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Hypertonic Saline Solution Reduces Microcirculatory Dysfunction and Inflammation in a Rat Model of Brain Death
Cristiano de Jesus Correia1, Roberto Armstrong, Priscila Oliveira de Carvalho
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 solution (HSS) improved mesenteric microcirculation and reduced inflammation in a rat model of brain death (BD). HSS treatment increased perfused small vessels and decreased leukocyte adhesion, offering potential therapeutic benefits for BD-induced organ dysfunction.
Area of Science:
- Physiology
- Pharmacology
- Immunology
Background:
- Brain death (BD) causes hemodynamic instability and microcirculatory hypoperfusion, leading to organ inflammation and dysfunction.
- Investigating interventions to mitigate these effects is crucial for improving patient outcomes.
Purpose of the Study:
- To evaluate the efficacy of 7.5% hypertonic saline solution (HSS) in addressing mesenteric microcirculatory dysfunction and inflammation in a rat model of BD.
Main Methods:
- Male Wistar rats underwent induction of brain death (BD) via intracranial balloon catheter.
- Rats were treated with either 0.9% NaCl (NS) or 7.5% HSS at different time points post-BD.
- Mesenteric microcirculation, leukocyte-endothelial interactions, and inflammatory markers were analyzed 180 minutes after BD induction.
Main Results:
- BD induced significant hypotension and reduced the proportion of perfused small mesenteric vessels compared to sham-operated rats.
- HSS treatment restored the proportion of perfused vessels and significantly reduced leukocyte rolling and migration.
- HSS modulated the expression of anti-endothelial nitric oxide synthase (eNOS) and endothelin-1, and decreased ICAM-1 levels.
Conclusions:
- HSS improves mesenteric perfused small vessel density in a rat model of BD, potentially via modulation of eNOS and endothelin-1.
- HSS demonstrates anti-inflammatory effects by decreasing leukocyte-endothelial interactions and ICAM-1 expression.
- These findings suggest HSS as a potential therapeutic agent for managing microcirculatory dysfunction and inflammation associated with brain death.
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