The Journal of surgical research
-
Chronic allograft nephropathy (CAN) is the leading cause of late kidney allograft loss. Recent studies have suggested that atorvastatin (ATO) may interact with the acute inflammatory process in the renal interstitium and suppress the proliferation of mesangial cells. We hypothesized that ATO could also inhibit the chronic inflammatory process and prevent the progression of CAN. ⋯ Atorvastatin showed excellent favorable effects on blocking renal inflammation and fibrosis, and thus, efficiently inhibited the development and progression of CAN, which might improve the long-term survival rate of renal allografts.
-
After extensive hepatectomy, excessive portal venous flow (PVF) and elevated portal venous pressure (PVP) may lead to postoperative liver damage. We have evaluated the use of portocaval shunt (PCS) to control PVF and PVP following partial hepatectomy (PH) to reduce the postoperative liver damage. ⋯ After 70% PH, extensive centrolobular necrosis and neutrophil aggregation were present and may have caused liver damage, manifested as hyperbilirubinemia and coagulopathy. The delayed liver regeneration with PCS may reduce the postoperative liver damages rather than the rapid liver hypertrophy. The diversion of PVF with PCS to maintain adequate PVP is a very effective procedure for avoiding the postoperative liver failure after extensive hepatectomy.
-
There are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO(2)) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO(2) in a rat model. ⋯ ETCO(2) increases when the small bowel is perforated during CO(2) pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO(2) through the bowel mucosa, causing ETCO(2) elevation. Therefore, an abrupt increase in ETCO(2) observed during laparoscopy may indicate small bowel injury.
-
In acute respiratory distress syndrome, pulmonary vascular permeability increases, causing intravascular fluid and protein to move into the lung's interstitium. The classic model describing the formation of pulmonary edema suggests that fluid crossing the capillary endothelium is drawn by negative interstitial pressure into the potential space surrounding extra-alveolar vessels and, as interstitial pressure builds, is forced into the alveolar air space. However, the validity of this model is challenged by animal models of acute lung injury in which extra-alveolar vessels are more permeable than capillaries under a variety of conditions. In the current study, we sought to determine whether extravascular fluid accumulation can be produced because of increased permeability of either the capillary or extra-alveolar endothelium, and whether different pathophysiology results from such site-specific increases in permeability. ⋯ Phenotypic differences between vascular segments resulted in site-specific increases in permeability, which have different pathophysiological outcomes. Our findings suggest that insults leading to acute respiratory distress syndrome may increase permeability in extra-alveolar or capillary vascular segments, resulting in different pathophysiological sequela.
-
Hemorrhagic shock with conventional resuscitation (CR) primes circulating neutrophils and activates vascular endothelium for increased systemic inflammation, superoxide release, and end-organ damage. Adjunctive direct peritoneal resuscitation (DPR) with intraperitoneal instillation of a clinical peritoneal dialysis solution decreases systemic inflammation and edema formation by enhancing tissue perfusion. The aim of this study is to determine the effect of adjunctive DPR on neutrophil and fluid sequestration. ⋯ Hemorrhagic shock and resuscitation produces time-dependent organ-specific trends of neutrophil sequestration as measured with tissue levels of myeloperoxidase, a marker of neutrophil infiltration. Modulation of the splanchnic blood flow by direct peritoneal resuscitation did not alter the time-dependent neutrophil infiltration in end-organs, suggesting a subordinate role of blood rheology in the hemorrhage-induced neutrophil sequestration. Vulnerable window for neutrophil-mediated tissue damage exists during the first 4 h following resuscitation from hemorrhagic shock in rats. Direct peritoneal resuscitation prevents the early obligatory fluid sequestration and promotes early fluid mobilization.