Pathophysiology of Renal Failure in Shock: Role of Lipid Mediators
Shock encountered in a variety of etiological conditions represents a generalized disease of microcirculation and involves most capillary networks. As a matter of fact, it could be considered as a disease of the endothelial layer, and perhaps of the sub-endothelial tissues of blood vessels (1). Endothelial cells are capable of synthesizing a number of vasoactive compounds which may dilate or constrict the media, as well as triggering white blood cells and platelets from the circulation, also capable of releasing vasoactive substances (2). Under most etiological conditions, shock is preceded by loss of vascular tone in most resistance vessels, by increased capillary permeability to circulatory macromolecules such as proteins, and by excessive loss of plasma volume into the interstitial space. Consequently, blood pressure collapses and perfusion of vital organs is compromised, leading to further deterioration of body fluid compartments homeostasis (1). The excess fluid and plasma proteins within the intersitial compartment where oxygen and substrates supply as well as removal of toxic end-products of cellular metabolism are dependent upon the physico-hemical characteristics responsible for their diffusion in opposite directions in this compartment of extracellular volume, probably represents the first deleterious step leading to impairment of function in vital organs during shock, and the first pathophysiological event responsible for the irreversible nature of certain shock syndromes (3, 4).
KeywordsGlomerular Filtration Rate Renal Plasma Flow Urinary Sodium Excretion Renal Hemodynamic Renal Perfusion Pressure
Unable to display preview. Download preview PDF.
- 1.Parker, M.M., Parillo, J.E. Septic Shock. Hemodynamics and pathogenesis. JAMA 250:3324, (1983).Google Scholar
- 5.Feurstein, G., Boyd, L.M., Ezra, D., Goldstein, R.E. Effect of platelet activating factor on coronary circulation of domestic pig. Am. J. Phvsiol. 246:H466, (1984).Google Scholar
- 6.Loegering, D.J. Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock. Am. J. Physiol. 232:H282, (1977).Google Scholar
- 13.Plante, G.E., Hebert, R.L., Braquet, P.,Sirois, P. Effects of PAF-Acether on renal function and its inhibitions with a new antagonist (BN-52021). New horizons in platelet activating factor research. C.M. Winslow, M.L. Lee, ed. (1986).Google Scholar
- Jobin, J., Nawar, T., Caron, C., Plante, G.E. Effect of acetazolamide on renal bicarbonate excretion in volume expanded dogs. Am. J. Physiol. 232:F484, (1977).Google Scholar
- 22.Plante, G.E., Erian, R., Petitclerc, C. Renal excretion of levamisole. J. Pharmacol. Exp. Therap. 216:617, (1981).Google Scholar
- 23.Hebert, R.L., Sirois, P., Braquet, P., Plante, G.E. Hemodynamic effects of PAF-Acether and the dog kidney. Prostaglandins, Leukotrienes and Med. in press.Google Scholar
- Plante, G.E., Hebert, R.L., Franco, N., St-Pierre, S. Vaso¬active intestinal peptide affects the renal transport of ions. Regulatory Peptides 54:136, (1985).Google Scholar
- 26.BRAQUET, P. BN-52021 and related compounds: a new series of highly specific PAF-Acether receptor antagonists. Proc. Int. Congr. Immunopharmacol., Florence, May 1985.Google Scholar