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[Myocardial apoptosis induced by delayed fluid resuscitation in a burned rat model]
1Burns Center, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
Objective:
To explore the possibility and the mechanism of myocardial apoptosis induced by delayed fluid resuscitation in a burned rat model and its relationship with nitric oxide (NO) and oxygen-derived free radicals.
Methods:
In a rat model with 30% III degree burn, the genomic DNA of the myocardial tissue was detected with ApoAlert(TMLM)-PCR Ladder Assay Kit and visualized with agarose gel electrophoresis. Meanwhile, the NO and the content of unsaturated fatty acids were measured.
Results:
In rats receiving delayed fluid resuscitation following burn, the myocardial genomic DNA exhibited DNA ladder-index of apoptosis, and the contents of myocardial NO and unsaturated fatty acid were much lower than those in rats receiving immediate resuscitation (P < 0.05).
Conclusion:
The myocardial tissue undergoes apoptosis in burned rats receiving delayed fluid resuscitation, and the decreased NO and the production of oxygen-derived free radicals are also observed in this process.
Insights
Delayed fluid resuscitation after severe burns triggers myocardial apoptosis in rats. This process is linked to reduced nitric oxide (NO) and increased oxygen-derived free radicals, impacting heart function.
Area of Science:
- Biomedical Science
- Physiology
- Pathology
Context:
- Severe burns cause significant physiological stress.
- Fluid resuscitation is a critical intervention following burn injury.
- Delayed resuscitation may lead to secondary organ damage.
Purpose:
- To investigate myocardial apoptosis in burned rats with delayed fluid resuscitation.
- To elucidate the role of nitric oxide (NO) and oxygen-derived free radicals in this process.
Summary:
- Burned rats with delayed fluid resuscitation showed DNA ladder-index of apoptosis in myocardial tissue.
- Myocardial nitric oxide (NO) and unsaturated fatty acid levels were significantly lower in delayed resuscitation compared to immediate resuscitation.
- These findings suggest a mechanism involving reduced NO and free radical production.
Impact:
- Highlights the detrimental effects of delayed fluid resuscitation on cardiac tissue post-burn.
- Suggests potential therapeutic targets for mitigating burn-induced myocardial injury.
- Provides insights into the pathophysiology of burn shock and organ dysfunction.