In 2 patients an active bleeding site could not be detected during selective angiography. Transarterial embolization was done in 19 patients and led to primary clinical success in 12 (63%), including 2 with grade

V parenchymal injury. In 6 of 7 cases (86%) in which primary treatment failed transarterial embolization was repeated. It resulted in clinical success in 4 of 6 patients (67%) with equal efficiency (p = 1). Three patients (16%) who could not be sufficiently treated with transarterial embolization underwent nephrectomy.

Conclusions: When conservative measures fail and clinical symptoms or a relevant hemoglobin decrease occur, transarterial embolization should be considered. Since the success rate is equally high for initial and repeat interventions, re-intervention is justified when the clinical course allows.”
“Rotenone is a mitochondrial poison that causes Adriamycin dopamine cell death and is used as a model of Parkinson’s disease in rodents. Recently, we

showed that rotenone augments currents evoked by N-methyl-D-aspartate (NMDA) by relieving voltage-dependent Mg(2+) block in rat substantia nigra compacta (SNC) dopamine neurons. Because rotenone is well known to generate reactive oxygen species (ROS), we conducted the present experiments to evaluate the role of ROS in mediating the effect of rotenone on NMDA current augmentation. Using patch pipettes MRT67307 ic50 to record whole-cell currents from SNC neurons in slices of rat brain, we found that the ability of rotenone (100 nM) to increase NMDA (3-30 mu M) current was antagonized by the antioxidant agent N-acetylcysteine (1 mM). In contrast, mercaptosuccinate (1 mM), which blocks glutathione peroxidase and raises tissue levels of H(2)O(2), mimicked rotenone by augmenting inward currents evoked by NMDA. Because oxidation of dopamine can also generate ROS, we explored the role of dopamine on to this action of rotenone. We prepared dopamine-depleted midbrain slices from rats that had been pretreated with reserpine

(5 mg/kg ip) and alpha-methyl-para-tyrosine (AMPT, 250 mg/kg ip). Dopamine depletion blocked the ability of rotenone (100 nM) to increase inward current evoked by NMDA (30 mu M). Rotenone-dependent augmentation of NMDA current was also blocked by the monoamine oxidase inhibitor pargyline (100 mu M) in slices prepared from normal rats. In contrast, the dopamine precursor levodopa potentiated the action of rotenone on NMDA current. These results suggest that ROS and/or dopamine oxidation products mediate the ability of rotenone to potentiate NMDA currents. Because excessive NMDA receptor stimulation can produce excitotoxicity, our results suggest that oxidative metabolism of dopamine might facilitate the neurotoxicity of rotenone. Published by Elsevier Ltd on behalf of IBRO.