PMID- 10454443
OWN - NLM
STAT- MEDLINE
DCOM- 19990915
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 34
IP  - 2
DP  - 1999 Aug
TI  - Microvascular responses to ischemia/reperfusion in normotensive and hypertensive 
      rats.
PG  - 212-6
AB  - The objective of the present study was to determine whether long-term arterial 
      hypertension renders the microvasculature more vulnerable to the deleterious 
      inflammatory responses elicited by ischemia and reperfusion (I/R). Intravital 
      fluorescence microscopy was used to monitor leukocyte adherence and emigration, 
      platelet-leukocyte aggregation, and albumin extravasation in mesenteric 
      postcapillary venules of spontaneously hypertensive rats (SHR) and normotensive 
      Wistar-Kyoto rats (WKY) after 10 minutes of ischemia and subsequent reperfusion. 
      Significant and comparable increases in leukocyte adherence/emigration and the 
      formation of platelet aggregates were elicited by I/R in both WKY and SHR. 
      Albumin extravasation was enhanced after I/R in SHR, but not in WKY. Monoclonal 
      antibodies directed against the adhesion glycoproteins CD18, P-selectin, or 
      ICAM-1 showed similar patterns of protection against the I/R-induced inflammatory 
      responses in WKY and SHR. The enhanced albumin extravasation noted in 
      postischemic venules of SHR was prevented by immunoneutralization of either CD18 
      on leukocytes or ICAM-1 on endothelial cells. These results suggest that, whereas 
      long-term arterial hypertension does not significantly modify the leukocyte and 
      platelet recruitment normally elicited in venules by I/R, it does result in an 
      exaggerated albumin leakage response, which is mediated by an interaction between 
      beta(2) (CD18) integrins on leukocytes and ICAM-1 on endothelial cells.
FAU - Kurose, I
AU  - Kurose I
AD  - Department of Molecular Physiology, Center of Excellence in Arthritis and 
      Rheumatism, Louisiana State University Medical Center, Shreveport, LA, USA.
FAU - Wolf, R
AU  - Wolf R
FAU - Cerwinka, W
AU  - Cerwinka W
FAU - Granger, D N
AU  - Granger DN
LA  - eng
GR  - HL-26441/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (CD18 Antigens)
RN  - 0 (P-Selectin)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Animals
MH  - CD18 Antigens/physiology
MH  - Data Interpretation, Statistical
MH  - Hypertension/blood/*physiopathology
MH  - Intercellular Adhesion Molecule-1/physiology
MH  - Leukocytes/physiology
MH  - Male
MH  - Mast Cells/physiology
MH  - *Microcirculation
MH  - Microscopy, Fluorescence
MH  - Oxidative Stress
MH  - P-Selectin/physiology
MH  - Platelet Aggregation
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Reperfusion Injury/blood/*physiopathology
MH  - Time Factors
MH  - Venules/physiopathology
EDAT- 1999/08/24 00:00
MHDA- 1999/08/24 00:01
CRDT- 1999/08/24 00:00
PHST- 1999/08/24 00:00 [pubmed]
PHST- 1999/08/24 00:01 [medline]
PHST- 1999/08/24 00:00 [entrez]
AID - 10.1161/01.hyp.34.2.212 [doi]
PST - ppublish
SO  - Hypertension. 1999 Aug;34(2):212-6. doi: 10.1161/01.hyp.34.2.212.