The present study was undertaken to ascertain the role of smooth muscles and pericytes in the microcirculation during hyperperfusion and hypoperfusion following ischemia in rats. Paired external carotids, the pterygopalatine branch of the internal carotids and the basilar artery were exposed and divided. Reversible inflatable occluders were placed around the common carotids. After 24 h, the unanesthetized rat underwent 10-min ischemia by inflating the occluders. Continuous cortical cerebral blood flow (c-CBF) was monitored by laser Doppler flowmetry. The measured c-CBF was below 20% of control (P < 0.001) during ischemia. A c-CBF of 227.5 +/- 54.1% (P < 0.001) was obtained during reperfusion hyperemia. A c-CBF of 59.7 +/- 8.8% (P < 0.001) occurred at the nadir of postischemic hypoperfusion, and this was followed by a second hyperemia. The cytoarchitecture of the vascular smooth muscles and pericytes was assessed by scanning electron microscopy. Samples were prepared using a KOH-collagenase digestion method. In control rats, arteriolar muscle cells showed smooth surfaces. Capillary pericytes were closely apposed to the endothelium. Immediately after reperfusion, transverse membrane creases were observed on the smooth muscle surfaces. During maximal hyperemia the creases disappeared. When c-CBF started to decrease the creases became visible again. Throughout the postischemic hypoperfusion the creases remained. Capillary endothelial walls became tortuous in the late phase of hypoperfusion. During the second hyperemia most arteriolar muscle cells showed smooth surfaces. Some pericytes appeared to have migrated from the vascular wall. The morphological changes of smooth muscle membranes suggest that they are related to specific perfusional disturbances during ischemia and reperfusion.

Objective?Advancements in endoscopic endonasal approaches have increased the extent and complexity of skull base resections, in turn demanding the development of novel techniques for skull base defect reconstruction. The objective of this pilot study was to investigate the effect of leukocyte?platelet-rich fibrin (L-PRF) on the postoperative healing after endoscopic skull base surgery. Methods?Between January and May of 2015, 47 patients underwent endoscopic endonasal resection of sellar, parasellar, and suprasellar lesions with the application of L-PRF membranes during the skull base reconstruction at two surgical centers. Early postoperative records were retrospectively reviewed. Results?We found that 21 days following the surgery, 17/41 patients (42%) demonstrated improvement in the crusting score as compared with their 7 day postoperative examination. Ten of these patients (23%) showed no crusting. Fourteen (34%) patients had no change in the crusting score. Six patient records were incomplete. A total of 4/47 cases (8.5%) had postoperative cerebrospinal fluid leak requiring surgical repair. Conclusion?This study demonstrates the potential utility of L-PRF membranes for skull base defect reconstruction. Future studies will be conducted to better assess the role of L-PRF in endoscopic skull base surgery.

Background Reconstruction of surgical defects following cranial base surgery is challenging. Others have demonstrated that leukocyte-platelet-rich fibrin (L-PRF) stimulates tissue healing and bone regeneration. However, these studies have addressed mostly maxillofacial surgical wounds. Objective The objective of this study was to assess the possible adjuvant role of L-PRF in inducing neoossification of the surgical bone defect in anterior skull base surgery. Methods We identified patients who had undergone an endoscopic endonasal surgery of the anterior skull base in which L-PRF membranes were used for the reconstruction of the bone defect and who were followed up with postoperative CT scans. CT findings were then correlated with baseline scans and with the CT scans of a patient who had undergone imaging and histologic analysis after maxillofacial surgery in which L-PRF was used and in which we demonstrated bone formation. Results Five patients fulfilled the inclusion criteria. In four patients, the CT scan demonstrated closure of the bony defect by neoosteogenesis; however, the bone appeared less dense than the surrounding normal bone. A comparison with the control patient yielded similar radiological features. Conclusion This case series suggests that L-PRF may induce bone healing and regeneration at the surgical site defect. Multi-institutional studies with a larger series of patients are required to confirm this possibility.

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