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The effect of experimental preeclampsia on cerebral blood flow autoregulation and cerebrovascular function (680.22)
Author(s) -
Johnson Abbie,
Chan SiuLung,
Moseley Janae,
LaMarca Babbette,
Cipolla Marilyn
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.680.22
Subject(s) - preeclampsia , endocrinology , chemistry , medicine , autoregulation , blood pressure , phenylephrine , cerebral blood flow , oxidative stress , in vivo , biology , pregnancy , genetics , microbiology and biotechnology
This study investigated changes in CBFAR and vascular function in SD rats that were normal pregnant (NP; d20) or with experimental preeclampsia (ePE; d20). ePE was induced by combining placental ischemia and a high cholesterol diet. CBFAR was determined in vivo during acute infusion of phenylephrine to raise blood pressure and measurement of CBF using laser Doppler. The slope (m) of the pressure vs. CBF curves were compared between ePE (n=9) and NP (n=6). Myogenic responses were determined in isolated and pressurized posterior cerebral arteries (PCA; n=5/gr). mRNA expression of iNOS was determined using qPCR (n=5/gr). ePE caused hypertension (123 ± 4 vs. 111± 2 mmHg, p<0.05) and a 25% increase in plasma 8‐isoprostane (p<0.01 vs. NP), indicating oxidative stress. CBFAR was intact in 7/9 ePE rats and not different from NP rats (m=0.54±0.06 vs. 0.45±0.04; p>0.05). However, 2/9 ePE rats had impaired CBFAR (m=0.93±0.05; p<0.05 vs. NP). PCA from NP rats displayed myogenic activity and were smaller than passive diameters at 150 mmHg (149±17 vs. 210±13 μm; p<0.05). In contrast, the myogenic response was absent in PCA from ePE rats with no difference between active and passive diameters. mRNA expression of iNOS increased 2‐fold in PCA from ePE rats (p<0.01 vs. NP). Thus, CBFAR appears to be intact in the majority of ePE rats. The lack of a myogenic response in PCA from ePE animals may be due to oxidative stress and vascular inflammation. Grant Funding Source : Supported by RO1 NS045940