PMID- 11254907
OWN - NLM
STAT- MEDLINE
DCOM- 20010621
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 155
IP  - 2
DP  - 2001 Apr
TI  - Dexamethasone inhibits macrophage accumulation after balloon arterial injury in 
      cholesterol fed rabbits.
PG  - 371-80
AB  - Macrophages play a critical role in the development and progression of 
      atherosclerosis. This study was designed to examine the effect of the 
      glucocorticoid, dexamethasone, (Dex), on macrophage accumulation after acute 
      arterial injury. Twenty New Zealand white rabbits were fed a 2% cholesterol, 6% 
      peanut oil, rabbit chow diet for one month prior to bilateral balloon dilatation 
      of the femoral arteries. Ten rabbits received Dex (1 mg/kg, im.) the day before 
      and then daily for 7 days after arterial injury; control rabbits received vehicle 
      only. Seven days after injury, Dex treatment resulted in a 96% and 77% reduction 
      (P < 0.002) in the mean number of macrophages accumulating in the intima and 
      media, respectively. This effect was apparently not due to a reduction in the 
      number of circulating monocytes or to the ability of monocytes from Dex treated 
      animals to adhere to endothelium or migrate in response to a chemotactic signal, 
      determined in vitro under static conditions. It was associated with a 61% 
      reduction in monocyte chemoattractant protein-1 (MCP-1) antigen (P < 0.004) in 
      the injured arterial wall (media+intima). Glucocorticoids may be useful in 
      attenuating the inflammatory response and subsequent foam-cell accumulation after 
      arterial injury.
FAU - Poon, M
AU  - Poon M
AD  - The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of 
      Medicine, New York, NY, 10029, USA.
FAU - Gertz, S D
AU  - Gertz SD
FAU - Fallon, J T
AU  - Fallon JT
FAU - Wiegman, P
AU  - Wiegman P
FAU - Berman, J W
AU  - Berman JW
FAU - Sarembock, I J
AU  - Sarembock IJ
FAU - Taubman, M B
AU  - Taubman MB
LA  - eng
GR  - HL43302/HL/NHLBI NIH HHS/United States
GR  - HL54469/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cholesterol, Dietary)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology/*therapeutic use
MH  - Arteriosclerosis/chemically induced/pathology/*surgery
MH  - Catheterization/*adverse effects
MH  - Cell Adhesion/drug effects
MH  - Chemokine CCL2/metabolism
MH  - Chemotaxis/*drug effects
MH  - Cholesterol, Dietary/*toxicity
MH  - Dexamethasone/pharmacology/*therapeutic use
MH  - *Diet, Atherogenic
MH  - Drug Evaluation, Preclinical
MH  - Endothelium, Vascular/drug effects/pathology
MH  - Femoral Artery/*injuries/metabolism/pathology
MH  - Graft Occlusion, Vascular/*prevention & control
MH  - Hyperplasia
MH  - Macrophages/*drug effects/pathology
MH  - Male
MH  - Monocytes/drug effects/pathology
MH  - Rabbits
MH  - Tunica Intima/drug effects/pathology
MH  - Wounds and Injuries/drug therapy
EDAT- 2001/03/20 10:00
MHDA- 2001/06/22 10:01
CRDT- 2001/03/20 10:00
PHST- 2001/03/20 10:00 [pubmed]
PHST- 2001/06/22 10:01 [medline]
PHST- 2001/03/20 10:00 [entrez]
AID - S0021-9150(00)00605-5 [pii]
AID - 10.1016/s0021-9150(00)00605-5 [doi]
PST - ppublish
SO  - Atherosclerosis. 2001 Apr;155(2):371-80. doi: 10.1016/s0021-9150(00)00605-5.