Thromb Haemost 1985; 53(01): 070-074
DOI: 10.1055/s-0038-1661239
Original Article
Schattauer GmbH Stuttgart

The Involvement of Platelets and the Coronary Vasculature in Collagen-Induced Sudden Death in Rabbits

G Mallarkey
The School of Pharmacy, Robert Gordon’s Institute of Technology Schoolhill, Aberdeen, UK
,
G M Smith
The School of Pharmacy, Robert Gordon’s Institute of Technology Schoolhill, Aberdeen, UK
› Author Affiliations
Further Information

Publication History

Received 14 May 1984

Accepted 07 November 1984

Publication Date:
18 July 2018 (online)

Summary

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 Fia (6-keto PGF). 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 PGF 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 KC1, 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.

 
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