Biological activity produced by ruthenium chloride on perfusion pressure, left ventricular pressure and heart failure using an isolated rat heart model
Background: Several drugs have been used to treat heart failure, including digoxin, spironolactone, captopril, and valsartan; however, some of these drugs can produce different secondary effects. Aim and Objectives: The aim of this investigation was to evaluate the biological activity of ruthenium...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Krishna Vishwa Vidyapeeth (Deemed to be University), Karad
2024-07-01
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| Series: | Journal of Krishna Institute of Medical Sciences University |
| Subjects: | |
| Online Access: | https://www.jkimsu.com/jkimsu-vol13no3/JKIMSU,%20Vol.%2013,%20No.%203,%20July-September%202024%20Page%2037-45.pdf |
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| Summary: | Background: Several drugs have been used to treat heart failure, including digoxin, spironolactone, captopril, and valsartan; however, some of these drugs can produce different secondary effects. Aim and Objectives: The aim of this
investigation was to evaluate the biological activity of ruthenium chloride on perfusion pressure, left ventricular pressure and heart failure. Material and Methods: Effects produced by ruthenium chloride (0.001 to 100 nM) on
perfusion pressure was evaluated using an isolated rat heart model. Besides, the biological activity of ruthenium chloride (1 to 100 nM) on Left Ventricular Pressure (LVP) was determined in the absence or presence of nifedipine,
indomethacin, prazosin, and WB-4101 at a dose of 1 nM. Finally, biological activity of ruthenium chloride (1 to 100 nM) against heart failure was evaluated using an ischemia/reperfusion injury model. Results: The results showed that ruthenium chloride increased the perfusion pressure from 1 to 100 nM; ruthenium chloride increased LVP in a dose-dependent manner, whose effect was inhibited by prazosin and WB-4101; and the ruthenium derivative significantly decreased the infarct area (p = 0.05) compared with the control conditions. Conclusion: These data suggest that ruthenium chloride may act as α -adrenoreceptor activator and could be a good agent to treat heart failure. |
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| ISSN: | 2231-4261 |