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1 flammation on I/R in a murine model of total hepatic ischemia.
2 rvival was determined using a model of total hepatic ischemia.
3 more vulnerable to necrosis after transient hepatic ischemia.
4 Numerous clinical circumstances lead to hepatic ischemia.
5 attenuate tissue injury after an episode of hepatic ischemia.
6 leotidase may be a potential therapeutic for hepatic ischemia.
7 is rats underwent 60 minutes of partial warm hepatic ischemia.
8 ingly, male rats were subjected to 1 hour of hepatic ischemia (70%) followed by reperfusion; animals
9 ute kidney injury, myocardial, intestinal or hepatic ischemia, acute lung injury, or during organ tra
10 d to 4 groups: 1.Sham; 2.IR: 40 min of lobar hepatic ischemia and 2 hr reperfusion; 3.RIPC+IR: 6 cycl
12 C57BL/6 mice underwent 90 minutes of partial hepatic ischemia and 4 hours of reperfusion in the prese
13 Rats were killed after 60 min of partial hepatic ischemia and after 2, 6, 24, and 48 hr of reperf
15 rculation, resulting in microscopic areas of hepatic ischemia and explaining the mechanism of IL-2-in
24 a unique role for Neo1 in the development of hepatic ischemia and reperfusion injury and identified N
26 d in a significant reduction of experimental hepatic ischemia and reperfusion injury, involving atten
41 ull mice were subjected to 60 min of partial hepatic ischemia, and at various times thereafter, blood
43 Analysis of microcirculatory events included hepatic ischemia, endothelial injury, including with gen
44 Rats were subjected to 60 minutes of partial hepatic ischemia followed by 0, 3, 6, 24, or 48 hours of
45 re subjected to 10 or 30 min of partial warm hepatic ischemia followed by 3 to 24 hr of reperfusion.
48 before subjecting them to 90 minutes of warm hepatic ischemia followed by reperfusion for 6 or 24 hou
50 C57BL/6 mice underwent 90 minutes of partial hepatic ischemia followed by reperfusion with or without
54 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 8 hours of reperfusio
55 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 96 hours of reperfusi
57 mice were subjected to 90 minutes of partial hepatic ischemia, followed by up to 8 hours of reperfusi
59 serotype O55:B5 (EC) and 90 min of secondary hepatic ischemia in EC + I/R and saline-infused (normal
62 ificantly improved after 75 minutes of total hepatic ischemia in P-selectin deficient mice when compa
66 , improved cell engraftment independently of hepatic ischemia or inflammation, without improving live
67 Systemic administration of DAR decreases hepatic ischemia-related events and thus indirectly impr
71 tate aminotransferase, a surrogate marker of hepatic ischemia reperfusion injury, was the only consis
72 m and xenon have additionally been tested in hepatic ischemia reperfusion injury, whereas neon was on
76 ment NO. bioavailability and protect against hepatic ischemia-reperfusion (I-R) injury in type 2 diab
77 CD4+ T cells play a critical role during hepatic ischemia-reperfusion (I/R) injury although the m
83 L/6 mice were subjected to 60-minute partial hepatic ischemia-reperfusion and posttreated with sirtui
84 n of sirtuin 1 attenuates liver injury after hepatic ischemia-reperfusion by restoring mitochondrial
88 play an essential role in the early phase of hepatic ischemia-reperfusion injury and determine the ex
89 ose tissue-derived mesenchymal stem cells in hepatic ischemia-reperfusion injury and the underlying m
93 ematopoietic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Pl
94 antibody and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the
95 Moreover, in animal models of peritonitis, hepatic ischemia-reperfusion injury, Salmonella infectio
104 zed that pulmonary injury is associated with hepatic ischemia-reperfusion resulting from descending t
105 hts into possible mechanisms responsible for hepatic ischemia-reperfusion-related acute lung injury a
106 rotects against inflammation and damage from hepatic ischemia/reperfusion (I/R) and other insults.
107 that drive sterile inflammatory injury after hepatic ischemia/reperfusion (I/R) injury are not comple
109 nflammatory responses play critical roles in hepatic ischemia/reperfusion (I/R) injury associating wi
111 catalysis of heme, in the protection against hepatic ischemia/reperfusion (I/R) injury needs to be es
112 he liver to examine their role in total warm hepatic ischemia/reperfusion (I/R) injury with bowel con
125 ever, their in vivo functional importance in hepatic ischemia/reperfusion (IR) injury is perplexing.
128 Therefore, we investigated the response to hepatic ischemia/reperfusion in STAT4-deficient mice.
133 stic target of rapamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and
136 ate that SLPI has protective effects against hepatic ischemia/reperfusion injury and suggest that end
137 The data suggest that IL-10 protects against hepatic ischemia/reperfusion injury by suppressing NFkap
139 er the LPS signaling pathway is activated by hepatic ischemia/reperfusion injury in the transplant se
144 ies with isolated cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 f
145 have previously employed an animal model of hepatic ischemia/reperfusion injury, and have shown that
146 Furthermore, P5779 can protect mice against hepatic ischemia/reperfusion injury, chemical toxicity,
147 R1, and IL-6 levels, are increased following hepatic ischemia/reperfusion injury, implying that TACE
148 Rgamma activation is hepatoprotective during hepatic ischemia/reperfusion injury, mice were treated w
160 as to determine whether IL-10 could suppress hepatic ischemia/reperfusion-induced NFkappaB activation
163 bjected to 70% hepatectomy and 30 minutes of hepatic ischemia showed significantly reduced regenerati
164 t) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight differen
165 R4 knockout (KO) mice were subjected to warm hepatic ischemia, there was significant protection in th
166 vival was observed after 75 minutes of total hepatic ischemia using both protective protocols, wherea
168 ncapsulated clodronate 48 h before 35 min of hepatic ischemia with bowel congestion, followed by 6 or
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