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Acute obstructive jaundice and chronic cirrhosis protect against the adverse renal effects of pneumoperitoneum: role of nitric oxide.

机译:急性阻塞性黄疸和慢性肝硬化可预防气腹对肾脏的不良影响:一氧化氮的作用。

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摘要

Obstructive jaundice and cirrhosis are associated with impaired renal function. Previously we demonstrated that increased intra-abdominal pressure (IAP, pneumoperitoneum) in normal rats induced renal dysfunction. This study investigated the renal effects of pneumoperitoneum in rats with acute jaundice and cirrhotic rats.Following a baseline period, rats with obstructive jaundice or cirrhosis induced by acute or chronic bile duct ligation (BDL), respectively, and their sham-controls were subjected to consecutive IAPs of 10 and 14 mmHg for 45 min each. Urine flow (V), Na(+) excretion (UNaV), glomerular filtration rate (GFR), renal plasma flow (RPF), and urinary NO metabolites ([Formula: see text]) and cGMP (UcGMP) were determined.Elevating IAP from 0 to 10 and 14 mmHg in normal rats caused IAP-dependent reductions in V, UNaV, GFR, RPF, [Formula: see text] and UcGMP. Basal renal function and hemodynamics were lower in rats with obstructive jaundice. In contrast to normal rats, application of elevated IAP of 10 and 14 mmHg significantly improved V, UNaV, GFR, RPF, and MAP along with increased [Formula: see text] and preserved UcGMP. Similarly, when identical IAP conditions were applied to cirrhotic rats, no deleterious changes in V, UNaV, GFR or RPF were observed.Application of pneumoperitoneum to rats with acute BDL improves kidney function and renal hemodynamics. Likewise, increased IAP does not exert adverse renal effects in cirrhotic rats. These effects are distinct from the deleterious renal consequences of increased IAP in normal rats. Perturbations in the generation of NO/cGMP during IAP in normal rats but not in rats with BDL or cirrhosis may contribute to these differences.
机译:阻塞性黄疸和肝硬化与肾功能受损有关。先前我们证明正常大鼠腹腔内压力升高(IAP,气腹​​)会引起肾功能障碍。这项研究调查了气腹对急性黄疸和肝硬化大鼠的肾脏作用。在基线期之后,分别对急性或慢性胆管结扎(BDL)诱发的梗阻性黄疸或肝硬化大鼠进行了假手术控制。分别进行10和14 mmHg的连续IAP,每次45分钟。测定了尿液流量(V),Na(+)排泄量(UNaV),肾小球滤过率(GFR),肾血浆流量(RPF)和尿中NO代谢物([公式:参见文字])和cGMP(UcGMP)。在正常大鼠中,IAP从0到10和14 mmHg导致V,UNaV,GFR,RPF,[公式:参见文本]和UcGMP的IAP依赖性降低。梗阻性黄疸大鼠的基础肾功能和血流动力学较低。与正常大鼠相反,应用升高的IAP分别为10和14 mmHg可以显着改善V,UNaV,GFR,RPF和MAP,同时增加[公式:参见文本]和保留UcGMP。同样地,当相同的IAP条件应用于肝硬化大鼠时,未观察到V,UNaV,GFR或RPF的有害变化。气腹对急性BDL大鼠的使用可改善肾脏功能和肾脏血液动力学。同样,IAP升高在肝硬化大鼠中不会产生不利的肾脏作用。这些作用不同于正常大鼠中IAP升高对肾脏的有害影响。在正常大鼠中,IAP期间NO / cGMP的产生受到干扰,而在BDL或肝硬化的大鼠中则没有,可能会导致这些差异。

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