Biomedical subjects

N S Gantenberg

Publications and source records attributed to N S Gantenberg.

5 recordsLinked to original sources

PubMed1992

A novel acetylcholine receptor-related peptide blocks canine cardiac ganglia and inhibits the nicotinic receptor of PC-12 cells.

A 13 amino acid peptide from the calf muscle acetylcholine receptor has been previously shown to bind both snake neurotoxins and acetylcholine. In the experiments reported here a modified complementary peptide (cAChR) derived from that acetylcholine receptor peptide was tested for biological activity in a canine heart preparation. It was expected that the modified complementary peptide would exhibit either acetylcholine-like effects or acetylcholine inhibiting effects, since, as a complementary peptide to the receptor, it should resemble acetylcholine. In these studies cAChR was administered via the sinus node artery of dog hearts in intact animals which were anesthetized with pentobarbital, intubated, and prepared with local cardiac electrograms and force gauges. cAChR was also injected directly into thoracic sympathetic ganglia. Both approaches demonstrated cAChR inhibition of neural transmission, cAChR was added to the medium of carbachol stimulated PC-12 cells. In these cells, derived from a rat pheochromocytoma, sodium flux is controlled by neural nicotinic receptors. With or without preincubation cAChR inhibited carbachol stimulation of sodium flux, exhibiting a Ki of approximately 9 x 10(-5) (similar to that of hexamethonium). Thus cAChR appears to be a novel synthetic peptide which interrupts nicotinic cholinergic neural transmission by acting as an antagonist of the neural nicotinic receptor.

Amino Acid Sequence↗

PubMed1992

Enhanced induction of ventricular arrhythmias during sympathetic stimulation before and during coronary artery occlusion.

We used programmed electrical stimulation to examine the arrhythmogenic influence of the sympathetic nervous system before and during coronary artery occlusion. In 29 anesthetized dogs the left and/or right stellate ganglia were stimulated at 2-8 hertz. Program-induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia and ventricular fibrillation. Both the number of extrastimuli and the duration of coronary occlusion significantly influenced ventricular arrhythmia induction. After pooling the number of extrastimuli, type of artery occluded, and the duration of occlusion, the influences of unilateral and bilateral stellate stimulations were evaluated. The incidence of induced ventricular arrhythmias was 54% during control conditions (prior to sympathetic stimulation). Right stellate stimulation had no influence on arrhythmogenesis, causing ventricular arrhythmia induction in 52% (NS) of the trials. Left stellate stimulation resulted in increased ventricular arrhythmias (68%; P less than 0.05) in response to programmed electrical stimulation. Bilateral stellate stimulation elevated program-induced ventricular arrhythmias (63%; P less than 0.05). The effects of the stellate stimulations on arrhythmia induction were similar during and up to 180 minutes of coronary occlusion. Thus, the arrhythmogenic influence of sympathetic stimulation was present before and during coronary artery occlusion.

Animals↗

PubMed1992

Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms.

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion. Autonomic decentralization was performed prior to the protocol in eight dogs. Induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia, and ventricular fibrillation. Intravenous cocaine, and subsequent adrenergic and muscarinic receptor blockade, or calcium channel blockade were evaluated for their influence on arrhythmogenesis. The incidence of induced ventricular arrhythmias was significantly elevated following cocaine and was reduced following propranolol and atropine. Verapamil, however, did not reduce the incidence of induced arrhythmias. In addition, cocaine significantly increased arrhythmia induction in decentralized animals, but propranolol, atropine, and phentolamine failed to reduce the proarrhythmic effects of cocaine in these animals. Thus, cocaine has a proarrhythmic effect on the heart with multiple mechanisms. The adrenergic mechanism appears to be a result of neurotransmitter uptake blockade, whereas the likely ionic mechanism is a neurally independent, direct effect on the heart.

Adrenergic beta-Antagonists↗

PubMed1991

Cocaine depresses cardiac sympathetic efferent activity in anesthetized dogs.

Increased use of cocaine has increased the incidence of sudden cardiac death concomitantly, likely due to life-threatening arrhythmias and/or myocardial ischemia. The effects of cocaine on regulation of the heart and circulation by the autonomic nervous system (which is active during arrhythmias and myocardial ischemia) are not fully understood, however. Therefore, we wished to evaluate the influence of intravenous (i.v.) cocaine on spontaneous thoracic cardiac sympathetic efferent nerve activity in anesthetized dogs. In six pentobarbital-anesthetized dogs, blood pressure (BP), heart rate (HR), and two cardiac sympathetic nerves (6 right-sided, 6 left-sided; 3 preganglionic, 9 postganglionic) were simultaneously recorded. Cocaine was infused for 15 min to a total dose of 6 mg/kg. Sympathetic multifiber efferent activities, HR, and BP were recorded continuously throughout the infusion and quantified at 5-min intervals during the infusion and for 45 min after infusion. Neural activities declined sharply to 54.7% of control (p less than 0.01) after only 5 min of infusion. After 15 min of infusion, nerve activity decreased to 39.4% of control (p less than 0.01). Cardiac nerve activity remained depressed (44.9%; p less than 0.01) 45 min after cocaine infusion. Cocaine caused a slight decrease in both HR and BP at 15 min. The rate-pressure product (RPP) decreased significantly during cocaine infusion. Comparable administration of lidocaine (6 mg/kg i.v. in 15 min) failed to influence cardiac sympathetic efferent activities significantly. We conclude that i.v. cocaine significantly depresses spontaneous cardiac sympathetic efferent neural activities in anesthetized dogs.

Animals↗

PubMed1990

A sample computer system for physiological data acquisition and analysis.

This report outlines a sample configuration of a system which records, stores and analyses, graphically and statistically, neurophysiological and cardiovascular recordings during an experiment. The system is composed of sensitive physiological amplifiers, an analog to digital signal conversion board, scientific software, a 80286-based computer with 640 Kb of RAM, and a laser printer. Each component of the system is described along with the specific task(s) it performs.

Analog-Digital Conversion↗