Statistical analysis was performed with using Dunnett’s test. All animals were euthanized with i.v. injection of pentobarbital (20 mg/kg) after blood sampling in 7 days. Organ samples including heart, lungs, liver, spleen and kidneys were harvested

after euthanasia. The brain of neurologically positive animal was obtained after perfusion with 10% buffered formalin via the right common carotid artery. Paraffin sections were cut at a thickness of 6 μm. Sections were stained with hematoxylin and eosin (HE), and Masson trichrome. Within 10 min after administration of SPN, animals in both PL and AA group showed a statistically significant decrease in SpO2 with rapid breathing (Fig. 3). However, in all cases, SpO2 recovered within 1 h. During signaling pathway this investigation, no animals showed

an elevated rectal core temperature. No animals showed signs of paresis, convulsion or anisocoria. One animal in the AA group showed transient horizontal nystagmus about 20 min after SPN administration, and the duration of nystagmus was 20 min (Table 1). There was no neuropathological damage, such as hemorrhage, ischemia GSK2656157 or any degeneration in brain tissue including the cerebellum and brain stem (Fig. 4). One animal in the PL group died 2 days after injection of SPN. The following description of pathological findings in this paragraph and biochemical plasma results from the PL group includes results from the seven surviving animals. No histological damage or leukocyte aggregation was found in any organ sample including the heart, lungs, liver, kidneys and spleen in any of the animals. No macrophage hypertrophy or vacuolation was found in the lung, liver or spleen of any animals (Fig. 5). On biochemical blood examination, including hepatobiliary,

renal function and plasma lipid, no significant differences were found between PL, AA, and Control groups (p > 0.05). In necropsy of the one dead animal in the PL group, diffuse alveolar damage with deposition of fibrin was apparent. Hyaline membrane formation and migration of macrophages were clear, suggesting a state of shock. However, a direct relationship between SPN injection and the histopathological findings could not be detected (Fig. 6). Canaud initially reported the “perfluorocarbon syndrome” as a previously unrecognized Suplatast tosilate hazard of a dialysis-related clinical pathologic event in 2002. He also pointed out that PFC foam was identified in blood mainly in the right ventricle in autopsied patients, leading to speculation that death was caused by gas embolism. Oxygen transport characteristic of PFC emulsions are fundamentally different from those of blood [11]. Nieuwoudt et al. reported that PFC is not metabolized, but rather is excreted from the respiratory system into the air. In the first 24 h, the PFC is cleared from the circulation by the mononuclear phagocyte system accumulating in the liver, spleen, and bone marrow [12].