Impact of Laparoscopic Prolapse Repair in the Levator Hiatus Area.

STUDY OBJECTIVE: To determine whether laparoscopic surgery by sacrocolpopexy or sacrocervicopexy with posterior mesh attachment to levator ani to treat pelvic organ prolapse reduces the levator hiatus area, as measured by transperineal 3- and 4-dimensional ultrasound. The secondary objective was to assess the risk factors for prolapse recurrence. DESIGN: This is a prospective cohort study. SETTING: A university tertiary hospital. PATIENTS: Women with symptomatic apical prolapse at a high risk of recurrence were included. High risk of recurrence was defined as age <60 years and levator injury (avulsion and/or ballooning) or stage III-IV prolapse Pelvic Organ Prolapse Quantification. INTERVENTIONS: Women were treated with laparoscopic sacrocolpopexy or sacrocervicopexy. MEASUREMENTS AND MAIN RESULTS: Women underwent clinical examination according to assessment by the Pelvic Organ Prolapse Quantification system and transperineal ultrasound for the levator hiatus area at Valsalva. We collected demographic, clinical, and ultrasound data before surgery from clinical records and performed a comparative analysis of the levator hiatus areas before and after surgery and univariate and multivariate analyses of the risk factors for recurrence. Among the 30 women who enrolled, the levator hiatus area at Valsalva decreased significantly after surgery by an average of 4.68 cm2 (p = .028). However, despite a recurrence rate of 13.3%, we found no risk factors associated with recurrence in either the univariate or the multivariate analyses. CONCLUSION: Laparoscopic surgery by sacrocolpopexy or sacrocervicopexy for pelvic organ prolapse with mesh posterior attachment to levator ani significantly reduces the levator hiatus area measured by transperineal ultrasound. Further large-scale studies will be needed to confirm our results and identify risk factors for recurrence.

Ozone oxidative preconditioning is mediated by A1 adenosine receptors in a rat model of liver ischemia/ reperfusion.

The liver is damaged by sustained ischemia in liver transplantation, and the reperfusion after ischemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischemia/reperfusion (I/R) injury. The aim of this study was to investigate the role of A(1) adenosine receptor on the protective actions conferred by OzoneOP in hepatic I/R. By using a specific agonist and antagonist of the A(1) subtype receptor (2-chloro N6 cyclopentyladenosine, CCPA and 8-cyclopentyl-1,3-dipropylxanthine, DPCPX respectively), we studied the role of A(1) receptor in the protective effects of OzoneOP on the liver damage, nitiric oxide (NO) generation, adenosine deaminase activity and preservation of the cellular redox balance. Immunohistochemical analysis of nuclear factor-kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha) and heat shock protein-70 (HSP-70) was performed. OzoneOP prevented and/or ameliorated ischemic damage. CCPA showed a similar effect to OzoneOP + I/R group. A(1)AR antagonist DPCPX blocked the protective effect of OzoneOP. OzoneOP largely reduced the intensity of the p65 expression, diminished TNF-alpha production, and promoted a reduction in HSP-70 immunoreactivity. In summary, OzoneOP exerted protective effects against liver I/R injury through activation of A(1) adenosine receptors (A(1)AR). Adenosine and (.)NO produced by OzoneOP may play a role in the pathways of cellular signalling which promote preservation of the cellular redox balance, mitochondrial function, glutathione pools as well as the regulation of NF-kappaB and HSP-70.

Role of protein synthesis in the protection conferred by ozone-oxidative-preconditioning in hepatic ischaemia/reperfusion.

The liver is damaged by sustained ischaemia during liver transplantation, and the reperfusion after ischaemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischaemia/reperfusion (I/R) injury through different mechanisms. The aim of this study was to investigate the influence of the inhibition of protein synthesis on the protective actions conferred by OzoneOP in hepatic I/R. Rats were treated with cycloheximide (CHX) in order to promote protein synthesis inhibition after OzoneOP treatment. Plasma transaminases, malondialdehyde and 4-hydroxyalkenals and morphological characteristics were measured as an index of hepatocellular damage; Cu/Zn-superoxide dismutase (SOD), Mn-SOD, catalase, total hydroperoxides and glutathione levels as markers of endogenous antioxidant system. OzoneOP increased Mn-SOD isoform and ameliorated mitochondrial damage. CHX abrogated the protection conferred by OzonoOP and decreased Mn-SOD activity. Cellular redox balance disappeared when CHX was introduced. Protein synthesis is involved in the protective mechanisms mediated by OzoneOP. Ozone treatment preserved mitochondrial functions and cellular redox balance.