ischemic canine ventricles. Ventricular fibrillation threshold was significantly increased and idioventricular automaticity was significantly suppressed after intravenous administration of 2 mg/kg of mexiletine. Diastolic threshold, effective refractory period and ventricular conduction time were all increased slightly after the drug administration, although the changes were not statistically significant. Rapidly repetitive responses and/or fibrillation were induced in the ischemic ventricle by two early premature beats in six of ten dogs, but these serious arrhythmias could be induced in none of the ten dogs after mexiletine pretreatment. The study indicates that the mode of action of mexiletine is similar to that of lidocaine and the drug is an effective antiarrhythmic agent in preventing ventricular arrhythmias in dog ventricles during myocardial ischemia.

Animals↗
PubMed1982

Effects of epinephrine on automaticity and the incidence of arrhythmias in Purkinje fibers surviving myocardial infarction.

The role of the sympathetic nervous system in the development of late-phase ventricular arrhythmias occurring 24 hr after myocardial infarction was investigated using canine ventricular preparations in vitro. One day after two-stage ligation of the left anterior descending coronary artery, transmembrane action potentials from subendocardial Purkinje fibers were monitored in noninfarcted (NZ) and infarcted (IZ) zones during Tyrode's superfusion at 37 degrees C. In combined preparations incorporating both NZ and IZ, epinephrine (10(-7)-10(-5)M) produced dose-dependent increases in spontaneous rates of depolarization, slope of phase 4 depolarization and incidence of spontaneous and induced arrhythmias. In particular, premature electrical stimulation induced increased numbers of unstimulated responses or rapid, repetitive depolarizations. These responses to the drug were antagonized by propranolol (10(-6)M) but not phentolamine (10(-7)M). Epinephrine appeared to promote the functional dissociation of conducted impulses often observed in the IZ of combined preparations. In preparations excised from either NZ or IZ alone, epinephrine induced elevated spontaneous firing rates, particularly in the IZ, but no increase in arrhythmias. These data suggest that elevated levels of beta adrenergic receptor stimulation 24 hr after myocardial infarction may increase ventricular vulnerability to arrhythmias arising through enhanced automaticity or reentry.

Animals↗
PubMed1981

Actions of verapamil on Purkinje fibers from normal and infarcted heart tissues.

Dogs were anesthetized and a two-stage occlusion of the left anterior descending coronary artery was performed. They were sacrificed 24 hr later and the experimental preparations, which included both normal and infarcted tissues, were dissected from the left ventricles. Effects of 1 microM verapamil on action potentials of Purkinje fibers from normal and infarcted zones (NZ and IZ) were studied using conventional microelectrode techniques. Verapamil produced a significant decrease in action potential amplitude in the cells from both NZ and IZ, with the IZ cells showing a greater reduction. A measured decrease in action potential duration (at 50% repolarization) was significant only in the NZ. Both NZ and IZ cells showed a significant increase in refractory period after verapamil superfusion Vmax was decreased only in the IZ in which slow responses were further depressed by the drug. The rapidly repetitive responses induced in some preparations by early premature stimuli were reduced or abolished during verapamil superfusion. These results suggest that verapamil may preferentially alter the slow responses seen in infarcted tissues, thereby reducing a source of reentrant activity and associated arrhythmias.

Animals↗
PubMed1980

Nonuniform epicardial depolarizations during coronary occlusion in dogs.

Epicardial electrograms were recorded before and after occlusion of the left anterior descending coronary artery. The greatest difference between the post-occlusion and pre-occlusion depolarization times were determined. These times were referred to as the normalized times of greatest disparity, delta tmax. It was found that following both one- and two-stage occlusion of the LAD there was a significant increase in delta tmax in the ischemic area of the myocardium. This indicates increased asynchrony of depolarization. However, no significant change in depolarization times occurred in the unaffected area. In one-stage occlusion with an increase in delta t max there was a linear correlation with the development of ventricular arrhythmias, especially ventricular premature beats and tachycardia. Thus, there is evidence which links the increase in depolarization times with the mechanism of reentry and ventricular arrhythmias.

Animals↗
PubMed1980

Effects of verapamil on action potentials of Purkinje fibers.

