Microvascular protection is essential for successful neuroprotection in stroke

Gursoy-Ozdemir Y., Yemisci M., DALKARA T.

JOURNAL OF NEUROCHEMISTRY, cilt.123, ss.2-11, 2012 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 123
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1111/j.1471-4159.2012.07938.x
  • Dergi Adı: JOURNAL OF NEUROCHEMISTRY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.2-11
  • Anahtar Kelimeler: cerebral ischemia, nitric oxide, neurovascular unit, no-reflow, peroxynitrite, pericyte, FOCAL CEREBRAL-ISCHEMIA, BLOOD-BRAIN-BARRIER, NITRIC-OXIDE SYNTHASE, SCANNING CONFOCAL MICROSCOPY, TISSUE-PLASMINOGEN ACTIVATOR, EVALUATION TRIAL EPITHET, OXIDATIVE STRESS, NADPH OXIDASE, MICROCIRCULATORY OBSTRUCTION, HEMORRHAGIC TRANSFORMATION
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Currently, the best way of neuroprotection for acute ischemic stroke appears to be restoration of blood flow to the ischemic area by thrombolysis. Unfortunately, a short therapeutic time window as well as thrombolysis-induced bleeding and edema limit the use of recanalization therapies. Here, we review the evidence suggesting that ischemia/reperfusion-induced microvascular injury plays a critical role in determining tissue survival after recanalization in focal cerebral ischemia by disrupting the bloodbrain barrier integrity and promoting microcirculatory clogging. Among many complex mechanisms of the ischemiareperfusion injury, overproduction of oxygen and nitrogen radicals on the microvascular wall appears to significantly contribute to these pathological processes. These developments bring about the exciting possibility that effective suppression of oxidative/nitrative stress during pharmacological or interventional re-opening of the occluded artery may significantly improve the outcome of recanalization therapies in stroke patients by improving microcirculatory reflow as well as by preventing hemorrhagic conversion and vasogenic edema. They also point to the critical (but partly neglected) importance of the microcirculation in neuroprotection.