Abstract
Background: It is known that ischemia-reperfusion damage in the kidney is one of the most common causes of acute kidney failure. It is also known that reduced renal damage has a nephroprotective effect by reducing the release of inflammatory and vasoactive peptides that cause tissue damage. Therefore, we think that reperfusion caused by ischemia in kidney damage may be an important focus for clinical research.Methods: A total of 21 healthy 230-250 g female rats were used in our experimental study. During the experiment, animals were randomly divided into three groups, each containing seven rats. Group 1: The group that underwent left nephrectomy with a sham operation. Group 2: Left renal ischemia for 60 minutes, then left nephrectomy followed by 45 minutes of reperfusion. Group 3: Left renal ischemia for 60 minutes, then reperfusion for 45 minutes, followed by left nephrectomy. In this group, sugammadex was given intravenously at a dose of 100 mg/kg at the beginning of reperfusion. In the histomorphological examination, damage findings of tubules atrophy, dilation and cast formation, tubular epithelial brush border loss and vacuolization, presence of fibrosis as interstitial structural change, capillary vasodilatation/congestion and neutrophilic cell infiltrates in interstitial spaces, and morphological changes in glomeruli were evaluated.Results: When evaluated based on tubular brush border, there were no significant differences between Group 2 and Group 1 (P = 0.454), while the damage in Group 3 was less significant than Group 2 (P = 0.017). When evaluated in terms of tubular vacuolization, there was no significant difference between Group 2 and Group 1 (P = 0.902), while the damage in Group 3 was less significant than Group 2 (P = 0.017).Conclusion: We believe that 100 mg/kg sugammadex given at the beginning of reperfusion after one hour of ischemic condition on rats has a histochemically detectable nephroprotective effect.
Highlights
IntroductionResumption of blood flow to an organ after a critical period of ischemia causes parenchymal injury
We believe that 100 mg/kg sugammadex given at the beginning of reperfusion after one hour of ischemic condition on rats has a histochemically detectable nephroprotective effect
In the IR model created with this experimental study on rats, we found findings that sugammadex may play a protective role in kidney damage
Summary
Resumption of blood flow to an organ after a critical period of ischemia causes parenchymal injury This phenomenon occurring through different clinical and laboratory findings is generally known as ischemiareperfusion (IR) injury [1]. It has been shown that acute tubular necrosis develops during/after renal IR injury [2] Organ dysfunction accompanying this condition is generally associated with increased microvascular permeability, interstitial edema, impaired vasoregulation, inflammatory cell infiltration, and parenchymal cell dysfunction and necrosis [3]. It is known that IR damage in the kidney is one of the most common causes of acute renal failure [4,5]. It is known that reduced renal damage has a nephroprotective effect by reducing the release of inflammatory and vasoactive peptides that cause tissue damage. We think that reperfusion caused by ischemia in kidney damage may be an important focus for clinical research
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