The involvement of platelets and the coronary vasculature in collagen-induced sudden death in rabbits.
The mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TXB2) and 6-keto prostaglandin F1a (6-keto PGF1a). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBS), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TXB2 levels. 6-keto PGF1a could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TXB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KCl, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBS physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects*; D003094:Collagen / Q000494:pharmacology*; D003331:Coronary Vessels / Q000187:drug effects*; D005260:Female; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D011817:Rabbits; D013928:Thromboxane A2 / Q000097:blood; D014661:Vasoconstriction / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology
D013928:Thromboxane A2; D003094:Collagen; D014700:Verapamil