ISSN:
1432-1440
Keywords:
Ischemia-reperfusion
;
Microcirculation
;
Oxygen radicals
;
Chemoattractants
;
PMN-endothelium interaction
;
No-reflow
;
Reflow-paradox
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Reperfusion after transient tissue ischemia constitutes an irrevocable need to preserve tissue viability. However, release of prolonged ischemia will either result in failure of the microcirculation to reperfusion (no-reflow) and thus the prolongation of hypoxia, or in restoration of blood flow resulting in reoxygenation of the inflicted tissue. While ischemia damages the tissue primarily through hypoxia-induced depletion of energy stores, reoxygenation paradoxically contributes to tissue damage through the formation of oxygen radicals, the release of chemoattractant mediators (TNF, IL-1, LTB4), and the activation of circulating polymorphonuclear leukocytes (PMNs). Through the action of chemoattractant mediators and the upregulation of leukocytic (CD11/CD18) and endothelial adhesion receptors (ICAM, GMP-140), activated PMNs adhere to the endothelium, release further chemoattractants and oxygen radicals and undertain a vicious circle, which will ultimately result in further tissue damage. Both theno-reflow phenomenon and the events initiated by reflow — termed herein as thereflow-paradox — contribute to the failure of the nutritive microvascular perfusion and loss of tissue viability following ischemia and reperfusion.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01645157
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