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Reduction of Cerebral Blood Flow (CBF) in Adenosine (ADO) Knock‐out (KO) Mice during Hypoxia
Author(s) -
Miekisiak Grzegorz Jerzy,
Beylin Alexander,
Kung David,
Yoo JiSuk Kristen,
Chandela Sidhartha,
Sandler Adam Lance,
Winn H. Richard
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1388-a
Subject(s) - hypoxia (environmental) , adenosine , vasodilation , cerebral blood flow , adenosine receptor , medicine , chemistry , anesthesia , endocrinology , oxygenation , receptor , oxygen , organic chemistry , agonist
: ADO has been suggested as being involved in the regulation of cerebral hypoxic hyperemia via ADO 2a receptor. Methods : Mice (22–30 gm) were intubated, anesthetized & ventilated. We continuously monitored end‐tidal CO 2 , arterial blood pressure (BP), & CBF (laser Doppler). WT and KO animals were randomly challenged for 30s. with 10% 0 2 /90% N 2 which resulted in a PaO 2 ~30–35mmHg. In a separate group of WT and KO animals, we controlled BP. Results: As indicated in Fig 1, the KO had an attenuated (~70%%) CBF response to hypoxia as compared to the WT animals (p<0.05). However, during hypoxia, the KO animals had a greater decrease in BP (p<0.05) than in the WT. When we controlled BP, the disparity in CBF response became even greater (181.9 ±.7.8 vs. 129.3 ± 6.5, p<0.05) Conclusion : The present study indicates that a significant component of the increase in CBF during moderate hypoxia is related to A2a receptor mediated vasodilatation. The persistence of some vasodilatation during hypoxia may be secondary to non A2a adenosine receptor mechanisms (i.e., A2b), by the adaptation of knockout animals and/or to non‐adenosine related mechanism. [supported by R01 (NS 21076 NINDS) to HRW] 1CBF [% change]2CBF [% change]