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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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]


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