The Role of Hemodynamic Shear Stress in Healing Chronic Wounds

Abstract

Wounds continue to pose significant challenges to clinicians. Data based on randomized controlled trials from the US Wound Registry showed that less than 50% of wounds heal in an unpredictable period of time. Chronic wounds are difficult to heal, with multiple barriers to healing that include inadequate nutrient flow, an inflammatory-coagulation vicious cycle, redox imbalance, and anatomical, physiological, and biochemical dysfunction in the endothelium. In clinical practice, wounds that fail to heal within an appropriate time are at higher risk for deterioration as well as development of infection that further complicates the pathology. Wounds complicated by deep abscess and osteomyelitis often result in amputation. Higher level amputations, below the knee and above the knee, are associated with increased morbidity and mortality rates. However, the most consequential barrier to healing is the prolonged inflammatory phase, which prevents progression to the proliferation phase of wound healing. Diabetic foot ulcers are especially difficult to heal because of angiopathy, hypoxia and ischemia, AGEs, and other factors related to impaired hemodynamics. Restoration of physiological levels of blood flow to DFUs will concomitantly bring about normalization of laminar SS on the endothelium. These multifaceted healing mechanisms, specifically related to the effects of vascular SS on the endothelium, are reviewed here. Such mechanisms involve anti-inflammation, anticoagulation, antioxidation, vasodilation, and angiogenesis. A concluding inference is made that if normalized SS could be produced in the vasculature serving chronic wounds, the sequential healing processes would be enhanced.

Pathophysiological Mechanisms of Deep Vein Thrombosis

“…Відомо, що напруга зсуву може модифікувати експресію багатьох генів [22]. Таким чином, пульсуюча або ламінарна напруга зсуву може сприяти експресії протизапальних та антиоксидантних факторів [23]. Навпаки, низька напруга зсуву або порушення кровотоку в результаті рефлюксу сприяють запальному та тромботичному фенотипу, наприклад, підвищеній експресії ICAM-1, молекули адгезії судинних клітин типу 1 (VCAM-1 -Vascular cell adhesion molecule 1) і Е-селектину [24].…”