Reversible blood-brain barrier dysfunction after intracarotid hyperthermic saline infusion


Oztas B., Kucuk M.

INTERNATIONAL JOURNAL OF HYPERTHERMIA, cilt.14, sa.4, ss.395-401, 1998 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 14 Sayı: 4
  • Basım Tarihi: 1998
  • Doi Numarası: 10.3109/02656739809018241
  • Dergi Adı: INTERNATIONAL JOURNAL OF HYPERTHERMIA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.395-401
  • İstanbul Üniversitesi Adresli: Evet

Özet

An animal model for reversible blood-brain barrier disruption has been developed. Retrograde infusion of hyperthermic saline solution 43 degrees C into the left external carotid artery of normothermic, Wistar rats, reversibly increases cerebrovascular permeability to Evans-blue albumin in the left cerebral hemisphere. Isotonic saline solutions at 37 degrees C for group I and 43 degrees C for group II were infused for 30-s at a constant rate of 0.12 ml/s into the left external carotid artery. Evans-blue, the barrier tracer was administered intravenously either prior to or at intervals of 5, 30, 180, 360 min after the hyperthermic saline infusion under pentobarbital anesthesia. All animals receiving hyperthermic saline perfusion had disturbed blood-brain barrier permeability. Based on visual inspection, disruption grade in the left hemispheres of six of 11 animals was grade 3+. Mean values for Evans-blue dye were found to be 0.28 +/- 0.06 mg/g of tissue in left hemisphere after normothermic saline infusion (group I), and 2.41 +/- 0.5 mg/g of tissue in the same hemisphere after hyperthermic saline infusion (group II). The difference was found to be significant between group I and group II (p < 0.OI). The increase in cerebrovascular permeability was temporary, even though Evans-blue albumin extravasation remained slightly elevated 3 h after infusion and was normal 6 h after infusion.