In the context of findings related to post-closure tensile strength, the implications of this observation are that the cavitation area may be a vulnerable point in the wound and likely to be more prone to wound recurrence. The ultrasound transducer used in the current study is capable of Doppler color flow imaging. While this technology platform is commonly used for diagnostic echocardiography, this work provides first evidence on BMN673 PARP inhibitor functional blood flow parameters in gated peripheral feeder artery supplying the wound site. In isolation, angiogenic factors or endothelial cell proliferation is not sufficient to induce angiogenesis. It is well documented that hemodynamic factors play a key role in driving inducible angiogenesis. Importantly, these biomechanical forces have to work synergistically with chemical factors in order to drive the proper establishment of vascular supply. A combination of biomechanical stimulation and chemical stimulation orchestrate various aspects of neo-vascularization including the proliferation of cells, regulation of permeability, stabilization of vessels and the production of the extracellular matrix. Modulation of simply one or the other of these regulatory arms may be insufficient to trigger functional angiogenesis to the full extent possible. This is evidenced from reports of gene therapies targeting the vascular endothelial growth factor that have failed in clinical trials possibly because they target only one aspect of the above mentioned combinatorial regulatory process. Because of technological limitations currently there is no functional evidence in the literature as to how wound angiogenesis is related to changes in blood flow velocity of the primary feeder artery that supplies the wound site. While pulse velocity is commonly used to assess arterial wall stiffness, it is also a key determinant of local hemodynamic performance. Higher pulse velocity can only be generated by healthy arteries and will propel blood flow within the given vessel resulting in higher sheer stress which in turn is likely to drive wound angiogenesis. As expected, pulse velocity was recorded as being low, comparable to that of homeostatic TWS119 baseline skin, immediately post-injury. Hypothetically one of the earliest drivers of wound angiogenesis is a sharp elevation of pulse velocity in the primary feeder artery that supplies the wound site. This remarkable change is noted on day 3 at the inflammatory phase as blood borne immune cells accumulate at the wound site. The mechanisms underlying this escalation remain unknown. During the course of the next two weeks of the healing process there appears to be a correction of pulse velocity wherein the velocity is still 5-fold of the baseline but has declined by about a third of where it was during the peak on day 3. This observation leads to the speculation that the noted rise in pulse velocity after wounding is not completely dependent on cells abundant during the inflammatory phase. As evident histologically with this wound model, the inflammatory phase has been largely resolved by the end of the second week. Of outstanding interest is the observation that as pulse velocity declines from day 3 to day 14, the system engages in a second boost of pulse velocity resulting in a bimodal peak as reported. This tight dual control of the arterial pulse velocity points towards an extraordinary significance of arterial hemodynamics in wound angiogenesis. Laser speckle imaging has previously been used for the assessment of spatio-temporal hemodynamic changes during excisional wound healing. We were able to visualize perfusion changes in the entire wound area as healing progressed and these were validated with histological analyses.