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Animal study reveals impaired osmoregulation and organ hydration after hemorrhagic shock in dysbiotic rat offspring, indicating lasting vulnerability from early antibiotic exposure.
Hemorrhagic shock is a major cause of trauma-related mortality, yet the contribution of the gut microbiome to systemic fluid and electrolyte regulation during acute blood loss remains unclear. This study investigated whether maternal antibiotic-induced dysbiosis alters the osmoregulatory and metabolic responses of offspring to hemorrhagic shock. Pregnant and lactating Sprague Dawley dams received vancomycin and amoxicillin, and antibiotic treatment was continued in male offspring until 8 weeks of age. Following a 4-week washout period, 12-week-old offspring underwent fixed-volume hemorrhagic shock (1.5 mL/100 g body weight), and serum biochemical variables and organ wet weights were evaluated. Compared with controls, dysbiotic offspring exhibited persistent hypernatremia and hyperchloremia (both p < 0.001), together with significantly higher calculated serum osmolarity (p = 0.030). These alterations were accompanied by significantly lower blood urea nitrogen and creatinine concentrations (p < 0.01), suggesting an attenuated metabolic and renal adaptive response. Lung and brain wet weights were also significantly lower in dysbiotic offspring (p = 0.002 and p = 0.01, respectively), whereas kidney and heart wet weights were unaffected. These findings suggest that maternal antibiotic-induced dysbiosis is associated with impaired systemic electrolyte regulation and organ-specific physiological responses during hemorrhagic stress. Clinically, closer monitoring of serum sodium and osmolarity may be warranted in trauma patients with a history of prolonged antibiotic exposure.
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Semen et al. (2026) studied this question.
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