Nitric oxide synthase inhibition aggravates the adverse renal effects of high but not low intraabdominal pressure

Bishara, Bishara; Ramadan, Rawi; Karram, Tony; Awad, Hoda; Abu-Saleh, Niroz; Winaver, Joseph; Assadi, Akram; Abassi, Zaid

doi:10.1007/s00464-009-0672-3

Cited by 13 publications

(6 citation statements)

References 43 publications

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“…A previous study revealed that the glomerular filtration rate decreased by 14 and 48% in rats when an intraabdominal pressure of 7 and 14 mmHg was applied, respectively. In parallel, the renal plasma flow decreased by 28 and 57% under these conditions ( 29 ). Certain studies have emphasized that high intraabdominal pressure can noticeably decrease renal blood flow, while other studies reported that renal blood flow returned to the normal range following deflation ( 30 , 31 ).…”

Section: Discussionmentioning

confidence: 99%

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

Zhao

Rao

et al. 2018

Int J Mol Med

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The primary aim of the present study was to investigate the potential effect of high-pressure carbon dioxide (CO2) pneumoperitoneum on kidneys with severe hydronephrosis and to investigate the possible underlying mechanism. A total of 18 rabbits underwent a surgical procedure inducing severe hydronephrosis. Rabbits were then divided at random into three groups (n=6 each) and subjected to intraabdominal pressure of 0, 8 or 18 mmHg, respectively. CO2 inflation lasted for 90 min in the pneumoperitoneum groups. Oxidative stress was assessed by measurements of reactive oxygen species (ROS). Activation of apoptosis was analyzed by western blot analysis of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated x protein (Bax), cytochrome c (Cyt c), caspase-3 and caspase-9 levels. In addition, TUNEL assay, hematoxylin and eosin (H&E) staining, measurement of mitochondrial membrane potential (MMP) and detection of changes to kidney ultramicrostructure were performed. In the 0 and 8 mmHg groups, all results were normal and similar. However, in the 18 mmHg group, the kidneys suffered oxidative damage and mitochondrial injuries, and increased ROS levels, lower MMP and mitochondrial vacuolization were observed. Furthermore, the mitochondrial/caspase-dependent pathway of apoptosis was activated, as indicated by the apoptotic index, and the expression levels and translocation of Bax, Bcl-2, Cyt c, caspase-3 and caspase-9. Therefore, it is concluded that high-pressure CO2 pneumoperitoneum induces oxidative damage and apoptosis in rabbit kidneys with severe hydronephrosis, which is associated with the mitochondrial apoptotic pathway.

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Section: Discussionmentioning

confidence: 99%

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

Zhao

Rao

et al. 2018

Int J Mol Med

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“…Essentially, blockade of NOS with L-NAME was found to aggravate pneumoperitoneum-induced renal hypoperfusion and oliguria, while pretreatment with nitroglycerine attenuated this effect. 2 9 Bishara, et al 18 reported the importance of IAP by showing that blockade of the NO system with L-NAME had adverse renal effects at high yet not moderate IAPs. Moreover, they found in another study that rats with decompensated congestive heart failure were more susceptible to the adverse renal effects of pneumoperitoneum when pretreated with L-NAME, implying a higher susceptibility to kidney function deterioration in patients with cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

“… 22 Moreover, the functional significance of arginase and its relevance with the activity of NOS was emphasized due to the fact that arginase and NOS share L-arginine as a substrate. 11 However, while oxidative stress, tissue injury, and reduction in kidney function during laparoscopic surgery have been suggested to be closely related to the NO system in several recent studies, 1 9 18 the role of arginase during CO 2 pneumoperitoneum has remained unknown. Considering the fact that competition for L-arginine supply is intensified under acute and chronic stress conditions, 23 arginase may contribute to the shortage of NO bioactivity during laparoscopic surgery.…”

Section: Discussionmentioning

confidence: 99%

Effect of Pneumoperitoneum on Oxidative Stress and Inflammation via the Arginase Pathway in Rats

