The Journal of surgical research
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Pulmonary edema is a complication of critical care fluid management that may be restricted by the use of oncotically effective resuscitation fluids. Potentially beneficial oncotic properties of starch-based plasma volume expanders such as hetastarch (Het), pentafraction (Pen), and Dextran-70 (Dex) may be compromised by their broad range of molecular masses, some of which are small enough to filter from the circulation. Leakage of these molecules into the pulmonary interstitium may limit their oncotic effectiveness and enhance fluid filtration. We measured the filtration of these three resuscitation solutions into lung lymph to evaluate their oncotic contribution to pulmonary edema formation. ⋯ Pen and Het demonstrated greater oncotic effectiveness because of restricted plasma-to-lymph macromolecular filtration and limited transvascular fluid flux. By comparison, Dex filtered rapidly and increased transvascular fluid filtration. Pen appears to possess filtration properties that optimize critical care fluid management compared to currently available colloid solutions such as Het and Dex.
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beta-2-Adrenergic agents can increase mesenteric blood flow under normal conditions. However, the effects of dobutamine on regional blood flow in sepsis are less well defined since diverging results had been obtained in some studies due to the differences in animal models. In this fluid-resuscitated hyperdynamic endotoxic dog model, we studied the effects of dobutamine on mesenteric, renal, and femoral perfusion. ⋯ Femoral VO2 remained stable. No statistical differences were found between 5 and 10 microgram/kg x min dobutamine. In this hyperdynamic endotoxic shock model, administration of a limited dose of dobutamine could be useful to increase mesenteric blood flow and urine output.
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Antibody against tumor necrosis factor-alpha (TNF-alpha) has improved survival in certain models of sepsis, but it remains unproven in clinical studies. In most of the successful animal studies, efficacy has been shown in previously healthy animals subjected to a septic challenge. Patients at risk for sepsis, however, may be ill for some time before the sepsis supervenes. ⋯ High doses of antibody (3.2 x 10(5) n.u.kg-1) were not beneficial and may have been detrimental. These results show that neutralizing antibody against TNF-alpha may reduce the susceptibility to infection seen after thermal injury, but the timing of administration of the antibody and the dose of antibody used are critical to the outcome. This should be considered when neutralizing antibody against TNF is used in the clinical setting.
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While it is well known that prolonged preservation of the intestinal graft causes severe mucosal damage after transplantation, little is known about the effect on neuromuscular function. The entire small intestine of adult hound dogs was flushed and preserved with cold lactated Ringer's solution and autotransplanted either immediately (n = 6) or after 24 hr (n = 6). Animals undergoing sham operation (n = 4) were used as a control. ⋯ The results of our study indicate that intestinal dysmotility is augmented in prolonged-preservation grafts compared to those with brief preservation. The dysmotility was transient and normalized 3 to 4 weeks after surgery. Preservation and reperfusion injury to the neuromuscular system of intestinal grafts are reversible and are attenuated by simple hypothermia.
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Protein kinase C (PKC) is an ubiquitous regulatory enzyme with dense myocardial distribution and activity; however, its physiologic relevance to myocardial function remains poorly understood. Although endogenous Ca2+ is a potent stimulus of PKC isoforms alpha and beta (cPKCs) it remains unknown whether exogenous Ca2+ activates these PKC isoforms, and if so, whether PKC plays any role in Ca2+-induced myocardial inotropy. To study this, ventricular sections from isolated rat hearts, with and without Ca2+-induced inotropy (CaCl2, 0.5 mM coronary concentration x 2 min), were probed for cPKC isoform translocation using immunofluorescence in order to determine if exogenous Ca2+ indeed activates cPKCs. ⋯ This dose of exogenous Ca2+ resulted in myocardial inotropy as determined by DP, dP/dt, and CF. Furthermore, myocardial inotropy was attenuated with concurrent inhibition of PKC activity. These findings link the physiologic effects of exogenous Ca2+ to PKC, providing a better understanding of the physiologic mechanism of Ca2+-induced inotropy.