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MECHANISMS OF CIRCULATORY FAILURE IN SHOCK

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One of the major contributory factors to mortality in septic shock is a fundamental circulatory abnormality with an altered relationship between cardiac output and systemic vascular resistance. Nonsurvivors tend to have a lower peripheral vascular resistance (unrelenting hypotension). This vascular failure results, in part, from reduced responsiveness to noradrenaline (and hence to sympathetic nerve stimulation) and to other endogenous and exogenous vasoconstrictor agents.

The most significant finding is the demonstration, for the first time, that endotoxin (a major constituent of the cell envelope of Gram negative bacteria which is released during sepsis) stimulates the l-arginine nitric oxide pathway. This results in the generation of a nitric oxide like substance which in turn activates guanylate cyclase and results in relaxation of vascular smooth muscle cells. This is perhaps the most significant response to endotoxin at the vascular level and it is this effect that leads to impairment of vasoconstrictor responses.
The mortality of patients who develop septic shock remains alarmingly
The mortality of patients who develop septic shock remains alarmingly high despite modern management and treatment. One key problem is an altered myocardial and vascular responsiveness to sympathetic nerve stimulation. The mechanisms involved in this dysfunction are poorly understood and the purpose of this application is to examine, especially in isolated cardiac and vascular smooth muscle preparations possible changes induced by Gram-negative infection and lipopolysaccharide in adrenoceptor binding excitation-contraction coupling, the second-messenger systems transmembrane action potentials and calcium flux. An understanding of these events will have an important bearing on therapy for patients with the 'sepsis syndrome'.

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CSC - Cost-sharing contracts

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University of Strathclyde
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Letzte Aktualisierung: 2 Oktober 1990

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Permalink: https://cordis.europa.eu/project/id/ST2*0457/de

European Union, 2024