Effects of tissue factor induced by oxygen free radicals on coronary flow during reperfusion

Author:  ["Paolo Golino","Massimo Ragni","Plinio Cirillo","V. Enrico Avvdimento","Antonio Feliciello","Nicolino Esposito","Annalisa Scognamiglio","Bruno Trimarco","Guido Iaccarino","Mario Condorelli","Massimo Chiariello","Giuseppe Ambrosio"]

Publication:  Nature Medicine

CITE.CC academic search helps you expand the influence of your papers.

Tags:     Medicine

Abstract

Tissue factor is a transmembrane protein that activates the extrinsic coagulation pathway by binding factor VII. Endothelial cells, being in contact with circulating blood, do not normally express tissue factor. Here we provide evidence that oxygen free radicals induce tissue factor messenger RNA transcription and expression of tissue factor procoagulant activity in endothelial cells in culture. Isolated, perfused rabbit hearts exposed to exogenous oxygen free radicals also showed a marked increase in tissue factor activity within the coronary circulation. Furthermore, in ex vivo and in vivo hearts subjected to ischemia and reperfusion, a condition associated with a production of oxygen free radicals in large amounts, a marked increase in tissue factor activity occurred. This phenomenon could be abolished by oxygen radical scavengers. This increase in tissue factor activity during postischemic reperfusion was accompanied by a significant decrease in coronary flow, suggesting that increase in tissue factor activity with the consequent activation of the coagulation cascade might impair coronary flow during reperfusion and possibly contribute to the occurrence of reperfusion injury.

Cite this article

Golino, P., Ragni, M., Cirillo, P. et al. Effects of tissue factor induced by oxygen free radicals on coronary flow during reperfusion. Nat Med 2, 35–40 (1996). https://doi.org/10.1038/nm0196-35

View full text

>> Full Text:   Effects of tissue factor induced by oxygen free radicals on coronary flow during reperfusion

Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis

Bcl–2 protects from lethal hepatic apoptosis induced by an ant–Fas antibody in mice