M E Peña1, C A Angeramo1, F Schlottmann1, E E Sadava2,3. 1. Department of Surgery, Hospital Alemán of Buenos Aires, Av. Pueyrredón 1640, 1118, Buenos Aires, CP, Argentina. 2. Department of Surgery, Hospital Alemán of Buenos Aires, Av. Pueyrredón 1640, 1118, Buenos Aires, CP, Argentina. esadava@hospitalaleman.com. 3. Division of Abdominal Wall Surgery, Department of Surgery, Hospital Alemán of Buenos Aires, Buenos Aires, Argentina. esadava@hospitalaleman.com.
Abstract
PURPOSE: Angiotensin II (AT II) receptor blockers have previously shown to reduce inflammatory response in many settings. We aimed to assess the effects of ATII receptor blocker (Losartan) on mesh integration after abdominal wall repair in a rat model. METHODS: A total of 16 Wistar-Kyoto (WKY) and 16 previously hypertensive (SHRSP) rats were isolated. An acute ventral hernia followed by a bridged repair with heavyweight polypropylene mesh was performed. Subjects received either normal saline (WKY-C n = 8 and SHRPS-C n = 8) or 40 mg/kg losartan (WKY-L n = 8) and SHRPS-L n = 8) in the postoperative period. Blood pressure was recorded preoperatively and weekly after surgery. Necropsy with en-bloc resection of the abdominal wall was performed at postoperative day 30. Macroscopic and microscopic evaluations of the specimens were conducted. H&E and Masson's trichrome were used for histologic evaluation. RESULTS: Both groups receiving Losartan showed a significant reduction of blood pressure after surgery (WKY-L: 130/85 vs 116/81 mmHg, SHRPS-L: 176/137 vs 122/101 mmHg, p < 0.01). A significant reduction in mesh incorporation and adherence scores were also observed on macroscopic analysis in Losartan groups (p < 0.01 and p = 0.02, respectively). Microscopically, higher immature fibroplasia was observed after Losartan, with a significant reduction in scar plate formation and inflammatory response on the prosthetic surface (p = 0.04 and p = 0.02, respectively). CONCLUSION: Losartan modifies the interaction between the host tissue and the prosthesis. An impairment in mesh integration and immature fibroplasia in both normotensive and hypertensive rats detected in our model warrants further research.
PURPOSE: Angiotensin II (AT II) receptor blockers have previously shown to reduce inflammatory response in many settings. We aimed to assess the effects of ATII receptor blocker (Losartan) on mesh integration after abdominal wall repair in a rat model. METHODS: A total of 16 Wistar-Kyoto (WKY) and 16 previously hypertensive (SHRSP) rats were isolated. An acute ventral hernia followed by a bridged repair with heavyweight polypropylene mesh was performed. Subjects received either normal saline (WKY-C n = 8 and SHRPS-C n = 8) or 40 mg/kg losartan (WKY-L n = 8) and SHRPS-L n = 8) in the postoperative period. Blood pressure was recorded preoperatively and weekly after surgery. Necropsy with en-bloc resection of the abdominal wall was performed at postoperative day 30. Macroscopic and microscopic evaluations of the specimens were conducted. H&E and Masson's trichrome were used for histologic evaluation. RESULTS: Both groups receiving Losartan showed a significant reduction of blood pressure after surgery (WKY-L: 130/85 vs 116/81 mmHg, SHRPS-L: 176/137 vs 122/101 mmHg, p < 0.01). A significant reduction in mesh incorporation and adherence scores were also observed on macroscopic analysis in Losartan groups (p < 0.01 and p = 0.02, respectively). Microscopically, higher immature fibroplasia was observed after Losartan, with a significant reduction in scar plate formation and inflammatory response on the prosthetic surface (p = 0.04 and p = 0.02, respectively). CONCLUSION: Losartan modifies the interaction between the host tissue and the prosthesis. An impairment in mesh integration and immature fibroplasia in both normotensive and hypertensive rats detected in our model warrants further research.
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