Severe burn injuries cause functional impairment in distant internal organs. Although this mechanism is not clear, it is possible that free radical toxicity plays an important role. Research in animals and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following thermal injury. It has been demonstrated that antioxidant treatment prevents oxidative tissue damage associated with thermal trauma. This study was designed to determine the possible protective effect of caffeic acid phenethyl ester (CAPE) treatment against oxidative damage in the kidney and lung induced by thermal injury. Rats were decapitated either 1, 3 or 7 days after burn injury. CAPE was administered intraperitoneally immediately after thermal injury. Kidney and lung tissues were taken for the determination of malondialdehyde (MDA) level, myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XO) activities. Severe skin thermal injury caused a significant decrease in SOD and CAT activities, as well as significant increases in MDA level, XO and MPO activities in tissues during the postburn period. Treatment of rats with CAPE (10 mol/kg) significantly elevated the decreased SOD and CAT activities, while it decreased MDA levels and MPO as well as XO activity.
The aim of this study was to assess the molecular basis of renal Na,K-ATPase disturbances in response to NO-deficient hypertension induced in rats by NO-synthase inhibition with 40 mg/kg/day NG-nitro-L-arginine methyl ester (L-NAME) for four weeks. After 4-week administration of L-NAME, the systolic blood pressure (SBP) increased by 30 %. Three weeks after terminating the treatment, SBP recovered to control value. When activating the Na,K-ATPase with its substrate ATP, a 36 % increase in Km and 29 % decrease in Vmax values were observed in NO-deficient rats. During activation with Na+, the Vmax was decreased by 20 % and the KNa was increased by 111 %, indicating a profound decrease in the affinity of the Na+-binding site in NO-deficient rats. After spontaneous recovery from hypertension, the Vmax remained at the level as in hypertension for both types of enzyme activation. However, in the presence of lower concentrations of substrate which are of physiological relevance an improvement of the enzyme activity was observed as documented by return of Km for ATP to control value. The KNa value for Na+ was decreased by 27 % as compared to hypertension, but still exceeded the corresponding value in the control group by 55 % thus resulting in a partial restoration of Na+ affinity of Na,K-ATPase which was depressed as a consequence of NO-dependent hypertension., N. Vrbjar, V. Javorková, O. Pecháňová., and Obsahuje bibliografii
This study evaluates bone mineral density (BMD) and trabecular bone score (TBS) in relationship with new markers of chronic kidney disease (CKD), fibroblast growth factor 23 (FGF23), and klotho. The patients in this cross-sectional study were divided as follows: group A -patients in stages G1-3; group B -patients in stages G4 - 5 according to KDIGO. Plasma levels of soluble klotho and FGF23 were determined by ELISA. Bone mineral density (BMD) and trabecular bone score (TBS) were measured. 74 patients with CKD (mean age 68.8 years) were included in the study. Higher levels of FGF23 were observed in group B (N=15) compared to group A (N=59; p=0.001) were observed. FGF23 was higher in group A compared to group B. Significant difference in TBS within the first 3 stages of CKD was observed (mean TBS in G1=1.375 vs. G2=1.340 vs. G3a=1.24; p<0.05) and negative correlation of FGF23 and TBS (R=-0.33; p=0.05) and positive correlation between klotho and TBS (R=0.419; p=0.04) was observed. This study confirmed that FGF23 and klotho are associated with TBS, but TBS reflects a decrease in kidney function only in the first 3 stages of CKD. Thus, FGF23 and klotho together with TBS are promising markers of early trabecular bone impairment in CKD., Zuzana Kužmová, Martin Kužma, Andrea Gažová, Magdaléna Kovářová, Peter Jackuliak, Zdenko Killinger, Ján Kyselovič, Juraj Payer., and Obsahuje bibliografii
Previous studies have reported a decreased incidence of delayed graft function after cadaveric transplantation with the use of lidocaine pretreatment of the donor. We evaluated the effects of lidocaine on prolonged cold ischemia and reperfusion injury in a canine model of isolated kidney perfusion (IPK). The purpose of this study was to evaluate the renal function of isolated perfused canine kidneys after 48 h of cold storage with Euro-Collins (EC) solution or EC solution plus lidocaine. Isolated perfused canine kidneys were randomized into four groups which contained six kidneys: I) cold flush with EC solution and immediately reperfused, II) cold flush with EC solution plus lidocaine and immediately reperfused, III) 48 h of cold storage with EC and reperfusion, IV) 48 h of cold storage with EC solution plus lidocaine and reperfusion. The measured renal functions were glomerular filtration rate, urine production, perfusate flow, urinary lactic dehydrogenase (ULDH), Na reabsorptive capacity, and tissue MDA levels. Histological examination was performed after reperfusion. The tubular functions of kidneys preserved with EC solution containing lidocaine were better when compared with the kidneys preserved with EC alone. Tubular injury marker levels (ULDH) in group IV were significantly lower than in group III and lidocaine also reduced lipid peroxidation during reperfusion. This is in agreement with the histological results. The results of the present study can be taken as evidence of the cytoprotective effect of lidocaine, which may therefore be accepted as a useful agent for kidney preservation., N. Erkasap, E. Ates, S. Erkasap, Z. Kaygisiz., and Obsahuje bibliografii