Neutrophils and the endothelium in post-ischemic alterations in skeletal muscle blood flow.
Thromboxane A2, leukotriene B4, and NE are all released from ischemic muscle during reperfusion. Thromboxane A2 levels peaked at 10 min and this potent vasoconstrictor may be responsible for low reflow. Neutrophil elastase levels did not rise until 240 min of reperfusion, following that of leukotriene B4 at 120 min, indicating that neutrophil recruitment and activation is a relatively late event following revascularization. In conclusion, it would appear that endothelial factors have a significant role in the vasomotor changes that account for low reflow. Equally altered neutrophil function almost certainly contributes to the final development of reperfusion injury.
Vascular Surgical Unit, University of Bradford, England.
J N
JN
Crinnion
S
S
Homer-Vanniasinkam
S M
SM
Parkin
M J
MJ
Gough
D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism*; D007511:Ischemia / Q000378:metabolism*; D019272:Leukocyte Elastase; D007975:Leukotriene B4 / Q000378:metabolism; D009132:Muscles / Q000098:blood supply*; D009504:Neutrophils / Q000378:metabolism*; D010196:Pancreatic Elastase / Q000378:metabolism; D051381:Rats; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000378:metabolism*; D013929:Thromboxane B2 / Q000378:metabolism
D007975:Leukotriene B4; D013929:Thromboxane B2; D010196:Pancreatic Elastase; D019272:Leukocyte Elastase