Neuropeptide Y in the Human Circle of Willis and Its Effect on Cerebral Cortical Blood Flow

1984 ◽  
Vol 67 (s9) ◽  
pp. 19P-19P
Author(s):  
J M Allen ◽  
F Schon ◽  
N Todd ◽  
J C Yeats ◽  
H A Crockard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Neuropeptide Y ◽  
Circle Of Willis ◽  
Cortical Blood Flow ◽  
Cerebral Cortical Blood Flow

Postnatal developmental changes in blood flow to choroid plexuses and cerebral cortex of the rat

1994 ◽  
Vol 266 (5) ◽  
pp. R1488-R1492
Author(s):  
J. Szmydynger-Chodobska ◽  
A. Chodobski ◽  
C. E. Johanson
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Vascular System ◽  
Developmental Changes ◽  
Choroidal Blood Flow ◽  
Flow Rates ◽  
Cortical Blood Flow ◽  
Choroid Plexuses ◽  
Choroidal Epithelium ◽  
Cerebral Cortical Blood Flow

Postnatal developmental changes in blood flow to choroid plexuses of the lateral (LVCP) and fourth (4VCP) ventricles and cerebral cortex were studied in pentobarbital-anesthetized rats at 2, 3, 5, and 7-8 wk. Blood flow was measured by indicator fractionation with N-isopropyl-p-[125I]iodoamphetamine as the marker. Blood flow to the LVCP and 4VCP was 2.5 +/- 0.1 and 2.7 +/- 0.1 ml.g-1.min-1, respectively, and did not change between the 2nd and 3rd wk. However, it increased by 34% between the 3rd and 5th wk. From the age of 5 wk on, 4VCP was characterized by higher blood flow rates than LVCP. Cerebral cortical blood flow gradually increased between the 2nd and 5th wk. There was no difference in cortical blood flow between 5-wk-old and adult animals. The changes in choroidal blood flow likely represent a continuing adjustment of the choroidal vascular system to steadily increasing secretory capabilities of the maturing choroidal epithelium.

scholarly journals Bexarotene Exerts Protective Effects Through Modulation of the Cerebral Vascular Smooth Muscle Cell Phenotypic Transformation by Regulating PPARγ/FLAP/LTB4 After Subarachnoid Hemorrhage in Rats

2019 ◽  
Vol 28 (9-10) ◽  
pp. 1161-1172 ◽  
Author(s):  
Zhaosi Zhang ◽  
Guosheng Zhao ◽  
Liu Liu ◽  
Junchi He ◽  
Rami Darwazeh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Vascular Smooth Muscle ◽  
Neurological Impairment ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Cortical Blood Flow ◽  
Phenotypic Transformation ◽  
Cerebral Cortical Blood Flow

Vascular smooth muscle cells (VSMCs) play an important role after a subarachnoid hemorrhage (SAH). The changes in VSMCs following bexarotene treatment after SAH are unknown. In the present study, neurological impairment, decreased cerebral cortical blood flow and transformation of cerebral VSMCs from a contractile to a synthetic phenotype were observed after SAH. Bexarotene reduced neurological impairment, improved cerebral cortical blood flow, inhibited VSMC phenotypic transformation and suppressed the expression of 5-lipoxygenase-activating protein (FLAP) and leukotriene B4 (LTB4), which was partly reversed by GW9662, an inhibitor of peroxisome proliferator-activated receptor gamma (PPARγ). Mechanistically, sh-PPARγ-mediated phenotypic transformation of VSMCs was partially suppressed by MK886, an antagonist of FLAP. Therefore, we conclude that bexarotene reduced neurological impairment, improved cerebral cortical blood flow and inhibited the VSMC phenotypic transformation after SAH, which was achieved by activating PPARγ-mediated inhibition of FLAP/LTB4 in VSMCs

scholarly journals Cerebral Cortical Blood Flow and Oxygen Metabolism in Normocythemic Hyperviscous Newborn Piglets

