PMID- 3596775
OWN - NLM
STAT- MEDLINE
DCOM- 19870805
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 9
IP  - 6 Pt 2
DP  - 1987 Jun
TI  - Mechanisms of protection of the blood-brain barrier during acute hypertension in 
      chronically hypertensive rats.
PG  - III101-5
AB  - Spontaneously hypertensive rats are less susceptible than normotensive rats to 
      disruption of the blood-brain barrier during acute hypertension. The purpose of 
      this study was to examine mechanisms that protect the blood-brain barrier from 
      disruption in chronically hypertensive rats during acute hypertension. 
      Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive 
      rats (SHRSP) were studied using intravital fluorescent microscopy and 
      fluorescein-labeled dextran. Disruption of the blood-brain barrier was 
      characterized by the appearance of microvascular leaky sites and quantitated by 
      the clearance of fluorescein-labeled dextran. We measured pressure (servo null) 
      in pial arterioles and venules 40 to 60 micron in diameter. In WKY, acute, 
      phenylephrine-induced hypertension increased pial arteriolar pressure by 47 +/- 7 
      mm Hg (mean +/- SE) and pial venous pressure by 20 +/- 2 mm Hg. Leaky sites 
      increased from 0 to 28 +/- 2. In SHRSP, acute hypertension increased pial 
      arteriolar pressure 44 +/- 8 mm Hg, but pial venous pressure increased only 6 +/- 
      1 mm Hg and leaky sites increased from 0 to only 6 +/- 1. All leaky sites were 
      venular. In another group of WKY and SHRSP, we increased pial venous pressure 
      passively with a neck cuff. In WKY, venous pressure increased by 22 +/- 2 mm Hg, 
      and leaky sites increased from 0 to 23 +/- 2. In SHRSP, venous pressure increased 
      by 19 +/- 1 mm Hg, and leaky sites increased from 0 to 24 +/- 2. Thus, when 
      venous pressure is increased to the same level in WKY and SHRSP, disruption of 
      the blood-brain barrier is similar. We conclude that protection of the 
      blood-brain barrier during acute hypertension in SHRSP is related to attenuation 
      of increases in pial venous pressure, not pial arteriolar pressure, and the 
      blood-brain barrier in venules of SHRSP probably is not inherently resistant to 
      disruption.
FAU - Mayhan, W G
AU  - Mayhan WG
FAU - Faraci, F M
AU  - Faraci FM
FAU - Heistad, D D
AU  - Heistad DD
LA  - eng
GR  - HL 14388/HL/NHLBI NIH HHS/United States
GR  - HL 35940/HL/NHLBI NIH HHS/United States
GR  - HL 7180/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Aorta/physiopathology
MH  - Biomechanical Phenomena
MH  - Blood Pressure
MH  - *Blood-Brain Barrier
MH  - Capillary Permeability
MH  - Constriction, Pathologic
MH  - Hypertension/*physiopathology
MH  - Male
MH  - Neck/blood supply
MH  - Pia Mater/blood supply
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Venous Pressure
MH  - Venules/metabolism
EDAT- 1987/06/01 00:00
MHDA- 1987/06/01 00:01
CRDT- 1987/06/01 00:00
PHST- 1987/06/01 00:00 [pubmed]
PHST- 1987/06/01 00:01 [medline]
PHST- 1987/06/01 00:00 [entrez]
AID - 10.1161/01.hyp.9.6_pt_2.iii101 [doi]
PST - ppublish
SO  - Hypertension. 1987 Jun;9(6 Pt 2):III101-5. doi: 10.1161/01.hyp.9.6_pt_2.iii101.