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Stimulation of the pterygopalatine ganglion elicits cerebral vasodilatation
Author(s) -
Talman William T.,
Corr Julie,
Wang DeQiang
Publication year - 2006
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.20.4.a294-b
Subject(s) - vasodilation , stimulation , cerebral blood flow , medicine , cerebral circulation , laser doppler velocimetry , anesthesia , blood flow
The pterygopalatine ganglia (PPG) provide parasympathetic nitroxidergic innervation to cerebral blood vessels. Stimulation of preganglionic input to the PPG leads to cerebral vasodilatation. Interruption of ganglionic fibers inhibits cerebral vasodilatation seen with breakthrough of autoregulation during hypertension and increases cerebral infarct volume. Thus, the pathway may influence outcomes in stroke. Having used a published approach to the PPG and finding no vasodilatation with ganglionic stimulation, we hypothesized that an approach that preserved delicate ganglionic fibers would permit vasodilatation during ganglionic stimulation. We modified a method (Rosen et al. Endocrinology 27:463‐68, 1940) for exposing the PPG in 6 adult rats. We then electrically stimulated the PPG while measuring cerebral blood flow (CBF) by means of a laser flow probe positioned over the parietal cortex on the same side as the stimulus. Stimulation produced no change in mean arterial pressure or arterial pCO 2 but significantly (p<0.05) increased CBF (from 28 ± 2.7 to 39 ± 4.3 laser Doppler units; LDU, mean ± SEM). Stimulation of ganglionic fibers also increased CBF (from 26 ± 3.3 to 41 ± 5.6 LDU). PPG stimulation after transection of those fibers failed to elicit any change in CBF. Thus the parasympathetic innervation of cerebral vessels may modulate cerebrovascular tone. Support: VA Merit Review and NIH R01 HL59593.