Cardiac sympathetic nerve activity and progressive vasoconstriction distal to coronary stenoses: feed-back aggravation of myocardial ischemia.

This study tested the hypothesis that the relative ischemia distal to a severe coronary stenosis increases the activity of cardiac sympathetic nerves which in turn results in poststenotic vasoconstriction and an aggravation of ischemia. An acute severe stenosis which reduced coronary blood flow to 50% of control was produced in 23 anesthetized, vagotomized dogs and maintained for 20 min. The activity of postganglionic cardiac sympathetic nerves increased by 23 +/- 4% within 20 min. In parallel, poststenotic coronary resistance increased from 0.48 +/- 0.03 to 0.61 +/- 0.03 mm Hg X min X 100 g/ml resulting in a net lactate production after 15 min. Pretreatment with aspirin (6 mg/kg i.v.; n = 5) was without any influence on these reactions. The selective alpha 2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.; n = 6) and the calcium antagonist nifedipine (10 micrograms/kg i.v.; n = 6) prevented the progressive increase in poststenotic resistance and lactate production, but still permitted an increase in sympathetic activity. Segmental anesthesia of cardiac sympathetic nerves by epidural infiltration of procaine at segments C7-T6 (n = 6) prevented the sympathetic activation, the progressive increase in poststenotic resistance and the resulting myocardial ischemia. Sympathetic activation and a concomitant increase in poststenotic resistance resulting in myocardial ischemia were also found in 6 dogs with intact vagus nerves. These data support the hypothesis of a vicious cycle between poststenotic coronary vasoconstriction and sympathetic activation resulting in severe myocardial ischemia.