Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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We assessed the effect of a cytokine inhibitor, compound SKF 86002 (a bicyclic imidazole), on changes in renal hemodynamics (renal blood flow and glomerular filtration rate) that occur acutely following immune injury of glomerular mesangial cells. ⋯ The observations indicate that in mesangial cell immune injury, cytokines mediate renal hemodynamic impairment.
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Comparative Study
Effects of Carbicarb and sodium bicarbonate on hypoxic lactic acidosis in newborn pigs.
Use of sodium bicarbonate (NaHCO3) may result in intracellular acidosis due to the generation of CO2. Carbicarb, has been reported to be superior to sodium bicarbonate (NaHCO3) because of lesser generation of CO2. The present study was designed to investigate whether Carbicarb or NaHCO3 is superior to normal saline in the treatment of hypoxic lactic acidosis. ⋯ The data demonstrate that 1) both Carbicarb and NaHCO3 significantly increase arterial pCO2; and 2) use of either alkalinizing agent in moderate acidosis does not alter the course of acidosis.
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Cytokine networks between immune and nonimmune cells of the alveolar-capillary membrane are necessary for cellular communication during pulmonary inflammation. The subsequent events of these cellular/humoral interactions are pivotal to the initiation and propagation of the inflammatory response leading to pulmonary injury. The studies cited in this paper underscore the interrelationship of early response cytokines, adhesion molecules, and the chemokine IL-8 that orchestrate the recruitment of neutrophils into the lung. ⋯ The participation of IL-8 and potentially other C-X-C chemokines in the inflammatory response appears to be critical for the orchestration of the directed migration of inflammatory leukocytes into the lung. After arriving in the lung, these activated leukocytes can respond to noxious stimuli or induce pulmonary injury through the release of reactive oxygen metabolites, proteolytic enzymes, and additional cytokines. Our current knowledge and future investigations regarding the mechanisms involved in neutrophil elicitation may allow us to employ clinical interventional strategies that will attenuate neutrophil-dependent acute lung injury, such as ARDS.