1988 ◽  
Vol 24 (4) ◽  
pp. 486-489 ◽  
Author(s):  
Marshall Goldstein ◽  
Barbara S Stonestreet ◽  
Benjamin S Brann ◽  
O H William
Keyword(s):  
Blood Flow ◽  
Oxygen Metabolism ◽  
Cortical Blood Flow ◽  
Newborn Piglets ◽  
Cerebral Cortical Blood Flow

Cervical spinal cord stimulation increases cerebral cortical blood flow in an experimental cerebral vasospasm model

2004 ◽  
Vol 147 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Ö. Karadağ ◽  
E. Eroğlu ◽  
M. Gürelik ◽  
H. M. Göksel ◽  
E. Kılıç ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cerebral Vasospasm ◽  
Spinal Cord Stimulation ◽  
Cervical Spinal Cord ◽  
Cortical Blood Flow ◽  
Cerebral Cortical Blood Flow

Isoflurane-induced Cerebral Hyperemia Is Partially Mediated by Nitric Oxide and Epoxyeicosatrienoic Acids in Mice In Vivo 

2002 ◽  
Vol 97 (6) ◽  
pp. 1528-1533 ◽  
Author(s):  
Franz Kehl ◽  
Hui Shen ◽  
Carol Moreno ◽  
Neil E. Farber ◽  
Richard J. Roman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Epoxyeicosatrienoic Acids ◽  
Acute Administration ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Oxide Synthase ◽  
Cerebral Cortical Blood Flow

Background Despite intense investigation, the mechanism of isoflurane-induced cerebral hyperemia is unclear. The current study was designed to determine the contributions of neuronal nitric oxide synthase, prostaglandins, and epoxyeicosatrienoic acids to isoflurane-induced cerebral hyperemia. Methods Regional cerebral cortical blood flow was measured with laser Doppler flowmetry during stepwise increases of isoflurane from 0.0 to 1.2, 1.8, and 2.4 vol% end-tidal concentration in alpha-chloralose-urethane-anesthetized, C57BL/6 mice before and 45 min after administration of the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI, 40 mg/kg, intraperitoneal), the cyclooxygenase inhibitor indomethacin (INDO, 10 mg/kg, intravenous), and the cytochrome P450 epoxygenase inhibitor N-methylsulfonyl-6-(2-proparglyoxyphenyl)hexanoic acid (PPOH, 20 mg/kg, intravenous). Results Isoflurane increased regional cerebral cortical blood flow by 9 +/- 3, 46 +/- 21, and 101 +/- 26% (SD) at 1.2, 1.8, and 2.4 vol%, respectively. The increases in regional cerebral cortical blood flow were significantly (*P < 0.05) smaller after 7-NI (5 +/- 6, 29 +/- 19*, 68 +/- 15%*) or PPOH (4 +/- 8, 27 +/- 17*, 67 +/- 30%*), but not after administration of INDO (4 +/- 4, 33 +/- 18 [NS], 107 +/- 35% [NS]). The effect of combined treatment with 7-NI, PPOH, and INDO was not additive and was equal to that of either 7-NI or PPOH alone (5 +/- 5, 30 +/- 12*, 76 +/- 24%*). Chronic treatment of mice for 5 days with 7-NI (2 x 40 mg/kg, intraperitoneal) produced similar decreases in regional cerebral cortical blood flow as those seen with acute administration. Neither PPOH nor INDO conferred a significant additional block of the hyperemia in these animals. Conclusions Nitric oxide and epoxyeicosatrienoic acids contribute to isoflurane-induced hyperemia. However, only approximately one third of the cerebral hyperemic response to isoflurane is mediated by autacoids. The remaining part of this response appears to be mediated by a direct action of isoflurane on smooth muscle by some yet-unknown mechanism.

Sign in / Sign up

Export Citation Format

Share Document