Early released lipid‐soluble cardiodepressant factor and elevated oestrogenic substances in human septic shock

Benassayag, C.; Christeff, Névéna; Auclair, Marie-Claude; Vernimmen, Catherine; Carli-Vielle, Claire; Nunez, Emmanuel A.; Carli, A

doi:10.1111/j.1365-2362.1984.tb01183.x

Cited by 28 publications

(5 citation statements)

References 11 publications

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“…We consider the pronounced peak in serum estrogens on postoperative days 1-2 a most fascinating finding. Elevated estrogen levels have been shown in different stressful conditions such as physical exercise (16 and references cited therein), myocardial infarction (17), surgical trauma (4) and septic shock (18). In a previous study on surgical trauma (4), we observed an increase in El levels of about 100 pmol.1-' after mastectomy and 200 pmol .1-' after cholecystectomy, compared with about 400 pmol.1-' in the present study.…”

Section: Surgical Trauma (1 3)supporting

confidence: 50%

“…In a previous study on surgical trauma (4), we observed an increase in El levels of about 100 pmol.1-' after mastectomy and 200 pmol .1-' after cholecystectomy, compared with about 400 pmol.1-' in the present study. Very high levels of El (1000-4000 pmol-I-') were reported in men in septic shock, especially in the fatal cases (18).…”

Section: Surgical Trauma (1 3)mentioning

confidence: 95%

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Serum steroids and prolactin during and after major surgical trauma

Lindh

Carlström

Eklund

et al. 1992

Acta Anaesthesiol Scand

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Serum levels of cortisol, dehydroepiandrosterone (DHA) and its sulfate (DHAS), 4-androstene-3,17-dione (A-4), 17-alfa-hydroxy-progesterone (17 OHP), testosterone (T, only in males), unconjugated (E1) and total estrone (tE1 greater than 85% estrone sulfate) were studied in six male and two female patients before, during and up to 30 days after aortic graft surgery. All steroids except 17 OHP decreased following induction of anesthesia but, except for testosterone, rose again during surgery to preoperative levels or slightly above. Extremely high peak values for E1 and tE1 and a less pronounced peak for cortisol were noted on postoperative day 2; after that, the levels of these steroids returned to normal. The levels of 17-OHP, DHA and DHAS decreased after surgery and were below preoperative values from postoperative day 4 to day 16 or (DHAS) day 30. In males, 17 OHP showed a pronounced peak 30 min after initiation of surgery, but decreased after that to below preoperative values. Testosterone levels decreased further during surgery and remained very low until postoperative day 16. Major surgical trauma has a rapid, profound and long-lasting effect on gonadal activity, as judged from decreased testosterone levels, while the effect on adrenal steroids is less pronounced. Adrenal delta 4 and delta 5-steroids showed different patterns in the postoperative period, indicating differences in their regulation. The highly elevated estrogen levels on postoperative day 2 probably reflect either transiently elevated peripheral aromatization or decreased estrogen metabolism rather than increased levels of substrate steroids (A-4). The biological significance of this remains to be elucidated.

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Section: Surgical Trauma (1 3)supporting

confidence: 50%

Section: Surgical Trauma (1 3)mentioning

confidence: 95%

Serum steroids and prolactin during and after major surgical trauma

Lindh

Carlström

Eklund

et al. 1992

Acta Anaesthesiol Scand

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“…Early studies of a myocardial depressant factor associated with endotoxic and septic shock (26,27) focused on a small (<1 kD) peptide of pancreatic origin. Later studies by other groups imphcated at least two distinct factors of unknown chemical composition with differing molecular masses (<1 kD and 1-10 kD; 28) or a heat-stable, lipid-soluble estrogenic compound of <1 kD (29,30). None of these substances was definitively identified or isolated.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor alpha and interleukin 1beta are responsible for in vitro myocardial cell depression induced by human septic shock serum.

Kumar

Thota

Dee

et al. 1996

The Journal of Experimental Medicine

678

346

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SummaryPrevious studies have demonstrated the presence of myocardial depression in clinical and experimental septic shock. This depression is associated with the presence of a circulating myocardial depressant substance with physical characteristics consistent with cytokines. The present study utilized an in vitro myocardial cell assay to examine the role of various human recombinant cytokines, including tumor necrosis factor (TNF)ot and interleukin (IL)113, in depression of cardiac myocyte contractile function induced by serum from humans with septic shock. The extent and velocity of electrically paced rat cardiac myocytes in tissue culture was quantified by a closed loop video tracking system. Individually, TNF-0c and IL-113 each caused significant concentration-dependent depression of maximum extent and peak velocity of myocyte shortening in vitro. In combination, TNF-cx and IL-1[3 induced depression of myocardial cell contractility at substantially lower concentrations consistent with a synergistic effect. Using immunoabsorption, removal of both TNF-cx and IL-113 (but not either alone) from the serum of five patients with acute septic shock and marked reversible myocardial depression resulted in elimination of serum myocardial depressant activity. IL-2, -4, -6, -8, -10, and interferon ~/failed to cause significant cardiac myocyte depression over a wide range of concentrations. These data demonstrate that TNF-0t and IL-113 cause depression of myocardial cell contraction in vitro and suggest that these two cytokines act synergistically to cause sepsis-associated myocardial depression in humans. Despite therapy with appropriate antibiotics and intensive supportive care, septic shock remains a serious disorder with significant morbidity and mortality. The typical human cardiovascular response to septic shock is characterized by hypotension, decreased systemic vascular resistance, and elevated cardiac index. In addition, myocardial depression manifested by reversible biventricular dilation and reduction of ejection fraction has been shown to be common in human septic shock (1-3).A previously described in vitro model of myocardial cell performance utilizes spontaneously beating rat cardiac myocytes in culture (4-6). This system allows assessment of myocardial cell performance (i.e., contraction) independent of changes in preload, afterload, and heart rate. In this system, serum from patients with acute septic shock produced in vitro depression of cardiac myocyte contractile function (decreased maximum extent and peak velocity of shortening) that correlated quantitatively and temporally with the

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“…Many investigators have attempted to characterise myocardial depressant factors in plasma or serum of patients with septic, haemorrhagic, or post-burn shock. [2][3][4][5][6] Attempts to identify the nature of these factors have produced differing data, including that the agent was of low molecular weight 2,4 or of a high molecular weight. 3 Water-soluble 2 and lipid soluble 5 factors that act acutely 2,3 or after prolonged incubation 6 have been reported.…”

Section: Introductionmentioning

confidence: 99%