Published January 1, 2025 | Version v1
Journal article Open

Role of adenosine A<sub>3</sub> receptor and endothelial nitric oxide synthase in patients with traumatic hemorrhagic shock

  • 1. Erciyes Univ, Fac Med, Dept Emergency Med, TR-38039 Kayseri, Turkiye
  • 2. Erciyes Univ, Genome & Stem Cell Ctr, TR-38280 Kayseri, Turkiye
  • 3. Gaziantep Univ, Fac Med, Dept Med Pharmacol, TR-27310 Gaziantep, Turkiye

Description

Background The aim of this research is to access the expression of adenosine A3 receptor (ADORA3) and nitric oxide synthase 3 (NOS3) genes and serum levels of ADORA3 and NOS3 in patients with multiple trauma with hemorrhagic shock. Materials and methods The study was performed at Erciyes University between November 2022 and March 2024, in a prospective and controlled manner. Patients diagnosed with traumatic hemorrhagic shock and requiring transfusion in the emergency department were selected as the patients group. Gene expressions were analyzed using quantitative real-time PCR analysis in total RNA samples and serum levels of NOS3 and ADORA3 were detected using ELISA measurements. Results In patients with multiple trauma, adenosine A3 receptor (ADORA3) gene expression showed a significant increase at discharge when compared to healthy controls (P < 0.05). However, serum levels of ADORA3 showed significant decreases at all stages (i.e. at admission, at 24 h, and at discharge) of patients. Although no significant changes were detected in NOS3 gene expression, marked decreases in serum NOS3 levels were observed at admission and at 24 h in multiple trauma patients (P < 0.05). ADORA3 and NOS3 gene expressions were found to be significantly diminished in nonsurvivors. Conclusion The study emphasizes the importance of ADORA3 and NOS3 gene expressions in influencing shock progression in multiple trauma patients. The increase in ADORA3 gene expression may play a role in restoring vascular reactivity after traumatic shock. Decreased serum NOS3 and ADORA3 levels can contribute to the shock progression in the pathophysiology of multiple trauma.

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