Stress and the Induction of Intravascular Platelet Aggregation in the Heart

Abstract

SUMMARYIntravascular aggregation of platelets similar to that found in dogs after norepinephrine infusion was demonstrated using the electron microscope in the hearts of 20 of 23 rats subjected to two forms of stress (immersion in hot water, 7 of 8 rats; repeated small electric shocks to the feet, 13 of 15 rats). Received January 9, 1973; revision accepted for publication March 5, 1973. 164 lodges in a coronary artery previously narrowed by atherosclerosis. To determine whether the catecholamines produced endogenously during stress are sufficient to cause intravascular platelet aggregation similar to that seen after exogenous infusion of norepinephrine,4 5 studies with rats stressed by immersion in ice water were conducted and similar platelet aggregates were noted on electron microscopic examination of the heart." It was not clear, however, what effect cold temperature per se had on the tendency for platelet aggregation to occur intravascularly in the heart. To further document that the intravascular platelet aggregates noted in the previous study were indeed due to the stress, 2 other forms of stress-immersion in hot water and repeated electrical shocks to the feet of rats-were studied and reported here. Electron microscopic findings in rats stressed in this way were similar to those found after cold stress, with intravascular platelet aggregates found in the small vessels of the heart.Material and Methods Thirty-seven white laboratory rats weighing 300-500 g were used for study.Eight rats were stressed by immersion in a tub that contained 4 to 5 inches of water kept at 500 by addition of small amounts of boiling water. The four to five inch water level was chosen to allow the rats to just touch bottom and keep their noses above the water. At the first sign of fatigue (inability to maintain head out of water), the rats were promptly removed from the water bath and killed with a blow on the head and removal of Circulation, Volume XLVIII,

Effects of Exercise-Induced Stress on Platelet Aggregation

“…With animal experiments available [7,8] suggesting that endo genous catecholamines secreted during stress were sufficient to induce platelet aggregates in myocardial small vessels, and with the present ob servation of increased platelet aggregability after exercise-induced stress, in human, it is tempting to postulate that the precipitating event in myo cardial infarction during a period of stress is a catecholamine-mediated phenomenon, inducing intraarterial platelet aggregates capable of oc cluding already narrowed segments of the coronary circulation.…”

“…In rats stressed by immersion in hot or iced water or by repeated elec trical shocks to their feet, the endogenously secreted catecholamines have been sufficient to cause platelet aggregates to occlude myocardial small vessels [7,8].…”

The syndrome of variant angina culminating in acute myocardial infarction.

“…Coronary artery spasm may be the stimulus initiating ischemic injury, although vasospasm could be the consequence of an initial ischemic injury,37' 38 occurring through some other mechanism. Platelet aggregates alone or in combination with coronary spasm could originate such ischemic injury.34 39 Intramyocardial spasm has followed myocardial ischemic injury in dogs subjected to transient coronary occlusion.37 Such spasm, occasionally spreading to epicardial vessels, could generate a vicious cycle perpetuating and extending the original ischemic injury. 38 Between episodes of variant angina, our patients showed persisting T-wave inversions, which probably indicate continuing ischemia.…”

Differences in platelet aggregation in coronary sinus and aortic blood in patients with coronary artery disease: Effect of propranolol

“…Abnormal platelet function has also been found in association with hyperlipidemia (1), diabetes mellitus (8) and hypertension (17), which are risk factors in the development of ischemic syndromes. Animal studies suggest that extension of myocardial infarction also may relate to excessive platelet aggregation (12) and that induction of platelet aggregation may result in focal myocardial necrosis (5,6). Recently, increased formation of platelet aggregates in the coronary circulation of dogs with narrowed coronary arteries (21) has been suggested as additional evidence implicating platelets in myocardial ischemia and necrosis.…”