Hydrosurgery as a safe and efficient debridement method in a clinical wound unit.

OBJECTIVE: Hydrosurgical debridement allows removal of non-viable tissue, preserving healthy tissues. This study was designed to analyse whether hydrosurgery, used in a clinical wounds unit, is an effective and safe method that may reduce debridement time. METHODS: Patients' wounds had the following characteristics: wounds with devitalised tissue needing rapid debridement, wounds with cavities, or non-healing wounds. Hydrosurgical debridement uses a pressurised stream of saline (0.9% sodium chloride) and a vacuum around this stream to remove the devitalised tissue of the wound, preserving healthy surrounding tissues. RESULTS: This prospective study comprised of 53 wounds from 39 patients. The wound aetiology included 39.7% arterial insufficiency, 22.6% pressure ulcers (PUs), 15.1% diabetic foot ulcers (DFUs), 9.4% venous leg ulcers (VLUs), and 13.2% from other aetiologies. The percentage of wounds according the size was the following: 32.1% (<10cm2), 43.4% (10-49cm2), 15.1% (50-99cm2), and 9.4% (≥100cm2). Superficial wounds were 43.4% of the total and 56.6% of wounds had cavities. Pain associated with the hydrosurgery was mild to moderate. There were no hydrosurgery-related adverse events. For effective debridement, the required sessions were as follows: one procedure (73.6%), two procedures (18.9%) and three procedures (7.5%). There was a statistical significant direct correlation (r=0.307) between the number of required sessions and wound size. All patients improved in a week (>80% of granulation tissue). CONCLUSION: We demonstrate that hydrosurgery is an effective and rapid debridement method that can be used safely in the outpatient setting.

Intracellular lipid accumulation, low-density lipoprotein receptor-related protein expression, and cell survival in vascular smooth muscle cells derived from normal and atherosclerotic human coronaries.

BACKGROUND: Vascular smooth muscle cell (VSMC) regulation during atherosclerotic plaque progression is determinant for plaque stability. AIMS: To study lipid accumulation, low-density lipoprotein receptor-related protein (LRP) expression, and cell survival in VSMCs isolated from nonatherosclerotic areas (normal VSMCs) and advanced atherosclerotic plaques (plaque-VSMCs) of human coronaries. DESIGN: Normal or plaque-VSMCs were obtained from the intima by modification of the explant technique. RESULTS: Aggregated low-density lipoprotein (agLDL) (100 micro g mL(-1)) internalization induced higher intracellular cholesteryl ester (CE) accumulation in plaque-VSMC compared with normal VSMCs (89.28 +/- 6.1 vs. 60.34 +/- 4.1 micro g CE mg(-1) of protein; P < 0.05). This internalization was associated with LRP expression, as plaque-VSMCs show higher levels of LRP mRNA (6.06 +/- 0.55 vs. 3.87 +/- 0.28; P < 0.05) and LRP protein expression than normal VSMCs. However, plaque-VSMCs showed a lower proliferative response than normal VSMCs (6536 +/- 636 vs. 11151 +/- 815 c.p.m. [(3)H]thymidine; P < 0.05) and did not respond to platelet-derived growth factor BB (PDGF-BB) stimulus. In agreement, the Bcl(2)/BAX ratio was significantly lower in plaque-VSMCs compared with normal VSMCs (0.14 +/- 0.05 vs. 0.51 +/- 0.07; P < 0.05) and it was independent of lipid loading. CONCLUSIONS: These results indicate that higher intracellular lipid deposition in plaque-VSMCs is related to higher LRP expression levels. However, LRP-mediated agLDL internalization is not directly related to the reduced survival of plaque-VSMCs.