Protective effect of nitric oxide on hepatopulmonary syndrome from ischemia-reperfusion injury

Figure 1 Hematoxylin and eosin staining and triphosphopyridine nucleotide-d staining and immunohistochemical staining for grafted liver and recipient’s lung tissues. A, C: Grafted liver tissues and the recipient’s lung tissues from group I of L-arginine revealed that the pathological damages of grafted liver and lung tissues significantly reduced after reperfusion 3 h (HE × 132, × 66); B, D: Grafted liver tissues and the recipient’s lung tissues from group III of the NOS inhibitor after reperfusion 3 h showed extensive cloudy swelling of hepatocytes, vacuolar degeneration, nuclear shrinkage, chromatin concentration, and marginalized or fragmented apoptotic body and severe structural damage to the recipient’s lung tissues, a large number of inflammatory cell infiltration, and intravascular thrombosis (HE × 33, × 66); E: NADPH diaphorase histochemistry staining of NO synthase and immunohistochemistry staining of cNOS for grafted liver tissues from group I after reperfusion 24 h (NADPH-d, × 66); F: Expressions of cNOS in grafted liver tissues were particularly significant in vascular endothelial cells and hepatocytes after 24 h in group II [immunohistochemical staining (IH), × 66]; G, H: Expressions of iNOS and ICAM-1 in grafted liver tissues were little in group I of L-arginine after reperfusion 24 h (IH × 66, × 66); I, J: Expression of ICAM-1 and TNF-α in grafted liver tissues were diffuse strong in group III of the NOS inhibitor after reperfusion 3 h (IH × 66, × 66). TNF-α: Tumor necrosis factor-α; NO: Nitric oxide; NOS: Nitric oxide synthase; NADPH: Triphosphopyridine nucleotide; ICAM-1: Intercellular adhesion molecule 1; cNOS: Constitutive nitric oxide synthase; iNOS: Inducible nitric oxide synthase; HE: Hematoxylin and eosin.