Background: Although hepatic ischemia-reperfusion (I/R) injury can be reduced by cooling of the ischemic organ, a systematic in vivo analysis of the influence of organ temperature in I/R injury is missing. The aim of this study was to systematically investigate the impact of defined temperatures of the ischemic liver tissue on microvascular I/R injury.
Methods: Ischemia of the left liver lobe was induced in C57BL/6 mice for 90 min. The ischemic lobe was placed in a polyethylene well and the temperature was adjusted to 37 degrees C, 26 degrees C, 15 degrees C, and 4 degrees C by superfusion with cooled/warmed saline solution. The ischemia groups (n=7 each) were compared with a sham-operated group (n=7). The sinusoidal perfusion index and the number of leukocytes firmly adherent to the endothelium of postsinusoidal venules were assessed using intravital fluorescence microscopy at 30 min, 120 min, and 240 min of reperfusion, respectively. At the end of the experiment, serum activities of the liver enzymes aspartate aminotransferase/alanine aminotransferase were determined, and tissue specimens were examined by electron microscopy.
Results: Core body temperature did not differ significantly between the groups. In the 37 degrees C group, the sinusoidal perfusion index was significantly reduced and the number of adherent leukocytes was significantly increased compared with the sham group. In all hypothermia groups, however, the microcirculatory parameters did not differ from the sham group. Serum activities of aspartate aminotransferase/alanine aminotransferase were significantly increased and hepatocellular integrity was severely affected in the 37 degrees C group as compared with all other groups.
Conclusions: These findings demonstrate that in the mouse liver the known protective effect of hypothermia is already encountered at 26 degrees C. Further reduction of temperature did not generate additional protection from I/R injury.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/00007890-200111150-00003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Synaptotagmin-1 attenuates myocardial programmed necrosis and ischemia/reperfusion injury through the mitochondrial pathway.
Cell Death Dis
January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
View Article and Find Full Text PDFHigh expression of SERPINE1 and CTSL in keratinocytes in pressure injury caused by ischemia-reperfusion injury.
Tissue Cell
January 2025
Institute of Regenerative Medicine, Binzhou Medical University, Yantai, Shandong 264003, PR China; Department of Histology and Embryology, Binzhou Medical University, Yantai, Shandong 264003, PR China. Electronic address:
Introduction: Pressure Injury (PI) is a complex disease process which is influenced by multiple factors, among which ischemia-reperfusion (I/R) injury is closely related to the progression of PI. But its biomarkers are still unclearly. Understanding its physiological mechanisms and related molecular biomarkers is a key to developing effective prevention and therapeutic strategies.
View Article and Find Full Text PDFsVEGFR3 alleviates myocardial ischemia/reperfusion injury through regulating mitochondrial homeostasis and immune cell infiltration.
Apoptosis
January 2025
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan II Rd, Guangzhou, 510080, China.
Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.
View Article and Find Full Text PDFAnalysis of the protective effect of hydrogen sulfide over time in ischemic rat skin flaps.
Ann Chir Plast Esthet
January 2025
Department of Plastic, Reconstructive, and Aesthetic Surgery, Faculty of Medicine, Çukurova University, Adana, Turkey.
Background: Hydrogen sulfide (HS) is a widely studied gasotransmitter, and its protective effect against ischemia-reperfusion damage has been explored in several studies. Therefore, a requirement exists for a comprehensive study about HS effects on ischemia-reperfusion damage in flap surgery. The aim of this study is to examine the effect of hydrogen sulfide by creating ischemia-reperfusion injury in the vascular-stemmed island flap prepared from the rat groin area.
View Article and Find Full Text PDFSivelestat sodium protects against renal ischemia/reperfusion injury by reduction of NETs formation.
Arch Biochem Biophys
January 2025
Department of Critical Care Medicine, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150001, China; Heilongjiang Provincial Key Laboratory of Critical Care Medicine, Harbin 150001, China; Central Laboratory of The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address:
Background: Ischemia-reperfusion injury (IRI) often results in renal impairment. While the presence of neutrophil extracellular traps (NETs) is consistently observed, their specific impact on IRI is not yet defined. Sivelestat sodium, an inhibitor of neutrophil elastase which is crucial for NET formation, may offer a therapeutic approach to renal IRI, warranting further research.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!