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

In: Septic Shock

12 Nov 2014

This activity may be a somewhat different molecular weight than depressant molecules that have been previously described. This difference may be due to the fact that the myocyte system in the present study is capable of assessing in vitro myocardial cell performance using unmodified serum. Previous studies analyzing the properties of cardiodepressant substances have used plasma ultrafiltrates of cat hemorrhagic shock or rat endotoxic shock models that have limited applicability to the myocardial depression seen in human septic shock. The difference might also be attributable to the occurrence in human septic shock of more than one myocardial depressant molecule, with differing molecular weights. Another possibility is that several active, identical low molecular weight molecules can combine to form a higher molecular weight macromolecule that also has depressant activity. www.cheap-asthma-inhalers.com

This could lead investigators to conclude that there are several active MDS molecules of different molecular weights, while in reality only a single active molecule existed, and combinations of several identical subunits were leading to a variety of molecular weights.
The potential diagnostic and therapeutic ramifications of MDS are in their preliminary stages. The data from this study and previous work strongly suggest that MDS depresses EF in vivo. It is not clear whether MDS directly increases EDVI or whether this ventricular dilatation is a compensatory mechanism stretching myocytes to increase preload, thus offsetting the depressed systolic function. Inhibition or neutralization of MDS might restore a normal EF, but this hypothesis awaits experimental verification in animal models. In a canine model which closely simulates the hemodynamic profile of human sepsis, plasmapheresis, which removes almost all noncellular blood elements, has not reversed myocardial depression or lethality.
In the present study, we have confirmed the existence of MDS in the blood of at least 41 percent of patients with septic shock. This substance was detected early in the course of septic shock, and we quantitatively and temporally correlated MDS to concomitant in vivo evidence of myocardial dysfunction, demonstrated by a depression of the EF and increased ventricular dilatation. Further studies are needed to evaluate the structural characteristics of MDS and to define biochemically its precise role in the complex pathophysiology of human septic shock.

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