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: Iraj Jafari Anarkooli[Show abstract] [Hide abstract]
ABSTRACT: This study aimed to investigate the effect of different pressures of CO2 on expression of P33 gene and apoptosis in liver and spleen cells during CO2 pneumoperitoneum. In this study, 30 male Sprague-Dawley rats, weighing approximately 280-340 grams were procured from Tehran Pasteur Institute’s animal house, and randomly divided into 3 equal groups of 10 each. Groups 1 and 2 received 10 and 20 mmHg respectively, and group 3 was the control group. CO2 was insufflated into abdominal cavity of rats in groups 1 and 2 for one hour using a cannula, and then, perfusion was performed for half an hour. In group 3, cannula was placed into abdominal cavity without releasing any gas. The rats were sacrificed afterwards, and their livers and spleens were removed after laparotomy to investigate expression of gene P33 and apoptosis using RT-PCR and TUNEL techniques. The TUNEL technique showed a significant increase in apoptosis in liver and spleen cells of rats that received 20 mmHg compared to rats that received 10 mmHg and control group (P<0.0001) and (P<0.006).respectively. Furthermore, RT-PCR revealed a significant decrease in P33 gene mRNA in liver and spleen cells in 20 mmHg group compared to other two groups (P<0.001). Too high a pressure or too long a duration of CO2 gas may cause release of cytokines and free-radicals from cells of these organs, which can lead to transient or serious dysfunction.Jokull 01/2015; 65(2):48-65. · 1.07 Impact Factor
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ABSTRACT: There is evidence that pneumoperitoneum (PNP) induces transient changes in renal function in healthy individuals. Its effect on malfunctioned kidney is not well known. We investigated the effects caused by PNP in animals with impaired renal function. Male Wistar rats underwent subtotal (5/6) nephrectomy in two sequential steps to induce renal failure. Two weeks after surgery rats were classified as suffering from acute kidney injury (AKI group), and 10 weeks after surgery - as chronic kidney injury (CKI group). All rats were exposed to PNP at the above time point, at 0, 5, and 8 mmHg for 60 min. Changes in creatinine (Cr), blood urea nitrogen (BUN) and creatinine clearance (CCT) levels were measured. Histopathological changes and apoptosis were also evaluated in the different subgroups. Thirty-six rats (18 with AKI, 18 with CKI) terminated the study. While Cr and BUN levels did not change after applying PNP in the different pressure subgroups, CCT decreased significantly in the 5 and the 8 mmHg subgroups, in both the AKI and the CKI rats. Histopathological findings in the AKI pressurized (5, 8 mmHg) subgroups revealed ischemic changes, while a compensatory hypertrophy was noticed in the CKI pressurized subgroups. Apoptotic count was significantly higher in the CKI subgroups as compared to their AKI pressurized counterparts. PNP seems feasible in animals with impaired baseline renal function. In particular, chronic cases should not be considered as contraindication for PNP, while in acute cases PNP might be detrimental.The Journal of urology 04/2014; 192(4). DOI:10.1016/j.juro.2014.03.114 · 3.75 Impact Factor
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ABSTRACT: Objective: Increased pneumoperitoneum pressure during laparoscopic surgery can result in acute kidney injury. We aimed to clarify whether intraabdominal pressure tolerance is modified in various degrees of unilateral kidney hydronephrosis in rabbits. Methods: A total 90 rabbits were randomly allocated to three groups (group PN, PM and PS, i.e. rabbits with no, mild and severe hydronephrosis, respectively, subjected to intraabdominal pressures). Rabbits in group PM (n = 30) and group PS (n = 30) underwent a surgical procedure inducing a mild or severe left hydronephrosis. Rabbits in all groups were then allocated to 5 subgroups. Then, they were subjected to intraabdominal pressures of 0, 6, 9, 12, and 15 mm Hg, respectively. Acute kidney injury was assessed by measuring serum creatinine (Scr), blood urea nitrogen (BUN), tubular cell apoptosis, kidney injury molecule-1 (KIM-1) and cysteine-rich 61 (Cyr-61/CCN1) expression. Results: Acute kidney injury with increased tubular apoptosis and KIM-1 and Cyr-61 expression occurred when intraabdominal pressure reached 15, 15 and 9 mm Hg in PN, PM and PS groups, respectively. The Scr and BUN levels were similar in all groups. Conclusions: In rabbits, kidneys with severe hydronephrosis were more likely to suffer acute injury when they were exposed to pneumoperitoneal pressure. © 2014 S. Karger AG, Basel.Urologia Internationalis 09/2014; 94(2). DOI:10.1159/000362845 · 1.15 Impact Factor