Hemodynamic parameters.

<p>CLP, cecal ligation and puncture; CERA, continuous erythropoietin receptor activator; MAP, mean arterial pressure.</p

Number of CD68-positive cells/0.087 mm² field in the tubulointerstitium at 24 h after CLP.

<p><b>A</b>, photomicrographs of immunohistochemical staining in control rats, rats submitted to cecal ligation and puncture only, and rats treated with continuous erythropoietin receptor activator prior to undergoing cecal ligation and puncture (magnification, ×40). <b>B</b>, Graphic representation of CD68-positive cell counts. Data are mean±SEM. p>0.05 for control vs. CLP+CERA. CLP, cecal ligation and puncture; CERA, continuous erythropoietin receptor activator.</p

Immunoblots reacted with anti-Toll-like receptor 4 antibody (1∶100), revealing an 89-kDa band.

<p>Semiquantitative immunoblots prepared from kidney samples. Densitometric analysis of samples from control rats, rats submitted to cecal ligation and puncture only, and rats treated with continuous erythropoietin receptor activator prior to undergoing cecal ligation and puncture. Differences among the means were compared by analysis of variance followed by the Student-Newman-Keuls test. p>0.05 for control vs. CLP+CERA. CLP, cecal ligation and puncture; CERA, continuous erythropoietin receptor activator; TLR4, Toll-like receptor 4.</p

Effects of continuous erythropoietin receptor activator on plasma levels of pro-inflammatory cytokines at 24 h after cecal ligation and puncture.

<p>CLP, cecal ligation and puncture; CERA, continuous erythropoietin receptor activator; IL, interleukin; TNF-α, tumor necrosis factor alpha; IFN-γ, interferon gamma.</p><p>*p<0.05 vs. CLP+CERA.</p

Physiological parameters.

<p>CLP, cecal ligation and puncture; CERA, continuous erythropoietin receptor activator; UV, urine volume; Cr, creatinine; Ccr, creatinine clearance; BW, body weight; U_Osm, urinary osmolality; UNaV, urinary excretion of sodium; UKV, urinary excretion of potassium; UureaV, urinary excretion of urea; AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDH, lactate dehydrogenase.</p><p>*p<0.01 vs. Control; †p<0.01 vs. CLP+CERA; ‡p<0.05 vs. Control; §p<0.05 vs. CLP+CERA; ‖p<0.001 vs. Control; ¶p<0.001 vs. CLP+CERA.</p

Representative light micrographs of Hematoxylin-Eosin stain.

<p>2a (Ec), 2b (Ec+NAC) and 2c (NAC+Ec) show areas of necrosis (*) and inflammatory infiltrations (macrophages)(arrows). 2d (Allo+Ec) shows no necrosis and slight inflammatory infiltration.</p

Acute tubular necrosis score in the four groups of studied rats: Control (C), <i>Bothrops</i> Venom (BV), <i>Schizolobium Parahyba</i> (SP) and treatment, which received <i>Schizolobium Parahyba</i> extract infusion immediately after <i>Bothrops</i> venom infusion (T).

<p>Acute tubular necrosis score in the four groups of studied rats: Control (C), <i>Bothrops</i> Venom (BV), <i>Schizolobium Parahyba</i> (SP) and treatment, which received <i>Schizolobium Parahyba</i> extract infusion immediately after <i>Bothrops</i> venom infusion (T).</p

Renal function, renal and systemic hemodynamics in control (C), <i>Bothrops</i> venom (BV), <i>Schizolobium parahyba</i> aqueous extract (SP) and BV followed by SP (T) groups.

<p>Data are mean ± SD or median (quartiles); (n); GFR: glomerular filtration rate; RBF: renal blood flow; RVR: renal vascular resistance; MAP: mean arterial pressure; UO: urinary output; FeNa: fractional excretion of sodium; FeK: fractional excretion of potassium; Uosm: urinary osmolality.</p>a<p>p<0.001 vs. control;</p>b<p>p<0.01 vs. control;</p>c<p>p<0.001 vs. SP;</p>d<p>p<0.01 vs. SP;</p>e<p>p<0.05 vs. control;</p>f<p>p<0.05 vs. SP.</p

Ecstasy induces reactive oxygen species, kidney water absorption and rhabdomyolysis in normal rats. Effect of N-acetylcysteine and Allopurinol in oxidative stress and muscle fiber damage

<div><p>Background</p><p>Ecstasy (Ec) use produces hyperthermia, excessive sweating, intense thirst, an inappropriate antidiuretic hormone secretion (SIADH) and a multisystemic toxicity due to oxidative stress (OS). Intense thirst induces high intake of pure water, which associated with SIADH, usually develops into acute hyponatremia (Hn). As Hn is induced rapidly, experiments to check if Ec acted directly on the Inner Medullary Collecting Ducts (IMCD) of rats were conducted. Rhabdomyolysis and OS were also studied because Ec is known to induce Reactive Oxygen Species (ROS) and tissue damage. To decrease OS, the antioxidant inhibitors N-acetylcysteine (NAC) and Allopurinol (Allo) were used.</p><p>Methods</p><p>Rats were maintained on a lithium (Li) diet to block the Vasopressin action before Ec innoculation. AQP2 (Aquaporin 2), ENaC (Epitheliun Sodium Channel) and NKCC2 (Sodium, Potassium, 2 Chloride) expression were determined by Western Blot in isolated IMCDs. The TBARS (thiobarbituric acid reactive substances) and GSH (reduced form of Glutathione) were determined in the Ec group (6 rats injected with Ec-10mg/kg), in Ec+NAC groups (NAC 100mg/Kg/bw i.p.) and in Allo+Ec groups (Allo 50mg/Kg/i.p.).</p><p>Results</p><p>Enhanced AQP2 expression revealed that Ec increased water transporter expression, decreased by Li diet, but the expression of the tubular transporters did not change. The Ec, Ec+NAC and Allo+Ec results showed that Ec increased TBARS and decreased GSH, showing evidence of ROS occurrence, which was protected by NAC and Allo. Rhabdomyolysis was only protected by Allo.</p><p>Conclusion</p><p>Results showed that Ec induced an increase in AQP2 expression, evidencing another mechanism that might contribute to cause rapid hyponatremia. In addition, they showed that NAC and Allo protected against OS, but only Allo decreased rhabdomyolysis and hyperthermia.</p></div

NGAL and KIM-1 in control (C), <i>Bothrops</i> venom (BV), <i>Schizolobium parahyba</i> aqueous extract (SP) and BV followed by SP (T) groups.

<p>Data are median (quartiles); (n); NGAL: neutrophil gelatinase-associated lipocalin; KIM −1: kidney injury molecule-1.</p>a<p>p<0.05 vs. control;</p>b<p>p<0.05 vs. SP.</p