A Circulating Myocardial Depressant Substance is Associated with Cardiac Dysfunction and Peripheral Hypoperfusion: Myocardial depression

In: Septic Shock

9 Nov 2014

A Circulating Myocardial Depressant Substance is Associated with Cardiac Dysfunction and Peripheral Hypoperfusion: Myocardial depressionA previous study excluded the possibility that myocardial depression resulted from electrolyte abnormalities or from circulating pharmacologic agents. The methods used to exclude electrolyte abnormalities or pharmacologic agents as causes of myocardial cell depression can be summarized as follows: (1) control groups receiving identical medications and having similar electrolyte derangements failed to show any myocardial cell depression; (2) measurements of the electrolyte solution bathing the myocardial cells reveal the same concentrations of electrolytes in the depressed and nondepressed cultures; (3) the assay is performed with 10 percent or 20 percent test serum added to a buffered electrolyte solution; this latter solution dilutes and corrects all electrolyte abnormalities; (4) as judged by Amicon filtration and gel filtration, MDS activity occurred at a molecular weight of greater than 2,000 daltons and probably greater than 10,000 daltons. Thus, the molecular weight of MDS was in a range inconsistent with any electrolyte molecule or pharmacologic agent. so

We have evaluated extensively a number of other cardiovascular factors that might have contributed to the decrease in EF that occurred in the patients with MDS. The patients with MDS had significantly higher preload (both initially and at two to four days, measuring preload by both pressure and volume methods) than patients without MDS. This difference in end-diastolic pressure and volume suggests that MDS also may be associated with a diastolic compliance abnormality of the ventricle, a finding that has been described previously in a canine sepsis model and in humans with septic shock. There were no differences noted between MDS positive and negative groups with respect to afterload, heart rate, or the quantity of exogenous catecholamines infused therapeutically during the shock syndrome. Thus, these cardiovascular parameters cannot account for the myocardial dysfunction, and the most likely explanation for this reversible in vivo myocardial depression is the occurrence of a molecule(s) that can directly affect cardiac performance. Using a spontaneously beating rat myocardial cell model in vitro, the present study demonstrated myocardial depressant activity that correlates both temporally and quantitatively with this myocardial depression.


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