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Direct action of endotoxin on cardiac muscle
R G Starr1, A S Lader, G C Phillips
1Department of Physiology, University of South Carolina, School of Medicine, Columbia 29208, USA.
Insights
Endotoxin directly depresses cardiac muscle function, contrary to previous beliefs. This study demonstrates endotoxin
Area of Science:
- Cardiovascular Physiology
- Toxicology
Background:
- Cardiovascular effects of endotoxin are primarily attributed to circulating substances.
- Endotoxin itself was not thought to directly impact cardiac muscle contractility.
Purpose of the Study:
- To investigate the direct effects of endotoxin on cardiac muscle contractility.
- To compare endotoxin's direct cardiac effects with its effects after systemic circulation.
Main Methods:
- Feline papillary muscle was used to assess contractile tension.
- Extracellular calcium concentrations were varied (0.5–8.0 mM) to evaluate muscle response.
- Endotoxin was administered directly to muscle baths and to intact animals.
Main Results:
- Endotoxin-exposed muscles showed reduced contractile tension increases with rising calcium levels.
- This direct depressant effect was observed without prior systemic circulation of endotoxin.
- NaOH-inactivated endotoxin did not produce similar depressant effects.
Conclusions:
- Endotoxin has a direct negative inotropic effect on cardiac muscle.
- This effect occurs independently of other circulating myocardial depressant substances.
- Findings challenge the established understanding of endotoxin's cardiovascular impact.
Abstract:
While the cardiovascular effects of endotoxin include myocardial depression, presumably due to circulating myocardial depressant substances, endotoxin itself is supposed to have no direct effect on the heart. In these experiments, we compared the direct effects of endotoxin on the contractile response of feline papillary muscle to calcium with that seen after administration to the intact animal. The contractile state of the muscle was assessed from developed tension as extracellular calcium concentrations were varied from .5 to 8.0 mM. When endotoxin was administered to the intact animal as well as given to the muscle directly in the bathing solution, endotoxin- exposed muscles showed smaller increases in contractile tension with increasing calcium concentrations than control muscles after 70-85 min. NaOH-inactivated endotoxin produced results similar to the control experiments. Previous experimenters have reported myocardial depression only after endotoxin had circulated in the intact animal for 1-2h; these experiments show a direct depressant effect of endotoxin on cardiac muscle without the release of a substance elsewhere in the body.