The microvascular impact of focal nerve trunk injury

The microvascular supply of the peripheral nerve trunk may be rendered vulnerable by acute focal injuries, particularly if they are associated with direct injury to the epineurial blood supply. In this work we tracked the impact of three clinically relevant forms of focal nerve trunk injury on serial measures of epineurial weighted erythrocyte flux and endoneurial blood flow: short-length crush injuries, long-segmental crush injuries, and crush injuries with superimposed vascular stripping to model added direct epineurial damage. Red blood cell (RBC) flux was measured using quantitative multiple sampling laser doppler flowmetry, and endoneurial blood flow by microelectrode hydrogen clearance polarography. Both short and long crush injuries transiently reduced epineurial RBC flux, most prominently in long injuries, to 34% by 1 h after injury. The changes were less prominent when deeper flux was examined, whereas endoneurial blood flow was not altered by either injury. Long crush injury with added stripping of the epineurial blood supply was associated with more profound declines in epineurial RBC flux, to 16% by 3 h, with recovery at 14 days to 70% of that of the contralateral intact nerve trunk. There was, however, only a minimal impact on endoneurial flow: mild reductions immediately and at 1 h after injury, with rebound hyperemia by 48 h. Despite the presence of prominent epineurial ischemia, regenerative sprouting was not impaired by longer segmental injuries with or without epineurial vascular stripping. Axon sprouting was more prominent in both of these types of injuries compared to short-crush lesions. Taken together, these results indicate that focal nerve trunk injury is remarkably resistant to endoneurial ischemia, and that it can sustain regenerative sprouting in spite of prolonged alterations in the epineurial circulation. Approaches to augment epineurial microvascular viability after nerve injury may not support better regeneration.