Sepsis Correlated with Increased Erythrocyte Na+ Content and Na+-K+ Pump Activity
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T. Hwang | Miin‐Fu Chen | H. Chen | Y. Lau | C. Hsieh | Yin-Fen Sun
[1] D. Jacobs,et al. Does endotoxin-activated complement alter myocellular sodium homeostasis during sepsis? , 2002, Journal of Trauma.
[2] D. Jacobs,et al. Complement activation alters myocellular sodium homeostasis during polymicrobial sepsis. , 2002, Critical care medicine.
[3] S. Ashley,et al. Sepsis increases the plasma membrane content of α1 and α2 isoforms of Na+-K+ adenosine triphosphatase in rat skeletal muscle , 2001 .
[4] T. Hwang,et al. Arginine-nitric oxide pathway in plasma membrane of rat hepatocytes during early and late sepsis. , 1999, Critical care medicine.
[5] E. Deitch. ANIMAL MODELS OF SEPSIS AND SHOCK: A REVIEW AND LESSONS LEARNED , 1998, Shock.
[6] T. Hwang,et al. Changes of adenosine triphosphate-dependent calcium uptake in microsomal fractions of rat liver during sepsis. , 1997, Surgery.
[7] C. Delclaux,et al. Acute bacterial pneumonia in rats increases alveolar epithelial fluid clearance by a tumor necrosis factor-alpha-dependent mechanism. , 1997, The Journal of clinical investigation.
[8] J. Fischer,et al. Linkage of aerobic glycolysis to sodium-potassium transport in rat skeletal muscle. Implications for increased muscle lactate production in sepsis. , 1996, The Journal of clinical investigation.
[9] D. Wilmore,et al. Glucocorticoid receptor antagonism by mifepristone alters phosphocreatine breakdown during sepsis. , 1996, Archives of surgery.
[10] J. Lingrel,et al. Sepsis increases skeletal muscle sodium, potassium-adenosinetriphosphatase activity without affecting messenger RNA or protein levels. , 1996, Journal of the American College of Surgeons.
[11] I. Chaudry,et al. Mechanism of hepatocellular dysfunction during hyperdynamic sepsis. , 1996, The American journal of physiology.
[12] R. L. Baldwin,et al. Structural changes of tumor necrosis factor alpha associated with membrane insertion and channel formation. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[13] C. Ellis,et al. Increased inward passive permeability in vitro to sodium in uraemic erythrocytes. , 1996, Clinical science.
[14] A. Klip,et al. Hormonal regulation of the Na(+)-K(+)-ATPase: mechanisms underlying rapid and sustained changes in pump activity. , 1995, The American journal of physiology.
[15] T. Hwang,et al. Erythrocyte Ca2+ pump is defective during sepsis. , 1994, Circulatory shock.
[16] J. Parrillo. Pathogenetic mechanisms of septic shock. , 1993, The New England journal of medicine.
[17] H. Dockrell. The Cytokine Handbook , 1993 .
[18] T. Hwang,et al. Calcium transport by rat liver plasma membranes during sepsis. , 1992, Circulatory shock.
[19] C. Hsieh,et al. Sodium transport in hypertension. , 1992, The Chinese journal of physiology.
[20] G. T. Shires,et al. Oxygen free radicals affect cardiac and skeletal cell membrane potential during hemorrhagic shock in rats. , 1992, The American journal of physiology.
[21] M. -. Chen,et al. Erythrocyte sodium-lithium countertransport in Chinese: its relationship to family history of hypertension. , 1992, Clinical and experimental hypertension. Part A, Theory and practice.
[22] F. Ognibene,et al. Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. , 1990, Annals of internal medicine.
[23] I. Chaudry,et al. Hepatocellular dysfunction occurs early after hemorrhage and persists despite fluid resuscitation. , 1990, The Journal of surgical research.
[24] R. Hotchkiss,et al. Sepsis does not alter red blood cell glucose metabolism or Na+ concentration: a 2H-, 23Na-NMR study. , 1990, The American journal of physiology.
[25] J. Skou. The Na,K-pump. , 1992, Methods in enzymology.
[26] K. Kako,et al. Depression of membrane-bound Na+-K+-ATPase activity induced by free radicals and by ischemia of kidney. , 1988, The American journal of physiology.
[27] M. Sayeed. Ion transport in circulatory and/or septic shock. , 1987, The American journal of physiology.
[28] K. Geering,et al. Regulation of the sodium pump: how and why? , 1987 .
[29] S. Hunt,et al. Three red cell sodium transport systems in hypertensive and normotensive Utah adults. , 1984, Hypertension.
[30] L. Stevens. Gauging the severity of surgical sepsis. , 1983, Archives of Surgery.
[31] I. Chaudry. Cellular mechanisms in shock and ischemia and their correction. , 1983, The American journal of physiology.
[32] D. Kaji,et al. Glucocorticoid-induced alterations in the sodium potassium pump of the human erythrocyte. , 1981, The Journal of clinical investigation.
[33] Y. Kitani,et al. Intracellular electrolytes in erythrocytes during and after shock: relation to impaired consciousness. , 1978, The Journal of trauma.
[34] E. Hirsch,et al. Elevated red cell sodium concentration in patients in shock: sources and significance. , 1976, Surgical forum.
[35] M. McCarron,et al. Septic Shock , 1964, International anesthesiology clinics.
[36] 山田 三郎. Na + , K + 促進性ATPaseについて , 1963 .