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Biomedical subjects

M S Yoon

Publications and source records attributed to M S Yoon.

At least 37 records · Page 2Linked to original sources
PubMed1994

Vasal anastomoses in dogs using contact neodymium:yttrium aluminum garnet (Nd:YAG) laser.

The purpose of this study is to evaluate the contact Nd:YAG laser system for vasal anastomosis in the animal model. Eighteen mongrel dogs were used. In this study, two major groups--control and laser--were defined. In the control group, vas anastomoses were performed with conventional microsurgical technique in six dogs. In the laser group, we performed contact laser assisted vas anastomosis (CLAVA) in 12 dogs by means of a contact Nd:YAG laser with synthetic sapphire probe (ERP4), emitted 2.0 sec pulse duration of minimum 1 watt to maximum 10 watts power. The time needed for completion of the vasal anastomosis in CLAVA group was 2-3 min; in the control group, approximately 25 min. The patency rate did not differ in these two groups; however, microscopic sperm granuloma formation was 16.7% (2/12) in the control group but 0% (0/12) in the CLAVA group. In conclusion, CLAVA is a fast and simple technique for vasal anastomosis and there were no significant complications, sperm granuloma, or even significant swelling or hematoma in any animal in this experiment.

Aluminum↗
PubMed1991

Two cases of nickel dermatitis showing vitiligo-like depigmentations.

The authors reviewed two patients showing "vitiligo-like depigmentations" where the skin had been in close contact with a metal spectacle frame made of nickel alloy. In spite of the hypersensitivity to nickel in both patients, they showed clinical and histologic findings indicate that the formation of "vitiligo-like depigmentation" does not result from posinflammatory hypopigmentation but from chemical hypomelanosis. We could not explain the underlying mechanisms; however, the speculation that the "vitiligo-like depigmentation" may come from the direct effect of the nickel itself, prompted us to report these cases.

Adult↗
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↗
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↗
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↗
PubMed1977

Effects of vagal stimulation, atropine, and propranolol on fibrillation threshold of normal and ischemic ventricles.

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.

Animals↗
PubMed1976

Facilitation of A-V nodal reciprocation by procainamide.

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.

Animals↗
PubMed1976

Effect of acetylcholine on automaticity of canine Purkinje fibers.

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.

Acetylcholine↗