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.[1]References
- The involvement of platelets and the coronary vasculature in collagen-induced sudden death in rabbits. Mallarkey, G., Smith, G.M. Thromb. Haemost. (1985) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
