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Regenerative cerebral arteriogenesis is induced by GM‐CSF and inhibited by anti‐inflammatory cardiovascular medications
Author(s) -
Persson Anja Bondke,
Duelsner André,
Gatzke Nora,
Buschmann Ivo R.
Publication year - 2013
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.27.1_supplement.1131.8
Subject(s) - arteriogenesis , medicine , cardiology , perfusion , collateral circulation , occlusion , monocyte , ischemia
Restoration of blood flow in case of stenotic brain‐supplying arteries relies on restoration of arterial inflow, achieved by an outgrowth of preexistent arterioles (arteriogenesis) and depends on monocyte migration into the vesel wall. It was assumed that a stimulation of monocytic function induces collateral growth, while anti‐inflammatory substances might interfere negatively. In two animal models of cerebral hypoperfusion (3‐vessel occlusion/rats, common carotid artery occlusion/mice), administration of the pro‐arteriogenic Granulocyte Colony‐ Stimulating Factor (40ug/kg) augmented angiographic collateral diameters and restored cerebrovascular reserve capacities (CVRC) (20+ 8%, cont. −14+14%). Acetylsalicylic acid (ASA), used in patients at risk for arterial stenosis, interfered with (a) CVRC restoration (1+4%), (b) collateral vessel growth and (c) monocyte migration, while Clopidogrel did not. Current data indicate similar effects for other anti‐inflammatory drugs and other vascular beds, which may explain why their effects on outcomes may fall behind effects on cardiovascular risk factors. Anti‐inflammatory drugs should be used with care in patients with vascular occlusions until large‐scale clinical data on antiarteriogenic effects have been obtained.