The effect of postischemic hyperemia on intracranial pressure and the no-reflow phenomenon

No-Reflow Phenomenon

“…25,26 Intravascular plugging by fibrin or platelets may also contribute to the no-reflow phenomenon. [27][28][29][30] Beneficial effects of ibuprofen, 31 prostaglandin E1, 32 and vascular washout with heparinized saline 33 support the concept that these blood elements may be important. In a no-reflow model of a New Zealand white rabbit study by Golino et al, 34 platelet depletion markedly reduced the extent of no-reflow zones.…”

“…94 General measures, including the use of intra-aortic balloon pumps, may be used as needed. 95,96 Because platelet and fibrin plugging is an important contributor to the pathogenesis of the no-reflow phenomenon, [27][28][29][30] glycoprotein IIb/IIIa platelet receptor inhibitor may be beneficial in the prevention of the no-reflow phenomenon during percutaneous coronary intervention. Studies have shown that this group of drugs is beneficial in reducing rates of death, reinfarction, and urgent revascularization when used in conjunction with percutaneous coronary intervention.…”

Local cerebral blood flow following transient cerebral ischemia. I. Onset of impaired reperfusion within the first hour following global ischemia.

“…61 The results of these experiments do not support some hypotheses presented by other investigators concerning the etiology of "no-reflow." Obstruction of capillaries by swollen astroglia,*' " • " blood aggregates and thrombi, 11 ' M microthrombi," swollen erythrocytes" and increased blood viscosity 8 have been implicated as major antecedents of "no-reflow." Wade et al ia reported that high concentration of extracellular potassium and consequent vascular constriction may account for "no-reflow."…”

“…It is highly unlikely that any heparin would have been in the cerebral vasculature during ischemia. If thrombi form during ischemia 11 -"• " heparin may inhibit thrombogenesis. Heparin was added after the brachiocephalic and left subclavian arteries were clamped and immediately prior to bypass from the aorta to the external reservoir.…”

“…Little, Kerr and Sundt 10 related impaired microcirculation to the compression of capillaries by perivascular glial swelling, but also noted that severe neuronal injury preceded the microvascular obstruction. Conversely, Cuypers and Matakas 11 concluded that no-reflow was produced by blood aggregates which obstructed larger vessels From the Department of Electrical Engineering, Monash University, Clayton, Victoria, Australia, 3168.…”