Endocrine – ARDS interactions in patients with heavy peritonitis and MOF

M. Tsareva, S. Todorova, A. Christova (Sofia, Bulgaria)

Source: Annual Congress 2001 - Monitoring acute lung disease
Session: Monitoring acute lung disease
Session type: Thematic Poster Session
Number: 1646
Disease area: Respiratory critical care

Congress or journal article abstract

Abstract

Adaptive endocrine response of organism to septic shock consisting in activation of the production of adrenal hormons, renin – angiotensin – aldosterone system (RAAS) and other hormonal systems has an influence over the microvascular changes in these states and for development of multiple organ failure (MOF).
In 25 patients with peritonitis of different origins (18 nonsurvivors and 7 survivors) were followed the changes in cortisol level and RAAS by radioimmunological methods and many variables for evaluation of respiratory, renal, hepatic function, coagulation etc. as a signs of MOF. It was observed significant increase of the level of cortisol (1099±]348 nmol/l), aldosterone (0.895±]0.687 nmol/l), renin (3.75±]4.95 pmol/i). By factorial statistical analysis we found significantly high correlations between hormonal changes and respiratory function (for example r = - 0.539, p<0.02 between cortisol and PaO2; r = 0.817, p<0.001 between cortisol and D(a-v)O2; also renin – CaO2 r = -0,824, p<0.001 etc. Such significant correlatins were found and for RAAS with respiratory, renal function, byproducts of arachidonic acid thromboxan B2 and PGF1 alpha etc. These correlations between the degree of endocrine changes and ARDS and MOF in patients with septic shock produced by peritonitis suggest that their effects upon peripheral vascular resistance and constriction of splenic, renal and other organ vasculatures are not always with physiologic expediency and there are perhaps the possibilites of therapeutic influence.


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M. Tsareva, S. Todorova, A. Christova (Sofia, Bulgaria). Endocrine – ARDS interactions in patients with heavy peritonitis and MOF. Eur Respir J 2001; 16: Suppl. 31, 1646

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