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Effects of mercury on the contractile activity of the right ventricular myocardium
F N Cunha1, G P de Assis, C E Silva
1Department of Physiological Sciences, Federal University of Espirito Santo and Health Science Center of Vitória-EMESCAM, Vitoria, ES, Brazil.
Insights
Mercury exposure can increase right ventricular systolic pressure, contrary to expectations. This study found mercury depresses isolated heart muscle but not in whole hearts or in vivo, suggesting protective mechanisms.
Area of Science:
- Cardiovascular Physiology
- Toxicology
- Myocardial Contractility
Background:
- Mercury (HgCl2) is a known cardiac toxin.
- Its effects on right ventricular function are not fully understood.
- In vivo studies show increased right ventricular systolic pressure after mercury administration.
Purpose of the Study:
- To investigate the acute effects of mercury on right ventricular myocardium.
- To determine if mercury depresses cardiac pump performance.
- To explore the mechanisms behind mercury's effects on the heart.
Main Methods:
- Isometric and tetanic contractions of isolated right ventricular strips.
- Measurement of right ventricular isovolumic systolic and diastolic pressures.
- Assessment of coronary perfusion pressure in Langendorff-perfused rat hearts.
Main Results:
- Mercury (0.1-2.5 microM) depressed contractile activity in isolated right ventricular strips.
- In perfused hearts and in vivo, mercury did not reveal a depressant effect.
- Increased coronary perfusion pressure was observed, potentially causing a positive inotropic effect.
Conclusions:
- Acute mercury effects on right ventricular myocardium are concentration-dependent and context-specific.
- Coronary circulation may protect against mercury's direct myocardial depressant effects.
- Further research is needed to elucidate the protective mechanisms of coronary circulation against mercury toxicity.
Abstract:
The increase in right ventricular systolic pressure observed in vivo after the administration of mercury opposes to the idea that the metal depresses the cardiac pump performance. We then investigated the effects of HgCl(2) (0.1 to 2.5 microM) on the contractile activity of the right ventricular myocardium, measuring isometric and tetanic contractions of right ventricular isolated strips, right ventricular isovolumic systolic and diastolic pressures, and the coronary perfusion pressure (0.03 to 3 microM) in constant-flow Langendorff-perfused rat hearts. The results presented here suggest that the acute effects of mercury on the right ventricular myocardium are distinct. When isolated strips of right ventricular wall are used, the contractile depression produced by mercury is manifested. However, when mercury is administered to isolated perfused hearts or in vivo this depressant effect is not revealed. The possible reasons for this behavior are the increased coronary perfusion pressure, which promotes a positive inotropic effect, manifested during the infusion of increasing concentrations of mercury, or the putative stretch of the ventricular fibers, which might cause the increment of diastolic pressure. An interesting finding is that the mechanical activity of the preparations, in which mercury is administered via coronary circulation, is not depressed and, even more, it can increase systolic pressure. However, the nature of this protective effect of coronary circulation cannot be explained by the results presented here.