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气腹可上调前内皮素-1信使核糖核酸。

Pneumoperitoneum upregulates preproendothelin-1 messenger RNA.

作者信息

Ambrose J A, Onders R P, Stowe N T, Simonson M S, Robinson A V, Wilhelm S, Schulak J A

机构信息

Department of Surgery, Case Western Reserve University, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106, USA.

出版信息

Surg Endosc. 2001 Feb;15(2):183-8. doi: 10.1007/s004640000313.

Abstract

BACKGROUND

Laparoscopic pneumoperitoneum has been shown to decrease glomerular filtration rate (GFR) and urine volume (UV). Endothelin-1 (ET-1), a potent renal vasoconstrictor, has been implicated. The purpose of this study was to determine renal function, ET-1 gene expression, and peptide localization in kidneys subjected to CO2 pneumoperitoneum.

METHODS

Experiments were performed in three groups of anesthetized Sprague-Dawley rats in which GFR and UV were measured before, during, and after insufflation. In the first group (n = 8), pneumoperitoneum (10 mmHg) was established for 30 min. The second group (n = 4) underwent a sham operation without pneumoperitoneum. In the final group (n = 4), kidneys were obtained from normal control animals without any prior surgical instrumentation. PreproET-1 (ppET-1) mRNA levels were measured by reverse transcription-polymerase chain reaction (RT-PCR). The ET-1 peptide was localized within kidneys by immunohistochemistry (IHC).

RESULTS

Pneumoperitoneum caused a significant (p < 0.05) 87% decrease in GFR and a 79% decrease in UV from baseline, with a return to baseline values after desufflation. RT-PCR showed a significant (p < 0.05) increase in expression of ppET-1 mRNA in the laparoscopic group; it was 3.52 +/- 0.33 densitometric units (DU), as compared to 0.35 +/- 0.06 DU and 0.57 +/- 0.12 DU in the control and sham groups, respectively. IHC showed enhanced expression of the ET-1 peptide in the vascular endothelium and proximal tubular cells of the laparoscopic group compared to the control and sham groups.

CONCLUSION

Pneumoperitoneum induces ET-1 gene and peptide upregulation in the kidney. Expression of ET-1 is increased in the renal vasculature and proximal tubular cells. The elevation of ET-1 and its localization may account for some of the renal dysfunction observed during pneumoperitoneum. This suggests that antagonism of ET-1 may be beneficial in patients with renal impairment undergoing prolonged laparoscopic procedures or in protecting allograft function during and after living donor nephrectomy.

摘要

背景

腹腔镜气腹已被证明会降低肾小球滤过率(GFR)和尿量(UV)。内皮素-1(ET-1),一种强效的肾血管收缩剂,被认为与此有关。本研究的目的是确定接受二氧化碳气腹的肾脏的肾功能、ET-1基因表达和肽定位。

方法

对三组麻醉的Sprague-Dawley大鼠进行实验,在气腹前、气腹期间和气腹后测量GFR和UV。第一组(n = 8)建立气腹(10 mmHg)30分钟。第二组(n = 4)进行无气腹的假手术。最后一组(n = 4)从没有任何先前手术操作的正常对照动物获取肾脏。通过逆转录聚合酶链反应(RT-PCR)测量前内皮素原-1(ppET-1)mRNA水平。通过免疫组织化学(IHC)在肾脏内定位ET-1肽。

结果

气腹导致GFR从基线显著(p < 0.05)下降87%,UV下降79%,放气后恢复到基线值。RT-PCR显示腹腔镜组中ppET-1 mRNA表达显著(p < 0.05)增加;为3.52 ± 0.33光密度单位(DU),而对照组和假手术组分别为0.35 ± 0.06 DU和0.57 ± 0.12 DU。IHC显示与对照组和假手术组相比,腹腔镜组血管内皮和近端肾小管细胞中ET-1肽的表达增强。

结论

气腹诱导肾脏中ET-1基因和肽上调。ET-1在肾血管系统和近端肾小管细胞中的表达增加。ET-1的升高及其定位可能是气腹期间观察到的一些肾功能障碍的原因。这表明拮抗ET-1可能对接受长时间腹腔镜手术的肾功能损害患者有益,或在活体供肾肾切除术中及术后保护移植肾功能。

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