AJP - Heart and Circulatory Physiology, Vol 249, Issue 6 1154-H1166, Copyright © 1985 by American Physiological Society
Impaired arteriolar vasodilation induced by thrombosis of a coronary arterial stenosis
H. Gewirtz, H. Sasken, M. Steiner and A. S. Most
This study tested the hypothesis that aggregation of platelets and release
of thromboxane A2 at the site of a coronary arterial stenosis may
contribute to myocardial ischemia by impairing flow regulation of the
distal coronary bed. Measurements of hemodynamics, flow (microspheres),
lactate metabolism, and prostaglandin (PG) metabolites (thromboxane B2 and
6-keto-PGF1 alpha) were made in closed-chest anesthetized pigs instrumented
with a stenosis (65% diam reduction) in the left anterior descending (LAD)
coronary artery. Data were acquired prior to stenosis insertion (control)
and 5 and 15 min after insertion, during which time thrombotic occlusion of
the device was occurring. Heart rate was controlled by atrial pacing.
Distal LAD zone endocardial flow (ml X min-1 X g-1) declined versus control
(1.15 +/- 0.20, mean +/- SD) at 5 min (0.89 +/- 0.40, P less than 0.05) and
15 min (0.41 +/- 0.36, P less than 0.01) of occlusion. Distal endocardial
resistance (mmHg X ml-1 X min X g), however, did not change versus control
(72 +/- 12) at 5 (66 +/- 12) or 15 min (61 +/- 38). Distal epicardial
resistance (mmHg X ml-1 X min X g) declined versus control (90 +/- 17) at 5
(66 +/- 35, P less than 0.05) and 15 min (43 +/- 26, P less than 0.01)
postinsertion. Finally, lactate extraction (%) at control (42 +/- 19)
changed to production 15 min postinsertion (-36 +/- 93, P less than 0.05)
and arterial-anterior interventricular vein thromboxane B2 difference
(pg/0.1 ml) changed from 13.1 +/- 17.8 pre to -15.8 +/- 30.0 at 5 min post
(P less than 0.05). Thus platelet aggregation and release at a
spontaneously thrombosing stenosis contribute to ischemia not only by
reduction of stenosis diameter but also by impairment of flow regulation in
endocardial layers distal to it.