The effects of verapamil (1 and 2 micro M) on automaticity, membrane responsiveness curve and action potential configuration were studied in canine Purkinje fibers using conventional microelectrode techniques. The drug effects were concentration dependent, and more statistically significant changes were obtained during superfusion with 2 micron M verapamil. In spontaneously active fibers, the rate of discharge was decreased due to a decrease in the phase 4 depolarization. Verapamil failed to produce a consistent shift in the membrane responsiveness curve (Vmax versus take-off membrane potentials), although the development of early, slow action potentials was blocked. This blocking resulted in an increased effective refractory period and a shortened membrane responsiveness curve at the lower end. Maximum diastolic potential and action potential amplitude were decreased, and action potential duration was increased by verapamil. The results suggest that verapamil may selectively depress or block the slower action potentials which are thought to be important in the genesis of ventricular arrhythmias.

Action Potentials↗
PubMed1979

Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties.

The effects of therapeutic and toxic doses of thioridazine (Mellaril) (10 and 50 mg/kg body weight, respectively) on ventricular electrophysiologic properties were studied in 12 anesthetized dogs. Threshold pacing currents (diastolic threshold), effective refractory period and conduction time were significantly increased, and idioventricular automaticity was suppressed after administration of 10 mg/kg of thioridazine; the effects were much more pronounced after administration of 50 mg/kg. Rapidly repetitive responses or tachycardia could be induced in the ventricle by two early premature beats in 9 of the 12 dogs after the 50 mg/kg dose, but they did not occur before drug administration or after the 10 mg/kg dose. These results indicate that the antiarrhythmic and arrhythmogenic effects of thioridazine are dose-dependent and that careful monitoring with frequent electrocardiograms is needed for patients receiving large doses of this drug.

Animals↗
PubMed1979

Effects of methylprednisolone on ventricular arrhythmias during acute myocardial ischaemia.

The effects of methylprednisolone (50 mg.kg-1) on the incidence of ventricular tachycardia and fibrillation and on ventricular fibrillation threshold were studied during acute coronary occlusion in anaesthetised dogs. Ventricular tachycardia and/or ventricular fibrillation occurred in 11 of the 16 animals (69%) both before and after methylprednisolone pretreatment. The mean ventricular fibrillation threshold of 10 dogs was 10.1 +/- 1.8 mA before methylprednisolone and it increased slightly to 13.3 +/- 2.3 mA after the drug. This difference was not statistically significant (P greater than 0.2).

Animals↗
PubMed1978

Effects of verapamil on ventricular rhythm during acute coronary occlusion.

The effects of verapamil on electrophysiologic parameters of the ventricle were studied during acute coronary occlusion in anesthetized open-chest dogs. Those parameters measured in the study were idioventricular automaticity, ventricular conduction, and fibrillation threshold. The incidence of rapidly repetitive beats and fibrillation induced by two successive premature beats was also studied. Verapamil significantly decreased idioventricular automaticity (in five dogs), improved conduction through the ischemic area (in six dogs), and increased fibrillation threshold of the ischemic ventricular (in eight dogs). The drug was effective in abolishing rapidly repetitive beats and fibrillation induced by closely coupled premature beats during acute coronary occlusion. Rapidly repetitive beats occurred in nine out of 15 dogs and these repetitive beats were degenerated into fibrillation in seven dogs before verapamil. Following pretreatment with the drug, rapidly repetitive beats and fibrillation occurred in none of the 15 dogs. The results indicate that verapamil can be very effective against ventricular arrhythmias occurring in association with myocardial infarction.

Animals↗
PubMed1978

Wolff-Parkinson-White syndrome in the neonate.

Of 16 infants who presented with paroxysmal supraventricular tachycardia in the neonatal period, 50 percent had an electrocardiographic pattern consistent with Wolff-Parkinson-White conduction, type A. It is suggested that infants have bypass pathways similar to or identical with a Kent pathway as part of normal maturation. Infants with paroxysmal supraventricular tachycardia have electrically active bypass tracts but these are documented in only about one half of the patients because of the short duration of recordings or because of concealment (the bypass tract conducts only in retrograde fashion). The activity of these pathways is enhanced by the predominant cholinergic innervation of the neonatal heart. Resolution of the arrhythmias and the Wolff-Parkinson-White pattern in most patients occurs because of anatomic maturation of the conduction tissue, development of adrenergic innervation and a decrease in cholinergic dominance. In some children, maturation is incomplete and the bypass fibers remain quiescent or become active under certain circumstances such as those associated with increased autonomic discharge. Extended surveillance is recommended for all infants who present with paroxysmal supraventricular tachycardia and the Wolff-Parkinson-White pattern.

Child, Preschool↗