• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.128-137
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• 1991

Peritoneal dialysis has been widely considered to be the dialytic treatment of choice for acute renal failure in infants and young children, because the technique is simple, safe and easily adapted for these patients. Also peritoneal dialysis in infants might have more effective ultrafiltration and clearance than in adults. In certain circumstances associated with hemodynamic instability, ordinary volume peritoneal dialysis(30-50 ml/kg body weight per exchange) or hemodialysis may not be suitable unfortunately. But frequent cycled, low volume, high concentration peritoneal dialysis may be more available to manage the hemodynamically untable acute renal failure of newborns and infants. Seven infants underwent peritoneal dialysis for hemodynamically unstable acute renal failure with low exchange volume($14.2{\pm}4.2ml/kg$), short exchange time(30 to 45 minutes) and hypertonic glucose solution(4.25% dextrose). Age was $1.9{\pm}1.3$ months and body weight was $4.6{\pm}1.6kg $. Etiology of acute renal failure was secondary to sepsis with or without shock(5 cases) and postcardiac operation(2 cases). Catheter was inserted percutaneously with pigtail catheter or Tenkhoff catheter by Seldinger method. Dialysate was commercially obtained Peritosol which contained sodium, chloride, potassium, magnesium, lactate and calcium. Net ultrafiltration(ml/min) showed no difference between low volume dialysis and control($0.27{\pm}0.09$ versus $0.29{\pm}0.09$) Blood BUN decreased from $95.7{\pm}37.5$ to $75.7{\pm}25.9mg/dl$ and blood pH increased from $7.122{\pm}0.048$ to $7.326{\pm}0.063$ after 24 hours of peritoneal dialysis. We experienced hyperglycemia which were controlled by insulin(2 episodes), leakage at the exit site(2), mild hyponatremia(1) and Escherichia coli peritonitis(1). Two children of low volume dialysis died despite the treatment. In our experience, low volume and high concentration peritoneal dialysis with frequent exchange may have sufficient ultrafiltration and clearance without significant complications in the certain risked acute renal failure of infants.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1236-1251
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• 1998

Background : TNF-$\alpha$ appears to be a central mediator of the host response to sepsis. While TNF-$\alpha$ is mainly considered a proinflammatory cytokine, it can also act as a direct cytotoxic cytokine. However, there are not so many studies about the relationship bet ween TNF-$\alpha$ level and lung injury severity in ALI, particularly regarding the case of ALI caused by direct lung injury such as diffuse pulmonary infection. Recently, a natural defense mechanism, known as the stress response or the heat shock response, has been reported in cellular or tissue injury reaction. There are a number of reports examining the protective role of pre-induced heat stress proteins on subsequent LPS-induced TNF-$\alpha$ release from monocyte or macrophage and also on subsequent LPS-induced ALI in animals. However it is not well established whether the stress protein synthesis such as HSP can be induced from rat alveolar macrophages by in vitro or in vivo LPS stimulation. Methods : We measured the level of TNF-$\alpha$, the percentage of inflammatory cells in bronchoalveolar lavage fluid, protein synthesis in alveolar macrophages isolated from rats at 1, 2, 3, 4, 6, 12, and 24 hours after intratracheal LPS instillation. We performed histologic examination and also obtained histologic lung injury index score in lungs from other rats at 1, 2, 3, 4, 6, 12, 24 h after intratracheal LPS instillation. Isolated non-stimulated macrophages were incubated for 2 h with different concentration of LPS (0, 1, 10, 100 ng/ml, 1, or 10 ${\mu}g/ml$). Other non-stimulated macrophages were exposed at $43^{\circ}C$ for 15 min, then returned to at $37^{\circ}C$ in 5% CO2-95% for 1 hour, and then incubated for 2 h with LPS (0, 1, 10, 100ng/ml, 1, or 10 ${\mu}g/ml$). Results : TNF-$\alpha$ levels began to increase significantly at 1 h, reached a peak at 3 h (P<0.0001), began to decrease at 6 h, and returned to control level at 12 h after LPS instillation. The percentage of inflammatory cells (neutrophils and alveolar macrophages) began to change significantly at 2 h, reached a peak at 6 h, began to recover but still showed significant change at 12 h, and showed insignificant change at 24 h after LPS instillation compared with the normal control. After LPS instillation, the score of histologic lung injury index reached a maximum value at 6 h and remained steady for 24 hours. 35 kDa protein band was newly synthesized in alveolar macrophage from 1 hour on for 24 hours after LPS instillation. Inducible heat stress protein 72 was not found in any alveolar macrophages obtained from rats after LPS instillation. TNF-$\alpha$ levels in supernatants of LPS-stimulated macro phages were significantly higher than those of non-stimulated macrophages(p<0.05). Following LPS stimulation, TNF-$\alpha$ levels in supernatants were significantly lower after heat treatment than in those without heat treatment (p<0.05). The inducible heat stress protein 72 was not found at any concentrations of LPS stimulation. Whereas the 35 kDa protein band was exclusively found at dose of LPS of 10 ${\mu}g/ml$. Conclusion : TNF-$\alpha$ has a direct or indirect close relationship with lung injury severity in acute lung injury or acute respiratory distress syndrome. In vivo and in vitro LPS stimulation dose not induce heat stress protein 72 in alveolar macrophages. It is likely that 35 kDa protein, synthesized by alveolar macrophage after LPS instillation, does not have a defense role in acute lung injury.