Gastrointestinal ischemia-reperfusi

Gastrointestinal ischemia-reperfusion (GI/R)3 generally
stems from interruption of blood flow within the superior
mesenteric artery or vein and leads to small intestinal hy-
poperfusion and a mortality rate of
70% (1). Clinically, GI/R is
commonly associated with sepsis, hemorrhagic shock, vascular sur-
gery, small bowel transplantation (2, 3), and multiple organ failure (4,
5). The complement system is a key component in GI/R, resulting in
local intestinal and secondary tissue injury (6 –11).
Research over the past 30 years has linked complement activa-
tion and consequent inflammation and tissue injury with I/R. Mod-
els of complement-dependent I/R injury include ischemia of the
intestine, hindlimb, kidney, myocardium infarction, hemorrhagic
shock, sepsis, and pulmonary injury (6 – 8, 12–15). Although the
exact molecular mechanisms of complement activation after GI/R
have not been fully elucidated, evidence from in vitro and in vivo
models suggest that complement activation is an early event; there

ผลลัพธ์ (อังกฤษ) 2:

Gastrointestinal ischemia-reperfusion (GI / R) 3 generally
stems from interruption of Blood flow Within the Superior
mesenteric artery or vein and Leads to Small intestinal HY-
Poperfusion and a mortality rate of? 70% (1). Clinically, GI / R is
commonly associated with sepsis, hemorrhagic Shock, vascular sur-
Gery, Small bowel Transplantation (2, 3), and multiple organ Failure (4,
5). System is a Key Component in the complement GI / R, resulting in
local intestinal tissue injury and Secondary (6 -11).
Research over the Past 30 years has linked complement Activa-
tion and consequent inflammation and tissue injury with I / R. MOD
els of complement-dependent I / R injury include ischemia of the
intestine, hindlimb, kidney, myocardium infarction, hemorrhagic
Shock, sepsis, and pulmonary injury (6 - 8, 12-15). Although the
molecular Exact Mechanisms of complement Activation after GI / R
have not been fully elucidated, in vitro and in vivo Evidence from
models suggest that complement Early Activation is an event; there

ผลลัพธ์ (อังกฤษ) 3:

Gastrointestinal ischemia-reperfusion (GI / R) 3 generally
stems from interruption of blood flow within the superior
mesenteric. Artery or vein and leads to small intestinal hy -
poperfusion and a mortality rate of
70% (1). Clinically GI / R, is
commonly. Associated sepsis with, shock vascular hemorrhagic, sur -
gery small bowel, transplantation, (2 3), and multiple organ failure. 4
5 (,).The complement system is a key component in GI / R resulting, in
local intestinal and secondary tissue injury (6 - 11).
Research. Over the past 30 years has linked complement Activa -
tion and consequent inflammation and tissue injury with I / R. Mod -
els. Of complement-dependent I / R injury include ischemia of the
intestine hindlimb kidney,,,,, myocardium infarction hemorrhagic
shock. Sepsis.And pulmonary injury (6 8 12 -, - 15). Although the
exact molecular mechanisms of complement activation after GI / R
have not. Been fully elucidated evidence from, in vitro and in vivo
models suggest that complement activation is an early event; there.