PMID- 17040967
OWN - NLM
STAT- MEDLINE
DCOM- 20070220
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 292
IP  - 1
DP  - 2007 Jan
TI  - The mechanism of flow-induced dilation in human adipose arterioles involves 
      hydrogen peroxide during CAD.
PG  - H93-100
AB  - Flow-induced dilation (FID) is an important physiological stimulus that regulates 
      tissue blood flow and is mediated by endothelium-derived factors that play a role 
      in vascular integrity and the development of atherosclerosis. In coronary artery 
      disease (CAD), conduit artery FID is impaired. The purpose of this study was to 
      determine the mechanism of FID in human visceral adipose and examine whether the 
      presence of conduit coronary atherosclerosis is associated with altered 
      endothelial function in visceral fat. FID was determined in isolated visceral fat 
      arterioles from patients with and without CAD. After constriction with 
      endothelin-1, increases in flow produced an endothelium-dependent vasodilation 
      that was sensitive to N(omega)-nitro-l-arginine methyl ester (l-NAME) in visceral 
      fat arterioles from patients without CAD. In contrast, l-NAME alone or in 
      combination with indomethacin had no effect on FID in similarly located 
      arterioles from patients with CAD. Flow increased dichlorofluorescein (DCF) and 
      dihydroethidium fluorescence accumulation in arterioles from patients with CAD 
      versus without, indicative of the production of oxidative metabolites and 
      superoxide, respectively. Both the dilation and DCF fluorescence to flow were 
      reduced in the presence of the H(2)O(2) scavenger polyethylene glycol-catalase. 
      Exogenous H(2)O(2) elicited similar relaxations of arterioles from patients in 
      both groups. These data indicate that FID in visceral fat arterioles is nitric 
      oxide dependent in the absence of known CAD. However, in the presence of CAD, 
      H(2)O(2) replaces nitric oxide as the mediator of endothelium-dependent FID. This 
      study provides evidence that adverse microvascular changes during CAD are evident 
      in human visceral adipose, a tissue associated with CAD.
FAU - Phillips, Shane A
AU  - Phillips SA
AD  - Cardiovascular Center, Dept. of Medicine, Medical College of Wisconsin, 8701 
      Watertown Plank Rd., Milwaukee, WI 53226, USA. shanep@mcw.edu
FAU - Hatoum, O A
AU  - Hatoum OA
FAU - Gutterman, David D
AU  - Gutterman DD
LA  - eng
GR  - HL-080704/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20061013
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
SB  - IM
MH  - Adipose Tissue/*blood supply/*physiopathology
MH  - Arterioles/*physiopathology
MH  - *Blood Flow Velocity
MH  - Coronary Artery Disease/*physiopathology
MH  - Humans
MH  - Hydrogen Peroxide/*metabolism
MH  - In Vitro Techniques
MH  - *Mechanotransduction, Cellular
MH  - Reactive Oxygen Species/*metabolism
MH  - Vasodilation
EDAT- 2006/10/17 09:00
MHDA- 2007/02/21 09:00
CRDT- 2006/10/17 09:00
PHST- 2006/10/17 09:00 [pubmed]
PHST- 2007/02/21 09:00 [medline]
PHST- 2006/10/17 09:00 [entrez]
AID - 00819.2006 [pii]
AID - 10.1152/ajpheart.00819.2006 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2007 Jan;292(1):H93-100. doi: 
      10.1152/ajpheart.00819.2006. Epub 2006 Oct 13.