The hemodynamic effects of CO2-induced pressure on the kidney in an isolated perfused rat kidney model.
ABSTRACT Variable mechanisms were suggested to mediate the changes in renal hemodynamics during pneumoperitoneum. To assess whether it can be pressure dependent only, we conduct a study in an isolated, pressurized, and perfused organ model.
Seventy Wistar rat kidneys were perfused with oxygenated, 3% albumin-contained Krebs-Henseleit solution. Experiments took place within Plexiglass chamber that provided conditions for perfusion of organs, humidity, and maintenance of intracameral CO2 pressures [0 (control), 3, 5, 8, 12, 15, and 18 mm Hg]. All kidneys (10/group) were perfused for 60 minutes. One-half of the groups were perfused for an additional 30 minutes, during which the perfusion pressures were reduced to 0 mm Hg. pH of the perfusate was measured as well.
The perfusion pressure increased and the kidney flow decreased slightly, in proportion with the intrachamber pressure. Urine output decreased to a minimum of 40% in >or=8 mm Hg pressure conditions, compared with the control group. The pH values were below normal, during experimental pneumoperitoneum.
Pneumoperitoneal conditions are a direct cause of changes in renal urinary output. The increase in pCO2 pressure and consequently low intraorgan pH may contribute to a mild transient renal damage during pneumoperitoneum.
- SourceAvailable from: synapse.koreamed.orgKorean Journal of Urology. 01/2009; 50(8).
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ABSTRACT: Molecular dynamics (MD) simulations have been used to study the adsorption of dodecylamine (DDA) on iron surfaces in aqueous solution in this paper. In strong acidic solution the protonated form of DDA, DDAH, can adsorb on the iron surface preferentially, while in weak acidic solution containing chloride ions the adsorption of DDA and DDAH forms can occur simultaneously. Different results were obtained when different simulation factors were considered. In order to obtain the correct results, a model close to the realistic inhibition system was fabricated.Corrosion Science - CORROS SCI. 01/2011; 53(5):2046-2049.
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ABSTRACT: Pneumoperitoneum-associated ischemia-reperfusion (IR) may initiate renal dysfunction. Whether oxidants are responsible for renal structural damage, such as cell apoptosis, has not yet been evaluated. We investigated such eventuality in an isolated rat kidney model. Thirty-five rat kidneys with their vessels and ureter were harvested and perfused within a closed environment at flow of 15 ml min(-1). After stabilization, kidneys were assigned to one of five groups (n = 7 per group): CO(2)-induced intrachamber pressure of 8, 12, or 0 mmHg (control), and 8 or 12 mmHg pressure applied to kidneys from rats treated pre-experimentally with tungsten for 14 days. Pressurization lasted 60 min. Organ perfusion pressure raised as intrachamber pressure increased. Urinary output decreased in the two pressurized nonpretreated groups. Intrachamber pressure was directly associated with an increase in postexperimental xanthine oxidase tissue levels. Twofold apoptosis was documented (p < 0.05) in cortex of nonpretreated kidney in the 12 mmHg group compared with the 8 or 0 mmHg groups. Tungsten pretreatment significantly (p < 0.05) attenuated the abnormalities documented in the 12 mmHg group, but less so in the 8 mmHg pressurized nontreated counterparts. Pneumoperitoneal pressure applied to isolated perfused kidney is associated with renal apoptosis. This rapidly induced structural renal damage is oxidant dependent and can be attenuated by antioxidants. Further studies may shed more light on the role of antioxidants in preventing pneumoperitoneum-induced kidney dysfunction.Surgical Endoscopy 12/2011; 26(5):1417-24. · 3.43 Impact Factor