Role of nitric oxide in hepatic ischemia-reperfusion injury

Figure 1 Multifaceted hepatic ischemia-reperfusion injury. Kupffer and endothelial cells produce cytokines and chemokines, recruiting neutrophils that further accentuate injury. EC: Endothelial cell; KC: Kupffer cell; ATP: Adenosine triphosphate; TNF: Tumor necrosis factor; IL: Interleukin; ICAM: Intercellular adhesion molecule; VCAM: Vascular adhesion molecule; PAF: Platelet activation factor; LTB4: Leukotriene B4; GMS-CSF: Granulocyte macrophage colony stimulating factor; INF: Interferon; ROS: Reactive oxygen species (Courtesy of Dr. Joan Rosello-Catafau, Barcelona, Spain).

Figure 2 Increased liver injury as assessed by serum alanine aminotransferase in endothelium-derived nitric oxide synthase knockout mice compared with their wild type controls. ^aP < 0.05 vs sham-operated controls. ^cP < 0.05 vs time-matched wild type control. ALT: Alanine aminotransferase; eNOS: Endothelium-derived nitric oxide synthase (Courtesy of Dr. Ianes N. Hines, Chapel Hill, NC).

Figure 3 Decreased apoptosis indicated by TUNEL staining in patients treated with inducible nitric oxide compared to controls (Courtesy of John D. Lang, MD, Seattle, WA). ^aP < 0.05. iNO: Inducible nitric oxide.