[Lung cancer associated with bulla found during an operation of pneumothorax; report of a case].

A 50-year-old man was admitted to our hospital because of dyspnea. His chest X-ray and computed tomography (CT) showed right pneumothorax and multiple bullae. His pneumothorax was drained with a chest tube, however, because of a persistent air leak, bullectomy was performed 18 days after the occurrence of pneumothorax. Intraoperatively, we found a palpable tumor in the bulla approximately 10 mm in diameter and resected it with the bullae. Histologically, the tumor was diagnosed as a large cell carcinoma.

[Successful removal of aberrant needles in the pericardium and lung].

A 28-year-old woman who had been diagnosed as schizophrenia was admitted to our hospital, complaining of chest pain. Her chest X-ray demonstrated 9 foreign bodies in the pericardium, lung and others. Her chest computed tomography (CT) confirmed needle-like shadows in the pericardium and lung. They were diagnosed as aberrant needles, and surgically removed. The intrapulmonary aberrant needle was removed with video-assisted thoracoscopic surgery. Aberrant needle in pericardium or lung should be removed surgically, because it is very dangerous. Intraoperative chest X-ray is always necessary before closing the wound to avoid leaving the residual fragments.

Up-regulation of oxygen-derived free radicals by interleukin-1 in hepatic ischemia/reperfusion injury.

BACKGROUND: Oxygen-derived free radicals (FRs) are critical mediators of ischemia/reperfusion injury. Inflammatory cytokines have been shown to play important roles in tissue injury. To examine the relationship between FRs and interleukin-1 (IL-1) in hepatic ischemia/reperfusion injury, we used interleukin-1 receptor antagonist (IL-1ra) to block endogenous IL-1 production in a rat model of hepatic ischemia/reperfusion. METHODS: Female SD rats were subjected to 30 min of hepatic ischemia followed by reperfusion. The animals were divided into two groups, control group and IL-1ra-treated group, according to the rinse solution. In both groups, FR production, histological changes, and interactions between leukocytes and endothelial cells were analyzed in the course of reperfusion. RESULTS: In the control group, production of FRs increased significantly after 60 min of reperfusion. After 60 and 180 min of reperfusion, histological examination showed atrophy and degeneration of hepatocytes. Hepatic microcirculation demonstrated a marked increase in the number of leukocytes adherent to endothelial cells and of injured cells after reperfusion. In the IL-1ra-treated group, IL-1ra pretreatment markedly reduced FR production after 60 min of reperfusion, the number of leukocytes adherent to endothelial cells, and tissue injury. CONCLUSION: These data clearly show an important role for IL-1 in the induction of FR production, leukocyte adhesion, and tissue injury after hepatic ischemia/reperfusion injury.

Efficacy of intraportal infusion of prostaglandin E1 to improve the hepatic blood flow and graft viability in porcine liver transplantation.

BACKGROUND: Prostaglandin E1 (PGE1) has been reported to have a protective effect in experimental and clinical models of liver damage. The aim of this study was to elucidate the effects of the intraportal infusion of PGE1 on hepatic blood flow and graft viability after orthotopic liver transplantation in pigs. METHODS: First, the hepatic arterial flow (HAF), portal venous flow (PVF), and liver tissue blood flow (LTBF) were measured during the continuous intravenous or intraportal infusion of PGE1. Second, two groups of pigs underwent orthotopic liver transplantation: group A, untreated controls; and group B, animals that received intraportal PGE1 for 2 hr after vascular reconstruction of the allograft. Changes in HAF, PVF, LTBF, and hepatic function were measured. RESULTS: The intraportal infusion of PGE1 significantly increased HAF and had no effect on blood pressure, PVF, or LTBF. In group B, HAF and LTBF increased significantly with time. In group A, HAF remained unchanged and a decrease in LTBF was observed. Group B exhibited a higher arterial ketone body ratio and a greater bile flow compared with group A. A significant elevation in serum glutamic oxaloacetic transaminase concentration was observed in group A, but not in group B. CONCLUSIONS: This study demonstrates that the intraportal infusion of PGE1 improves hepatic allograft blood flow, predominantly through an effect on HAF, and may improve graft viability after orthotopic liver transplantation.

Anti-interleukin-8 monoclonal antibody reduces free radical production and improves hemodynamics and survival rate in endotoxic shock in rabbits.

BACKGROUND: Although high levels of interleukin-8 (IL-8) have been found in patients with sepsis and a monoclonal antibody (MoAb) against IL-8 has been successfully used in some animal models of inflammation, no specific therapeutic agent against IL-8 has been tested for the treatment of sepsis. We studied the effects of a MoAb against IL-8 in the treatment of endotoxic shock with a prospective randomized rabbit endotoxic shock model. METHODS: Twenty New Zealand white rabbits were anesthetized and divided into four groups: normal, anti-IL-8, control-Ab, and lipopolysaccharide (LPS). Anti-IL-8 and control-Ab groups received a MoAb (immunoglobulin G, 3 mg/kg) 5 minutes before the LPS injection. All groups, except the normal group, received a continuous 20-minute infusion of LPS (500 micrograms/kg). The normal group received NaCl (0.9%) rather than LPS. RESULTS: The 7-day survival rates were 100% for normal group, 80% for anti-IL-8 group, 40% for control-Ab group, and 0% for LPS group. Compared with the LPS group, anti-IL-8 rabbits had a smaller decrease in mean arterial blood pressure (p < 0.05) and increased urinary volume (p < 0.05). Anti-IL-8 rabbits had lower plasmatic levels of IL-1 beta, less free radical production (p < 0.05), and a higher survival rate (p < 0.01). CONCLUSIONS: IL-8 plays a significant role in endotoxic shock, and IL-8 blockage results in attenuation of the hypotensive and tachypneic effects of LPS, reduced free radical production, and an increased survival rate after lethal endotoxic shock.

[Microcirculatory disturbances after surgical insults--important role of inflammatory cytokines].

Microcirculatory disturbances in the gastric mucosa was investigated in rats after thermal injury using intravital video microscopy. Mucosal blood flow decreased significantly 5 hrs after thermal injury and increased neutrophil-endothelial cell interaction was observed at the same time. Zymosan stimulated-free radical production from peripheral blood was also increased and acute gastric mucosal lesion (AGML) appeared 5 hrs after thermal injury. These data suggest that neutrophil-endothelial cell interaction and increased free radical production induce AGML formation and that microcirculatory disturbance is one of the main reasons for organ failure after surgical insults. The role of inflammatory cytokines in hepatic microcirculatory disturbance was also studied in endotoxin-injected rats using IL-1 receptor antagonist (IL-1Ra) or TNF binding protein (TNFbp). Pretreatment with IL-1Ra or TNFbp significantly improved hepatic microcirculatory disturbance and reduced both the number of leukocytes adhered to the sinusoidal wall and the number of injured cells as well. These data suggest that inflammatory cytokines play a crucial role in microcirculatory disturbance after surgical insults by promoting neutrophil-endothelial cell interaction and systemic excessive inflammation.