PMID- 11166274
OWN - NLM
STAT- MEDLINE
DCOM- 20010329
LR  - 20190513
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 49
IP  - 3
DP  - 2001 Feb 16
TI  - Time course of arteriogenesis following femoral artery occlusion in the rabbit.
PG  - 609-17
AB  - OBJECTIVE: We examined the time course of arteriogenesis (collateral artery 
      growth) after femoral artery ligation and the effect of monocyte chemoattractant 
      protein-1 (MCP-1). METHODS: New Zealand White rabbits received MCP-1 or phosphate 
      buffered saline (PBS) for a 1-week period, either directly or 3 weeks after 
      femoral artery ligation (non-ischemic model). A control group was studied with 
      intact femoral arteries and another 1 min after acute femoral artery ligation. 
      RESULTS: Collateral conductance index significantly increased when MCP-1 
      treatment started directly after femoral artery ligation (acute occlusion: 
      0.94+/-0.19; without occlusion: 168.56+/-15.99; PBS: 4.10+/-0.48; MCP-1: 
      33.96+/-1.76 ml/min/100 mmHg). However, delayed onset of treatment 3 weeks after 
      ligation and final study of conductance at 4 weeks showed no significant 
      difference against a 4-week control (PBS: 79.08+/-7.24; MCP-1: 90.03+/-8.73 
      ml/min/100 mmHg). In these groups increased conductance indices were accompanied 
      by a decrease in the number of visible collateral vessels (from 18 to 36 
      identifiable vessels at day 7 to about four at 21 days). CONCLUSION: We conclude 
      that the chemokine MCP-1 markedly accelerated collateral artery growth but did 
      not alter its final extent above that reached spontaneously as a function of 
      time. We show thus for the first time that a narrow time window exists for the 
      responsiveness to the arteriogenic actions of MCP-1, a feature that MCP-1 may 
      share with other growth factors. We show furthermore that the spontaneous 
      adaptation by arteriogenesis stops when only about 50% of the vasodilatory 
      reserve of the arterial bed before occlusion are reached. The superiority of few 
      large arterial collaterals in their ability to conduct large amounts of blood 
      flow per unit of pressure as compared to the angiogenic response where large 
      numbers of small vessels are produced with minimal ability to allow mass 
      transport of bulk flow is stressed.
FAU - Hoefer, I E
AU  - Hoefer IE
AD  - Department of Experimental Cardiology, Max-Planck-Institute for Physiological and 
      Clinical Research, Benekestr. 2, D-61231, Bad Nauheim, Germany. 
      ihoefer@kerkhoff.mpg.de
FAU - van Royen, N
AU  - van Royen N
FAU - Buschmann, I R
AU  - Buschmann IR
FAU - Piek, J J
AU  - Piek JJ
FAU - Schaper, W
AU  - Schaper W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Chemokine CCL2)
SB  - IM
CIN - Cardiovasc Res. 2012 Nov 1;96(2):152-3; discussion 154-6. PMID: 22977003
MH  - Animals
MH  - Arterial Occlusive Diseases/diagnostic imaging/drug therapy/*physiopathology
MH  - Chemokine CCL2/*therapeutic use
MH  - Collateral Circulation/*drug effects
MH  - Disease Models, Animal
MH  - *Femoral Artery/diagnostic imaging
MH  - Hemodynamics/drug effects
MH  - Hindlimb/blood supply
MH  - Ligation
MH  - Microspheres
MH  - Neovascularization, Physiologic/*drug effects
MH  - Rabbits
MH  - Radiography
MH  - Random Allocation
MH  - Time Factors
EDAT- 2001/02/13 11:00
MHDA- 2001/04/03 10:01
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/04/03 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
AID - S0008636300002431 [pii]
AID - 10.1016/s0008-6363(00)00243-1 [doi]
PST - ppublish
SO  - Cardiovasc Res. 2001 Feb 16;49(3):609-17. doi: 10.1016/s0008-6363(00)00243-1.