To discuss the complexity of septic microvascular dysfunction and the role of shear stress in this process.
Approach:
Biological vs. Physical Models: Biological models elucidate the complexity of septic microvascular dysfunction, while physical models isolate variables to understand their effects.
Shear Model Hypothesis: The shear model's relevance to sepsis requires experimental testing to determine if altering shear signaling can mitigate microvascular shutdown.
Key Findings:
Septic microvascular dysfunction involves leucocyte adhesion, coagulation, and endothelial shedding.
The shear model remains experimentally untested and requires validation.
Current dominant theories, such as the 'cytokine storm', have not successfully improved patient outcomes.
Interpretation:
The author emphasizes the need for fresh approaches in sepsis research, advocating for the use of models to enhance understanding despite biological complexity.
Limitations:
The shear model is not yet experimentally validated.
The anatomical complexity of arterioles is not fully recreated in models.
Conclusion:
The author hopes the discussion around the shear model will continue to stimulate scientific dialogue on sepsis.
