Arch Surg Chicago
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Review
Signaling mechanisms of altered cellular responses in trauma, burn, and sepsis: role of Ca2+.
Alterations in cellular responses in various organ systems contribute to trauma-, burn-, and sepsis-related multiple organ dysfunction syndrome. Such alterations in muscle contractile, hepatic metabolic, and neutrophil and T-cell inflammatory-immune responses have been shown to result from cell-signaling modulations and/or impairments in the respective cell types. Altered Ca(2+) signaling would seem to play an important role in the myocardial and vascular smooth muscle contractile dysfunction in the injury conditions; Ca(2+)-linked signaling derangement also plays a crucial role in sepsis-induced altered skeletal muscle protein catabolism and resistance to insulin-mediated glucose use. ⋯ The injury conditions would seem to cause an inappropriate up-regulation of Ca(2+)-signal generation in the skeletal myocyte, hepatocyte, and neutrophil, while they lead to a down-regulation of Ca(2+) signaling in T cells. The crucial signaling derangement that causes T-cell proliferation suppression seems to be a decrease in the activation of protein tyrosine kinases, which subsequently down-regulates Ca(2+) signaling. The delineation of cell-signaling derangements in trauma, burn, or sepsis conditions can lead to development of therapeutic interventions against the disturbed cellular responses in the vital organ systems.
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Subcutaneous perfusion and oxygen during acute severe isovolemic hemodilution in healthy volunteers.
Acute severe isovolemic anemia (to a hemoglobin [Hb] concentration of 50 g/L) does not decrease subcutaneous wound tissue oxygen tension (PsqO(2)). ⋯ The level of PsqO(2) was maintained at baseline levels during hemodilution to Hb 50 g/L in healthy volunteers, whether they were initially well-perfused or mildly underperfused peripherally. Given the significant increase in Tsq and flow index, this resulted from a compensatory increase in subcutaneous blood flow sufficient to maintain oxygen delivery. Wound healing depends to a large extent on tissue oxygen delivery, and these data suggest that even severe anemia by itself would not be sufficient to impair wound healing. Thus, transfusion of autologous packed red blood cells solely to improve healing in surgical patients with no other indication for transfusion is not supported by these results.
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Biography Historical Article
Moments in surgical history: William Stewart Halsted.
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Intra-arterial lipiodol labeled with iodine 131 ((131)I-lipiodol) can be safely used as adjuvant therapy following curative liver resection for hepatocellular carcinoma (HCC). ⋯ This pilot study failed to demonstrate any clinically significant adverse effect of adjuvant therapy by intra-arterial (131)I-lipiodol after curative liver resection for HCC. Long-term survival compares favorably with those undergoing only surgery and suggests a benefit in lowering tumor recurrence. A randomized, multicenter, prospective trial comparing patients treated with intra-arterial (131)I-lipiodol with a nontreated control group seems appropriate.
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A shift in the balance of helper T cells type 1 (T(H)1) toward type 2 (T(H)2) has been suggested as a possible mechanism for impaired immune responses after severe trauma. We suggest that major injuries (polytrauma) induce an alteration in the pattern of T(H)1/T(H)2 cells. ⋯ Patients with multiple injuries have no significant alteration in the ratio of circulating T(H)1/T(H)2 cells. Thus, our results suggest pathomechanisms in posttraumatic T-cell suppression apart from alterations in the T(H)1/T(H)2 pattern.