Thromb Haemost 1981; 46(01): 027
DOI: 10.1055/s-0038-1652028
Platelets, Drugs – I
Platelets, Drugs – II
Schattauer GmbH Stuttgart

Protection Against Epinephrine Exacerbated Platelet Thrombi Formation In Stenosed Dog Coronary Arteries With Chlorpromazine

J Folts
Department of Medicine, University of Wisconsin, Madison, WI
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Publication Date:
24 July 2018 (online)

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.