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Are the upper limits of cerebral autoregulation at gross and microcirculatory levels different? Does nitric oxide play a role? (1183.1)
Author(s) -
Thompson Emma,
Coney Andrew,
Marshall Janice
Publication year - 2014
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.28.1_supplement.1183.1
Subject(s) - cerebral circulation , cerebral blood flow , vasoconstriction , medicine , middle cerebral artery , phenylephrine , nitric oxide synthase , cerebral arteries , vasodilation , autoregulation , chemistry , cardiology , anatomy , anesthesia , endocrinology , nitric oxide , blood pressure , ischemia
In Alfaxan‐anaesthetised, male Wistar rats, we infused phenylephrine (0.1‐200µg/kg/min i.v.) to raise arterial pressure (ABP). Dual‐line least‐squares analysis of gross cerebral blood flow (CBF), recorded from the common carotid with external carotid ligated, vs ABP, gave an autoregulatory upper limit (UL) of 168±3mmHg (n=14). By contrast, after neuronal NO synthase (nNOS) inhibition (ЅMTC; 0.56mg/kg i.v, or 7‐NI, 25mg/kg i.p. n=24), or non‐selective NOS inhibition (L‐NAME, 10mg/kg, n=9), the UL was either not reached, even when ABP reached 171±2 or 186±6* (vs Control; P<0.05) respectively or was increased to 173±2 (n=11) and 187±2mmHg* (n=4) respectively. When laser speckle imaging was used to follow tissue red cell flux (RCF) and diameters of arterial and venous vessels in the cerebral cortex, gross CBF UL was 168±5mmHg, but cortical tissue UL was higher; 170±5mmHg† (vs gross CBF UL, n=6). Further, in 4 rats after L‐NAME, the UL was not reached (either gross CBF or cortical tissue RCF) even when ABP was increased to 190±2mmHg*. We suggest that autoregulatory constriction of proximal cerebral arterial vessels when ABP rises is protective of cerebral tissue circulation, as indicated by the higher cortical tissue UL. We propose that NO synthesised mainly by nNOS induces tonic dilatation of cerebral circulation, such that its absence allows greater scope for autoregulatory vasoconstriction, leading to a raised UL. Grant Funding Source : Supported by the British Heart Foundation