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Updated: Feb 15, 2026

A Structured Approach to Extubation in Mechanically Ventilated Rats
Published on: July 18, 2025
Mechanical ventilation strategies alter cardiovascular biomarkers in an infant rat model
Philipp Baumann1,2, Susanne Wiegert1,2,3, Francesco Greco1,2,3
1Department of Intensive Care Medicine and Neonatology, University Children's Hospital of Zurich, Zurich, Switzerland.
Insights
Mechanical ventilation impacts infant cardiovascular biomarkers. Positive end-expiratory pressure (PEEP) affected B-type natriuretic peptide (BNP), while vascular endothelial growth factor (VEGF) responded to various ventilation strategies, indicating potential for monitoring lung injury.
Area of Science:
- Pediatric Critical Care Medicine
- Cardiovascular Physiology
- Respiratory Physiology
Background:
- Mechanical ventilation (MV) is essential in pediatric critical care but can impact cardiovascular function.
- Cardiovascular biomarkers are crucial for assessing patient status and guiding treatment.
- The effects of specific MV strategies on infant cardiovascular biomarkers are not well understood.
Purpose of the Study:
- To investigate the impact of different mechanical ventilation strategies on key cardiovascular biomarkers in infant rats.
- To determine if biomarkers like BNP, VEGF, and ET-1 change in response to varying positive end-expiratory pressure (PEEP), oxygen levels, and CO2 levels.
- To explore the potential of these biomarkers as indicators of ventilation-induced cardiovascular compromise and lung injury.
Main Methods:
- A retrospective study using a validated in vivo infant rat model (14-day-old Wistar rats).
- Rats were subjected to 2 hours of mechanical ventilation with controlled variations in PEEP (high and low), hyperoxemia, hypoxemia, hypercapnia, and hypocapnia.
- Plasma concentrations of B-type natriuretic peptide (BNP), vascular endothelial growth factor (VEGF), and endothelin-1 (ET-1) were measured and compared to control groups.
Main Results:
- B-type natriuretic peptide (BNP) levels were significantly altered by both high (9 cmH2O) and low (1 cmH2O) PEEP.
- Vascular endothelial growth factor (VEGF) concentrations were associated with high PEEP, hyperoxemia, hypoxemia, and hypocapnia.
- Endothelin-1 (ET-1) levels showed a significant change specifically in response to hypoxemia.
Conclusions:
- The specific strategy of mechanical ventilation significantly influences plasma biomarker concentrations in infants.
- BNP and VEGF may serve as valuable surrogate markers for detecting ventilation-induced cardiovascular compromise and lung tissue damage.
- Sudden hyperoxemia may rapidly induce VEGF release, potentially as a protective cellular response.
Abstract:
Mechanical ventilation (MV) is routinely used in pediatric general anesthesia and critical care, but may adversely affect the cardiocirculatory system. Biomarkers are increasingly measured to assess cardiovascular status and improve clinical treatment decision-making. As the impact of mechanical ventilation strategies on cardiovascular biomarkers in ventilated infants is largely unknown, we conducted this retrospective study in a healthy in vivo infant rat ventilation model using 14-days old Wistar rats. We hypothesized that 2 h of mechanical ventilation with high and low positive end-expiratory pressure (PEEP), hyperoxemia, hypoxemia, hypercapnia, and hypocapnia would significantly impact B-type natriuretic peptide (BNP), vascular endothelial growth factor (VEGF), and endothelin-1 (ET-1). We found BNP to be driven by both high (9 cmH2 O) and low (1 cmH2 O) PEEP compared to ventilated control animals (P < 0.05). VEGF concentrations were associated with high PEEP, hyperoxemia, hypoxemia, and hypocapnia (P < 0.05), whereas ET-1 levels were changed only in response to hypoxemia (P < 0.05). In conclusion, the mode of mechanical ventilation alters plasma biomarker concentrations. Moreover, BNP and VEGF might serve as surrogate parameters for ventilation induced cardiovascular compromise and lung tissue damage. Furthermore, our data support the hypothesis, that sudden onset of hyperoxemia may trigger a quick VEGF release as a possible cellular survival reflex.
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