Shin

Kim

et al. 2016

Yonsei Med J

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PurposeOxidative stress during CO2 pneumoperitoneum is reported to be associated with decreased bioactivity of nitric oxide (NO). However, the changes in endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and arginase during CO2 pneumoperitoneum have not been elucidated.Materials and MethodsThirty male Sprague-Dawley rats were randomized into three groups. After anesthesia induction, the abdominal cavities of the rats of groups intra-abdominal pressure (IAP)-10 and IAP-20 were insufflated with CO2 at pressures of 10 mm Hg and 20 mm Hg, respectively, for 2 hours. The rats of group IAP-0 were not insufflated. After deflation, plasma NO was measured, while protein expression levels and activity of eNOS, iNOS, arginase (Arg) I, and Arg II were analyzed with aorta and lung tissue samples.ResultsPlasma nitrite concentration and eNOS expression were significantly suppressed in groups IAP-10 and IAP-20 compared to IAP-0. While expression of iNOS and Arg I were comparable between the three groups, Arg II expression was significantly greater in group IAP-20 than in group IAP-0. Activity of eNOS was significantly lower in groups IAP-10 and IAP-20 than in group IAP-0, while iNOS activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10. Arginase activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10.ConclusionThe activity of eNOS decreases during CO2 pneumoperitoneum, while iNOS activity is significantly increased, a change that contributes to increased oxidative stress and inflammation. Moreover, arginase expression and activity is increased during CO2 pneumoperitoneum, which seems to act inversely to the NO system.

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“…In rat studies, the administration of nitric oxide alleviates the renal effect of pneumo-peritoneum at a higher (14 mmHg compared to 7 and 10 mmHg) pressure by about 40%, as can be gleaned from a bar chart in Bishara et al, while the nitric oxide synthase inhibitor aggravates it by approximately 50% [ 117 , 118 ].…”

Section: Humoral Factorsmentioning

confidence: 99%

Mediators of Regional Kidney Perfusion during Surgical Pneumo-Peritoneum Creation and the Risk of Acute Kidney Injury—A Review of Basic Physiology

Kopitkó

Medve

Gyökeres

et al. 2022

JCM

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Acute kidney injury (AKI), especially if recurring, represents a risk factor for future chronic kidney disease. In intensive care units, increased intra-abdominal pressure is well-recognized as a significant contributor to AKI. However, the importance of transiently increased intra-abdominal pressures procedures is less commonly appreciated during laparoscopic surgery, the use of which has rapidly increased over the last few decades. Unlike the well-known autoregulation of the renal cortical circulation, medulla perfusion is modulated via partially independent regulatory mechanisms and strongly impacted by changes in venous and lymphatic pressures. In our review paper, we will provide a comprehensive overview of this evolving topic, covering a broad range from basic pathophysiology up to and including current clinical relevance and examples. Key regulators of oxidative stress such as ischemia-reperfusion injury, the activation of inflammatory response and humoral changes interacting with procedural pneumo-peritoneum formation and AKI risk will be recounted. Moreover, we present an in-depth review of the interaction of pneumo-peritoneum formation with general anesthetic agents and animal models of congestive heart failure. A better understanding of the relationship between pneumo-peritoneum formation and renal perfusion will support basic and clinical research, leading to improved clinical care and collaboration among specialists.

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Nitric oxide synthase inhibition aggravates the adverse renal effects of high but not low intraabdominal pressure

Abstract: Decreased renal function/perfusion is induced by IAP pressures of 10 and 14 mmHg but not 7 mmHg. Inhibition of NOS aggravates the adverse renal effects of high (14 mmHg) but not low (7 or 10 mmHg) IAP, indicating that NO deficiency may contribute to the renal dysfunction during high IAP.

Cited by 13 publications

References 43 publications

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

Effect of Pneumoperitoneum on Oxidative Stress and Inflammation via the Arginase Pathway in Rats

Mediators of Regional Kidney Perfusion during Surgical Pneumo-Peritoneum Creation and the Risk of Acute Kidney Injury—A Review of Basic Physiology

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