AI Article Synopsis

  • The study aimed to assess how hemorrhagic shock without resuscitation affects Toll-like receptor (TLR) expression in the heart of rats, highlighting its significance.
  • Forty-five mice were divided into three groups, with the hemorrhagic shock model created via heart puncture; TLR2 and TLR4 expression levels were measured, and heart function was evaluated through left ventricular pressure.
  • Results showed that both hemorrhagic shock and lipopolysaccharide (LPS) reduced blood pressure and heart function, while increasing TLR2 and TLR4 expression in the heart, indicating a link between these receptors and cardiac dysfunction in shock conditions.

Article Abstract

Objective: To investigate the effect of hemorrhagic shock without resuscitation on expression of Toll-like receptor (TLR) in myocardium of rats and its significance.

Methods: Forty-five C57BL/6 mice were randomly divided into 3 groups: hemorrhagic group, sham operation group and lipopolysaccharide (LPS) group, with 15 mice in each group. The hemorrhagic shock mouse model was reproduced by heart puncture. Expression levels of TLR2 mRNA and TLR4 mRNA were determined by reverse transcription-polymerase chain reaction (RT-PCR). Left ventricular end-systolic pressure (LVESP) was determined and adopted as an index of left ventricle contractile function.

Results: (1)Both hemorrhagic shock and LPS challenge led to a reduction in arterial blood pressure in mice when compared with sham operation group. Both hemorrhagic shock and LPS challenge could result in left ventricle contractile dysfunction when compared with sham operation group. (2)Expression levels for TLR2 and TLR4 genes were upregulated in myocardium to various extents after hemorrhagic shock and LPS challenge, while in contrast the changes were absent in sham operation group.

Conclusion: (1)The up-regulation of TLR2 and TLR4 genes is closely related with hemorrhagic shock and LPS-induced left ventricle contractile dysfunction, and there may exist a difference in signal transduction pathway between the two pathological conditions. (2)The host ability of innate immune response may be reinforced by the up-regulation of TLR2 and TLR4, whereas overexpression of them may also impair the function of tissues or organs.

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