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Myocardial function during hypoxia: protective effect of dimethyl sulfoxide (DMSO)
Research Communications in Chemical Pathology and Pharmacology
|January 1, 1975
Summary
Dimethyl sulfoxide (DMSO) protected rabbit heart atria from contractile decline during hypoxia. However, DMSO slowed recovery after hypoxia, suggesting altered metabolic pathways during oxygen deprivation.
Area of Science:
- Cardiovascular Physiology
- Cellular Metabolism
- Pharmacology
Background:
- Hypoxia significantly impairs cardiac contractility.
- Understanding protective agents against hypoxic damage is crucial for cardiovascular health.
- Dimethyl sulfoxide (DMSO) is a potential cryoprotectant and metabolic modulator.
Purpose of the Study:
- To investigate the protective effects of dimethyl sulfoxide (DMSO) and sucrose on cardiac contractility during hypoxia in rabbit left atria.
- To elucidate the mechanism of DMSO's action during hypoxic conditions.
Main Methods:
- Electrically driven rabbit left atria were subjected to 20-minute hypoxic periods.
- Tissues were treated with either DMSO or sucrose, or served as controls.
- Contractile strength was measured during hypoxia and reoxygenation.
- Kinetic analysis was performed on tension decline during hypoxia.
Main Results:
- DMSO significantly attenuated the decline in contractile strength during hypoxia compared to controls.
- Sucrose offered no protection against hypoxia-induced contractile dysfunction.
- DMSO-treated tissues exhibited slower recovery of contractile strength upon reoxygenation.
- Kinetic analysis revealed DMSO decreased the rate of tension loss and shifted decline to a slower component during hypoxia.
Conclusions:
- DMSO provides protection against cardiac contractile dysfunction during hypoxia, potentially by affecting energy metabolism or utilization.
- The protective mechanism of DMSO during hypoxia is distinct from its effects during the recovery phase.
- Sucrose does not confer protection under these experimental conditions.