ABSTRACT
Background & objectives: Acute tubular necrosis (ATN) caused by renal ischaemia, renal hypo-perfusion, or nephrotoxic substances is the most common form of acute kidney injury (AKI). There are a few treatment options for this life-threatening disease and the mortality rate exceeds 50 per cent. In critical cases of AKI the only option is renal transplantation. In the present study we evaluated whether bone marrow cells (BMCs) are involved in regeneration of kidney tubules following acute tubular necrosis in the mouse. Methods: Six to eight week old C57BL6/J and congenic enhanced green fluorescence protein (eGFP) mice were used. The relative contributions of eGFP-expressing BMCs were compared in two different approaches to kidney regeneration in the mercuric chloride (HgCl2)-induced mouse model of AKI: induced engraftment and forced engraftment. In vitro differentiation of lineage-depleted (Lin-) BMCs into renal epithelial cells was also studied. Results: In the forced engraftment approach, BMCs were found to play a role in the regeneration of tubules of renal cortex and outer medulla regions. About 70 per cent of donor-derived cells expressed megalin. In vitro culture revealed that Lin- BMCs differentiated into megalin, E-cadherin and cytokeratin-19 (CK-19) expressing renal epithelial cells. Interpretation & conclusions: The present results demonstrate that Lin- BMCs may contribute in the regeneration of renal tubular epithelium of HgCl2-induced AKI. This study may also suggest a potential role of BMCs in treating AKI.
Subject(s)
Acute Kidney Injury/therapy , Acute Kidney Injury/etiology , Animals , Bone Marrow Cells , Kidney Tubules , Kidney Tubular Necrosis, Acute/therapy , Mercuric Chloride/adverse effects , MiceABSTRACT
The effects of increasing concentrations of mercury (Hg2+) chloride (0.5, 1, 2 and 10 uM) on the myocardial electromechanical activity were studied on 10 Langendorff-perfused rat hearts. Hg2+ decreased the development of isovolumic systolic pressure from 20.3 ñ 2.13 mmHg under control conditions to 6.25 ñ 1.32 mmHg at 10 uM HgCl2 (P<0.01) (diastolic pressure = 0 mm Hg). The atrial and ventricular rates also decreased at uM, 1 uM and 2 uM HgCl2 when compared to the Hg2+ - free solution (from 201 ñ 4 to 126 ñ 15 bpm). However, at 10 uM Hg2+ the atrial rate increased (155 ñ 19 bpm) whereas the ventricular rate did not change significantly (119 ñ 13 bpm). A delay in atrioventricular conduction occured at 0.5 uM Hg2+ (64 ñ 4 ms in the Hg2+ free solution to 91 ñ 14 ms in the presence of 0.5 uM Hg2+, P<0.05) with no further changes at higher Hg2+ concentrations. The QRS-T duration also increased as a function of increasing Hf2+ concentrations (58 ñ 5.5 ms in the Hg2+ -free solution to 123 ñ 15 ms in the presence of 10 uM Hg2+ , P<0.01). Qualitative changes of ECG such as extrasystoles , atrial or ventricular arrhythmias and A-V blocks were also observed. The inhibitory action of Hg2+ on ATP hydrolysis and on Ca2+ and Na+-K+ ATPases suggested to occur in other tissues could be the mechanism responsible for the observations reported here
Subject(s)
Rats , Blood Volume , Mercuric Chloride/adverse effects , Electrocardiography , Heart , Myocardium , Perfusion , Mercuric Chloride/toxicityABSTRACT
Se presenta el caso de un adolescente intoxicado por mercurio por intento autodestructivo. Se analizan las diversas formas de intoxicación por este metal así como su sintomatología, haciendo énfasis en la terapéutica utilizada y al mismo tiempo se mencionan las causas que pueden motivar esta autodestrucción.