We have previously shown that platelet thrombi (PTH) form in stenosed canine coronary
arteries in five to ten minutes producing reductions in coronary flow (RCF) and that
these can be exacerbated by IV infusions of epinephrine (E) by an alpha adrenergic
mechanism in spite of pretreatment with aspirin, indomethacin, ibuprofen, or sulfinpyrazone.
We have also shown an apparent active involvement of lysed red blood cells (RBC) packed
together proximal and in the area of stenosis releasing ADP and exacerbating the PTH
formation. On high magnification using carstairs stain and fluoresceine conjugated
antisera, fused platelets, lysed RBCs and some fibrin are noted. Eight dogs were prepared
with an EMF probe in the circumflex coronary artery along with a fixed mechanical
stenosis of 75% of the artery. RCF were noted and 5 ug of E/minute for ten minutes
IV raised arterial blood pressure (ABP) 15 ± 6 mm Hg and exacerbated RCF in all dogs,
but after administration of .6 mg/kg of chlorpromazine (C) IV the RCF were abolished
and repeated infusions of E did not provoke RCA but did lower ABP 10 ± 6 mm Hg. In
vitro platelet aggregation (ADP stimulus) decreased from 61 ± 11 LTU to 39 ± 13 LTU
(p < .05). Red cell osmotic fragility tests were done on samples obtained before and
after C and the curve was significantly shifted to the right after C suggesting more
stable RBC membranes. We postulate that C may stabilize RBCs, preventing ADP release
and inhibit platelet aggregation by an alpha adrenergic mechanism. C or an agent like
it may prevent PTH from forming in patients with stenosed coronary or cerebral arteries
who smoke or otherwise have elevated plasma E.
