Delayed myocardial ischemia following the cessation of sympathetic stimulation.
A phenomenon entitled "delayed myocardial ischemia" has been described, in which there is a significant degree of coronary malperfusion following the cessation of behavioral stress. The primary objective of the present study was to develop a model for the delayed ischemic response in anesthetized animals to gain insights into the underlying mechanisms. In 15 morphine and chloralose-anesthetized dogs, a moderate degree of stenosis was applied to the left circumflex coronary artery by means of a toroidal balloon occluder. The pulsed Doppler technique was used to monitor coronary flow. After baseline data were obtained, the left stellate ganglion was stimulated for 30 seconds. Heart rate increased (63%), as did systemic blood pressure (41%) and flow in the left circumflex artery (47%). These parameters rapidly returned to control levels when stimulation was terminated. Forty-five to 90 seconds later, coronary flow decreased by 65% and coronary vascular resistance increased by 45%. These hemodynamic changes were accompanied by ECG abnormalities indicative of regional myocardial ischemia. The delayed ischemic response could be prevented by pretreatment with either nifedipine (20 micrograms/kg) or prazosin (0.3 mg/kg). These data indicate that the primary mechanism for the delayed ischemic response is alpha-adrenergically mediated contraction of the smooth muscle in the coronary artery wall.
Hagestad
E L
EL
Cardiovascular Laboratories, Harvard School of Public Health, Boston, MA 02115.
Verrier
R L
RL
D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004558:Electric Stimulation; D006439:Hemodynamics / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D013233:Stellate Ganglion / Q000503:physiopathology*
D009543:Nifedipine; D011224:Prazosin