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Updated: Jan 30, 2026

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
Published on: June 11, 2020
Hypertonic Saline Modulates Heart Function and Myocardial Inflammatory Alterations in Brain-Dead Rats
Daniel Marcelo S Magalhães1, Fernando Luiz Zanoni1, Cristiano Jesus Correia1
1Laboratório Cirúrgico de Pesquisa Cardiovascular (LIM-11), Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Hypertonic saline (HS) improves left ventricular (LV) systolic function and reduces myocardial injury in brain death (BD) rats. This study shows HS can be an effective treatment even when administered after BD onset.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Brain death (BD) in organ donors causes hemodynamic instability and myocardial dysfunction.
- Hypertonic saline (HS) is a volume expander with potential hemodynamic and immunomodulatory benefits.
Purpose of the Study:
- To investigate the efficacy of HS in preventing left ventricular (LV) dysfunction and myocardial injury in a rat model of BD.
- To assess the impact of HS timing on cardiac function and myocardial integrity post-BD.
Main Methods:
- BD was induced in rats using a subdural balloon catheter.
- Animals received either normal saline (Control) or HS (7.5%) at 1 or 60 minutes post-BD.
- Cardiac function was monitored for 6 hours using LV pressure-volume analysis; inflammatory markers and apoptosis were also assessed.
Main Results:
- HS treatment improved LV ejection fraction and systolic function compared to controls.
- HS administration increased antiapoptotic protein expression and decreased inflammatory markers.
- No significant differences in histological or structural protein changes were observed between groups.
Conclusions:
- Hypertonic saline ameliorates LV systolic dysfunction in BD rats.
- HS may reduce myocardial tissue compromise, even when treatment is initiated after BD onset.
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