Related Experiment Video
Updated: Jul 14, 2026

Developing a Clinically Relevant Hemorrhagic Shock Model in Rats
Published on: March 22, 2024
[Damage effects of shock lymph on the pulmonary micro-vascular endothelial cells of rats]
Chun Yu Niu1, Zi Gang Zhao, Ji Cheng Li
1Department of Pathophysiology, Hebei North University, Zhangjiakou 075029, China. ncylxf@126.com
Abstract:
The model of serious hemorrhagic shock was established under the condition of asepsis and mesentery lymph was taken out. As control, normal mesentery lymph fluid, normal portal vein blood, and shock portal vein blood of rats were taken out. The primary pulmonary microvascular endothelial cells (PMVECs) of passages 3 were treated by different treatment factors, respectively. The morphology and ultrastructure changes of PMVECs were observed under optics microscope, transmit electronic microscope and scan electronic microscope. The cells proliferation under different final concentrations of shock lymph and normal lymph were measured with MTT method. The cell cycle arrest was analyzed by flow cytometry and the DNA of cell nucleus was analyzed by electrophoresis. The results showed that shock lymph played a role in damaging PMVECs. The contracted cells and condensed nucleus were found, and apoptosic bodies were observed under a transmission electron microscope. The proliferation of PMVECs was decreased when the concentration of shock lymph increased to some extent and showed statistic significance compared with normal lymph group. The cells cocultured with shocking lymph fluid at 4% final concentration showed that G0-G1 cell population was higher and the proportion of S+G2-M cell population was lower than that of other groups, and the DNA ladder was observed in electrophoresis of cell nucleus DNA at same time. The results demonstrated that shock lymph could damage the morphology and ultra-structure of PMVECs, reduce the cells proliferation, interfere with cell cycle, and induce the apoptosis.
Insights
Hemorrhagic shock lymph damages pulmonary microvascular endothelial cells (PMVECs). It reduces cell proliferation, alters cell cycle, and induces apoptosis, highlighting shock lymph
Area of Science:
- Endothelial Cell Biology
- Hemorrhagic Shock Pathophysiology
- Lymphatic System Research
Context:
- Serious hemorrhagic shock models are crucial for understanding systemic injury.
- Pulmonary microvascular endothelial cells (PMVECs) are vital for lung function and susceptible to shock-induced damage.
- Mesenteric lymph composition changes during shock, potentially impacting distant organs.
Purpose:
- To investigate the direct effects of shock-induced mesenteric lymph on PMVECs.
- To analyze morphological, ultrastructural, proliferative, and cell cycle changes in PMVECs exposed to shock lymph.
- To determine if shock lymph induces apoptosis in PMVECs.
Summary:
- Shock lymph induced significant morphological changes in PMVECs, including cell contraction and nuclear condensation.
- Transmission electron microscopy revealed apoptotic bodies in PMVECs treated with shock lymph.
- MTT assays and flow cytometry demonstrated reduced PMVEC proliferation and cell cycle arrest (G0-G1 phase) in response to shock lymph, with DNA laddering indicating apoptosis.
Impact:
- Shock lymph directly damages PMVECs, contributing to microvascular dysfunction during hemorrhagic shock.
- Findings suggest mesenteric lymph plays a role in mediating shock-induced endothelial injury.
- This research provides insights into the cellular mechanisms underlying multi-organ damage in severe shock.

