Oxygen Transport to Tissue XIX pp 333-341 | Cite as
Skeletal Muscle Function, Oxygenation and Biochemistry in an Endotoxemic Model of Sirs
Abstract
Traditionally, “sepsis” refers to bacteremia leading to arteriolar vasodilatation and signs of generalized infection. Sepsis may progress to septic shock, often characterized by hypotension, classically explained as pooling of blood in the peripheral microcirculation.1 A similar clinical picture in patients with no laboratory evidence of infection has been called the “septic syndrome.”9 Many of the characteristics of sepsis and the septic syndrome are mediated by host inflammatory products. The more comprehensive title systemic inflammatory response syndrome (SIRS) encompasses both states as well as states with similar clinical characteristics such as burn injuries.16 The clinical signs of SIRS are fever, tachycardia, low systemic vascular resistance, tachypnea, and leukocytosis or leuk- openia. Organ dysfunction may ensue despite adequate cardiac output and arterial oxygen tension. When more than 2 organs are dysfunctional, the patient is said to have multiple organ dysfunction syndrome (MODS). In patients the development of MODS leads to high mortality and great expense. Understanding the pathophysiology of SIRS may lead to improved therapy, lower mortality and reduced cost.16
Keywords
Mean Arterial Blood Pressure Multiple Organ Dysfunction Syndrome Muscle Blood Flow Gracilis Muscle Skeletal Muscle FunctionPreview
Unable to display preview. Download preview PDF.
References
- 1.R.S. Cotran, V. Kumar, and S.L. Robbins, Robbins Pathologic Basis of Disease, W.B.Saunders Company, Philadelphia, (1989).Google Scholar
- 2.J. Olgin, R.J. Connett, and B. Chance, Mitochondrial redox changes during rest-work transition in dog gracilis muscle. Advances In Experimental Medicine & Biology 200:545–54 (1986).CrossRefGoogle Scholar
- 3.R.J. Connett, T.E. Gayeski, and C.R. Honig, Lactate accumulation in fully aerobic, working, dog gracilis muscle, American Journal of Physiology 246:H120–H128(1984).PubMedGoogle Scholar
- 4.T.E. Gayeski and C.R. Honig, 02 gradients from sarcolemma to cell interior in red muscle at maximal VO2, American Journal of Physiology 251:H789–H799 (1986).PubMedGoogle Scholar
- 5.T.E. Gayeski, R.J. Connett, and C.R. Honig, Minimum intracellular PO2 for maximum cytochrome turnover in red muscle in situ, American Journal of Physiology 252:H906–l5 (1987).PubMedGoogle Scholar
- 6.W. Karzai, J.M. Reilly, W.D. Hoffman, R.E. Cunnion, R.L. Danner, S.M. Banks, J.E. Parrillo, and C. Natanson, Hemodynamic effects of dopamine, norepinephrine, and fluids in a dog model of sepsis, American Journal of Physiology 268:H692–H702 (1995).PubMedGoogle Scholar
- 7.W.A. Voter and T.E.J. Gayeski, Determination of Myoglobin Saturation of Frozen Specimens Using a Reflecting Cryospectrophotometer, American Journal of Physiology 269: H1328–H1341 (1995).PubMedGoogle Scholar
- 8.B.R. Berg and I.H. Sarelius, Functional capillary organization in striated muscle, American Journal of Physiology 268:H1215–H1222 (1995).PubMedGoogle Scholar
- 9.R.C. Bone, The pathogenesis of sepsis. [Review], Annals of Internal Medicine 115:457–469 (1991).PubMedGoogle Scholar
- 10.R.M. Palmer, The discovery of nitric oxide in the vessel wall. A unifying concept in the pathogenesis of sepsis. [Review], Archives of Surgery 128:396–401 (1993).PubMedCrossRefGoogle Scholar
- 11.P. Eggleton, S.R. Elsden, and N. Gough, The estimation of creatine and diacetyl. Biochem. J. 37:526–529 (1943).PubMedGoogle Scholar
- 12.A. Clark, Jr. and P.A.A. Clark, Capture of spatially homogeneous chemical reactions in tissue by freezing, Biophys J 42:25–30(1983).PubMedCrossRefGoogle Scholar
- 13.N.K. Boughton-Smith, S.M. Evans, F. Laszlo, B.J. Whittle, and S. Moncada, The induction of nitric oxide synthase and intestinal vascular permeability by endotoxin in the rat, British Journal of Pharmacology 110:1189–1195(1993).PubMedCrossRefGoogle Scholar
- 14.C. Thiemermann, C.C. Wu, C. Szabo, M. Perretti, and J.R. Vane, Role of tumour necrosis factor in the induction of nitric oxide synthase in a rat model of endotoxin shock, British Journal of Pharmacology 110:177–182(1993).PubMedCrossRefGoogle Scholar
- 15.J.A. Lorente, L. Landin, E. Renes, R. De Pablo, P. Jorge, E. Rodena, and D. Liste, Role of nitric oxide in the hemodynamic changes of sepsis, Critical Care Medicine 21:159–161 (1993).Google Scholar
- 16.A.L. Beal and F.B. Cerra, Multiple organ failure syndrome in the 1990s. Systemic inflammatory response and organ dysfunction. [Review], JAMA 271:226–233 (1994).PubMedCrossRefGoogle Scholar
- 17.M.S. Rangel-Frausto, D. Pittet, M. Costigan, T. Hwang, C.S. Davis, and R.P. Wenzel, The natural history of the systemic inflammatory response syndrome (SIRS). A prospective study [see comments], JAMA 273:117–123(1995).PubMedCrossRefGoogle Scholar
- 18.R.W. Samsel, D.R Nelson, W.M. Sanders, L.D. Wood, and P.T. Schumacker, Effect of endotoxin on systemic and skeletal muscle 02 extraction, Journal of Applied Physiology 65:1377–1382 (1988).PubMedGoogle Scholar
- 19.B. Vallet, N. Lund, S.E. Curtis, D. Kelly, and S.M. Cain, Gut and muscle tissue PO2 in endotoxemic dogs during shock and resuscitation, Journal of Applied Physiology 76:793–800 (1994).PubMedGoogle Scholar
- 20.C. Lam, K. Tyml, C. Martin, and W. Sibbald, Microvascular perfusion is impaired in a rat model of nor-motensive sepsis, Journal of Clinical Investigation 94:2077–2083 (1994).PubMedCrossRefGoogle Scholar
- 21.K.A. Wichterman, A.E. Baue, and I.H. Chaudry, Sepsis and septic shockߞxa review of laboratory models and a proposal. [Review], Journal of Surgical Research 29:189–201 (1980).PubMedCrossRefGoogle Scholar
- 22.M.P. Fink and S.O. Heard, Laboratory models of sepsis and septic shock. [Review], Journal of Surgical Research 49:186–196 (1990).PubMedCrossRefGoogle Scholar
- 23.A. Marston, The bowel in shock; the role of mesenteric arterial disease as a cause of death in the elderly, Lancet 2:365–369 (1962).PubMedCrossRefGoogle Scholar
- 24.U. Heinrich, J. Hoffmann, and D.W. Lubbers, Quantitative evaluation of optical reflection spectra of blood-free perfused guinea pig brain using a nonlinear multicomponent analysis, Pflugers Archiv-European Journal of Physiology 409:152–7 (1987).PubMedCrossRefGoogle Scholar
- 25.L. Mela, Direct and indirect effects of endotoxin on mitochondrial function, Progress in Clinical & Biological Research 62:15–21 (1981).Google Scholar