Background Subsidiary mammalian cardiac pacemakers are normally kept under inhibition because they are driven by the sinus node at a rate that is faster than their own intrinsic rate. Failure of this inhibition can result in cardiac dysrhythmias and death. The mechanism by which this inhibition is brought about is still under study. The degree to which the sympathetic system is able to influence both the suppression and the initiation of ventricular automaticity following over-drive remains unclear. The purpose of this study is to examine the role of neural and hormonal sympathetic influences on ventricular overdrive suppression and the possible role of potassium as an associated mediator.
Methods Mongrel open-chest dogs with surgically induced atrioventricular block (in vivo) were used to study ventricular drive-suppression relationships and associated changes in coronary sinus blood effluent potassium concentrations under conditions of stellate ganglion isolation and stimulation, chemically induced hypotension with amyl nitrite, intravenous infusion of noradrenaline, beta receptor blockade with propranolol, and chronic catacholamine depletion by pretreatment with reserpine. Small canine hearts were studied using a modified Langendorf isolated perfused heart preparation (in vitro) in a manner analogous to those studies performed in the intact animals.
Results Factors that reduce sympathetic influences such as bilateral stellate ganglionectomy, beta blockade, catecholamine depletion, and perfusing an isolated heart with blood free crystalloid were observed to reduce ventricular automaticity while at the same time increasing the effect of over-driving the ventricular pacemaker. Enhancing sympathetic factors by stellate ganglion stimulation, induced hypotension, and noradrenaline infusion had the opposite effect. Increasing the rate of overdrive enhanced the inibitory effects and delayed recovery, whereas reducing the rate of overdrive had the opposite effect. Regardless of the methods employed to alter the overdrive suppression relationships, in both in vivo and in vitro hearts, the coronary sinus effluent potassium concentration rose during overdrive and slightly after it's cessation and then fell below baseline during the recovery period.
Conclusions Sympathetic neural and humoral factors significantly affect the overdrive suppression of ventricular pacemakers over a physiologic range, as demonstrated by their shifting of overdrive-suppression relationships used in the present models. The role of extracellular potassium concentration appears to be related, but the exact mechanism remains unclear.
|Advisor:||Brooks, Chandler McC.|
|School:||State University of New York Downstate Medical Center|
|School Location:||United States -- New York|
|Source:||DAI-B 73/06, Dissertation Abstracts International|
|Subjects:||Neurosciences, Pharmacy sciences, Physiology|
|Keywords:||Ganglionic blockade, Sympathetic nervous system, Ventricular pacemakers|
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