Abstract

kidneys of any group. The addition of TUDCA in group 3 reduced apoptosis in the lung to a level similar to controls. There were significant differences in WW/DW and PaO2/FIO2 between the control and the 2 experimental groups but not between groups 2 and 3. TUDCA appears to reduce the rise in pulmonary vascular resistance associated with VILI and help maintain cardiac output. Conclusion Ventilation with high pressure induced cellular apoptosis in lung but not kidneys. TUDCA significantly reduced ventilator-induced apoptosis in the lungs. This study is the first to demonstrate that the reduced cardiac output, increased pulmonary vascular resistance and apoptosis in the lungs associated with VILI is reduced by TUDCA.

Highlights

  • Apoptosis has been implicated in the process of lung injury

  • tauroursodeoxycholic acid (TUDCA) appears to reduce the rise in pulmonary vascular resistance associated with ventilatorinduced lung injury (VILI) and help maintain cardiac output

  • This study is the first to demonstrate that the reduced cardiac output, increased pulmonary vascular resistance and apoptosis in the lungs associated with VILI is reduced by TUDCA

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Summary

Introduction

Apoptosis has been implicated in the process of lung injury. A drug that inhibits apoptosis could be very helpful to understand the role of programmed cell death in ventilatorinduced lung injury (VILI). We examined whether tauroursodeoxycholic acid (TUDCA), an anti-apoptotic bile acid prevents ventilator-induced apoptosis in rabbit model of VILI

Materials and methods
Conclusion
Discussion

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