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Updated: Feb 10, 2026

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Early Postnatal Stress as a Risk Factor for Cardiac Pathology in Systemic Inflammatory Conditions: An Experimental

E E Pinaeva1, E N Sazonova2, D V Yakovenko2

  • 1Far-East State Medical University, Ministry of Health of the Russian Federation, Khabarovsk, Russia. ekaterinabaglaevakhv@gmail.com.

Bulletin of Experimental Biology and Medicine
|February 9, 2026
PubMed

Insights

Early life stress in rats amplifies the heart

Area of Science:

  • Cardiovascular Physiology
  • Neuroimmunology
  • Developmental Biology

Background:

  • Early life stress, such as maternal separation, can have long-lasting effects on physiological systems.
  • Lipopolysaccharide (LPS) is a potent immune stimulant that can induce inflammation and affect cardiac function.
  • Understanding the interplay between early life stress and immune challenges is crucial for cardiovascular health.

Purpose of the Study:

  • To investigate the impact of early postnatal stress on the myocardial response to lipopolysaccharide (LPS) in adult rats.
  • To compare the cardiac effects of LPS in stressed versus non-stressed animals.

Main Methods:

  • Adult male Wistar rats were subjected to maternal separation (early stress) or not.
  • Animals received an intraperitoneal injection of LPS or saline.
  • Cardiac response was assessed by measuring p53+ cardiomyocytes, plasma troponin I, cardiomyocyte nucleoli, and eNOS+ cardiomyocytes.

Main Results:

  • Both LPS-treated groups showed increased p53+ cardiomyocytes and elevated troponin I compared to controls.
  • The MS + LPS group exhibited a higher number of nucleoli per cardiomyocyte and more eNOS+ cardiomyocytes than control and LPS groups.
  • Early postnatal stress exacerbated the myocardial response to LPS.

Conclusions:

  • Early life stress primes the heart for an exaggerated response to immune challenges like LPS.
  • This heightened cardiac sensitivity in stressed animals involves specific cellular changes in cardiomyocytes.
  • Findings highlight the long-term cardiovascular consequences of early life adversity.

Keywords:
cardiomyocytesearly postnatal stresslipopolysaccharidesystemic inflammatory response

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