Shock pathophysiology

Novelli, G.P. (1992). Oxygen radicals in experimental shock. Effects of spin-trapping nitrones in ameliorating shock pathophysiology. Grit. Care Med. 20, 499-507. 

Lipopolysaccharide A Mediator of Septic Shock -Pathophysiological Properties... 

Z4. Zenichi, M., Masakazu, U., Koichi, A., Masao, E., and Masaki, K Pathophysiologic role of en-dothelin-l in renal function in rats with endotoxin shock. Surgery 115,199-204(1994). 

Urban, N. and Porth, C.M., Heart failure and circulatory shock, in Pathophysiology Concepts of Altered Health States, 5th ed., Porth, C.M., Ed., Lippin-cott-Raven Publishers, Philadelphia, 1998, chap. 20. 

First described in the 1980s as "endothelium-derived relaxing factor," nitric oxide (NO) is a vasodilator believed to play a role in regulation of blood pressure under physiologic and pathophysiological conditions. For example, inhibition of NO synthesis under normal conditions and during septic shock results in a significant elevation of blood pressure. 

It should also be mentioned that superoxide and not nitric oxide production by eNOS may have implications for atherosclerosis and septic shock due to imbalance between NO and superoxide formation, for example due to an increase in TNF-a production [164]. These pathophysiological functions of NO synthases will be considered in detail in Chapter 31. 

Shock results in failure of the circulatory system to deliver sufficient oxygen (02) to body tissues despite normal or reduced 02 consumption. General pathophysiologic mechanisms of different forms of shock are similar except for initiating events. 

Figure 2.2 Proposed mechanism of inducible gene expression mediated by heat shock and certain other pathophysiological conditions. Adapted from Zou et al. (1998). Terminology HSF1 (heat shock factor 1) HSP (heat shock proteins) HSE (heat shock element in DNA) P (phosphorylation).

The cellular heat shock response can be initiated by physical or pathophysiological stresses, as depicted in Figure 2.2. In most organisms, HSPs are activated in response to sublethal heat shock and other stresses, including UV light and different chemicals. Several HSPs are normally and/or differentially expressed... 

Leppa, S. and Sistonen, L. (1997) Heat shock response-pathophysiological implications. Ann. Med., 29,73-78. 

Loppnow, H., Flad, H.-D., Rietschel, E.Th., Brade, H. The active principle of bacterial lipopolysac-charides (endotoxins) for cytokine induction. In Schlag, G., Redl, H.(eds), Pathophysiology of Shock, Sepsis, and Organ. Springer-Verlag, Heidelberg (1993), pp. 405-416. 

Hossmann KA (1997) Reperfusion of the brain after global ischemia hemodynamic disturbances. Shock 8 95-101 Hossmann K-A (1987) Pathophysiology of cerebral infarction. In Vinken PJ, Bruyn GW, Klawans HL (eds) Handbook of clinical neurology. Elsevier, Amsterdam, pp 107-153 Hossmann K-A (1991) Animal models of cerebral ischemia. 1. 

Szabo, C., The pathophysiological role of peroxynitrite in shock, inflammation, and ischemia-reperfusion injury. Shock 6, 79-88 (1996). 

The decision how to treat shock depends on assessment of the pathophysiology ... 

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