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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.
Background:
Brain death (BD) in potential organ donors is responsible for hemodynamic instability and organ hypoperfusion, leading to myocardial dysfunction. Hypertonic saline (HS) is a volume expander with positive effects on hemodynamics and immunomodulation and was tested in this study to prevent left ventricular (LV) dysfunction and myocardial injury.
Methods:
BD was induced in anesthetized Wistar rats by inflating a subdural balloon catheter, except in sham-operated animals (n = 6). After BD induction, Control animals received only normal saline solution (NaCl 0.9%, 4 mL/kg; n = 6), and treated animals were divided to receive HS (NaCl, 7.5% 4 mL/kg) at 1 min (HS1, n = 6) or 60 min (HS60, n = 6) thereafter. We continuously assessed cardiac function for 6 h with LV pressure-volume analysis. Inflammatory response, markers of myocardial injury, and cellular apoptosis-related proteins were investigated.
Results:
BD was associated with decreased LV systolic and diastolic function. In comparison with the Control group, HS treatments improved LV ejection fraction (HS1, 51% [40-66]; HS60, 71% [28-82]; Control, 46% [23-55]; P < 0.05) and other parameters of LV systolic function 6 h after BD induction. However, no ventricular relaxation advantages were observed during the same period. HS treatments increased antiapoptotic protein expression and decreased vascular adhesion molecule and tumor necrosis factor alpha expression. No significant differences in histologic or structural protein changes were observed between groups.
Conclusions:
The observed data suggest that HS ameliorates LV systolic dysfunction and seems to reduce myocardial tissue compromise in BD rats, even when the treatment is performed during the process triggered by this event.
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