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Nditions. One hour later, 50 mg/kg of L-NAME was injected IP.
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Nditions. One hour later, 50 mg/kg of L-NAME was injected IP. Two additional CSD waves were induced one and two hours after L-NAME injection. The experiment and the monitoring period continued 1.5 hours after the last initiation of CSD wave. In another group of rats (n=11) 4 CSD waves were induced with an interval of one hour between each wave under normoxic conditions. This group of rats was considered as a control group for hypoxia and L-NAME groups. Ischemia Protocol Partial ischemia (n=9) was induced by permanent bilateral carotid artery occlusion. Twenty-four hours later the rats were reanesthetized and underwent [https://dx.doi.org/10.1089/jir.2010.0108 jir.2010.0108] preparation for the experiment and monitoring. Sham rats (n=8) underwent the same experimental [http://www.medchemexpress.com/GLPG0187.html GLPG0187 custom synthesis] procedure without carotids occlusion. CSD waves were induced (by epidural application of 0.5-2M KCl solution, using the lowest concentration that induced CSD), in lightly anesthetized rats in the partial ischemic and in sham rats. Data Acquisition The NADH fluorescence, reflected light, CBF, [K +]e and DC steady potential that were monitored by the MPA system were recorded continuously, simultaneously and in real time using Codas software for a 16-channel computerized acquisition and storage system (DATAQ Instruments, MN, USA). Data Analysis and Calculation Various time and amplitude values were calculated during the CSD wave cycles. In the present article we will present: The maximum (VTmax) and minimum (VTmin) amplitude values, as well as wave duration that were calculated for every parameter recorded by the MPA system. Wave duration was calculated as the time it took the CSD wave toThe Open Neurology Journal, 2012, VolumeSonn and MayevskyFig. (2). Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R ?reflectance, NADH ?mitochondrial NADH redox state; CBF?cerebral blood flow; K+e ?corrected extracellular potassium concentration; DC ?DC steady potential. The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneous minimum and maximum responses in CBF and NADH during CSD.propagate from the beginning of the changes in the measured parameters, (as a result of KCl application), until the wave's initial recovery. Base line levels of reflectance, NADH and CBF were determined in steady state conditions prior to CSD wave initiation and were defined as 100 . The baseline DC potential levels were determined as Zero mV under the same conditions. Values at maximum - the maximum level of the increased amplitudes; Minimum - the minimum level of the decreased amplitudes (during CSD wave propagation) were calculated relative to their levels before the CSD episode. The mV output values of the ion selective K+ electrode were transformed to mM values to provide the [K+]e. Statistical Analysis Statistical analysis was performed by using the SPSS software version 15.0. Student's paired and unpaired t-test was performed to evaluate the changes in amplitude values during CSD, [https://dx.doi.org/10.4278/ajhp.120120-QUAN-57 ajhp.120120-QUAN-57] between control and during the three pathological conditions tested. Results are presented as Mean ?SEM and a value of p

Версия 14:21, 2 апреля 2018

Nditions. One hour later, 50 mg/kg of L-NAME was injected IP. Nditions. One hour later, 50 mg/kg of L-NAME was injected IP. Two additional CSD waves were induced one and two hours after L-NAME injection. The experiment and the monitoring period continued 1.5 hours after the last initiation of CSD wave. In another group of rats (n=11) 4 CSD waves were induced with an interval of one hour between each wave under normoxic conditions. This group of rats was considered as a control group for hypoxia and L-NAME groups. Ischemia Protocol Partial ischemia (n=9) was induced by permanent bilateral carotid artery occlusion. Twenty-four hours later the rats were reanesthetized and underwent jir.2010.0108 preparation for the experiment and monitoring. Sham rats (n=8) underwent the same experimental GLPG0187 custom synthesis procedure without carotids occlusion. CSD waves were induced (by epidural application of 0.5-2M KCl solution, using the lowest concentration that induced CSD), in lightly anesthetized rats in the partial ischemic and in sham rats. Data Acquisition The NADH fluorescence, reflected light, CBF, [K +]e and DC steady potential that were monitored by the MPA system were recorded continuously, simultaneously and in real time using Codas software for a 16-channel computerized acquisition and storage system (DATAQ Instruments, MN, USA). Data Analysis and Calculation Various time and amplitude values were calculated during the CSD wave cycles. In the present article we will present: The maximum (VTmax) and minimum (VTmin) amplitude values, as well as wave duration that were calculated for every parameter recorded by the MPA system. Wave duration was calculated as the time it took the CSD wave toThe Open Neurology Journal, 2012, VolumeSonn and MayevskyFig. (2). Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R ?reflectance, NADH ?mitochondrial NADH redox state; CBF?cerebral blood flow; K+e ?corrected extracellular potassium concentration; DC ?DC steady potential. The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneous minimum and maximum responses in CBF and NADH during CSD.propagate from the beginning of the changes in the measured parameters, (as a result of KCl application), until the wave's initial recovery. Base line levels of reflectance, NADH and CBF were determined in steady state conditions prior to CSD wave initiation and were defined as 100 . The baseline DC potential levels were determined as Zero mV under the same conditions. Values at maximum - the maximum level of the increased amplitudes; Minimum - the minimum level of the decreased amplitudes (during CSD wave propagation) were calculated relative to their levels before the CSD episode. The mV output values of the ion selective K+ electrode were transformed to mM values to provide the [K+]e. Statistical Analysis Statistical analysis was performed by using the SPSS software version 15.0. Student's paired and unpaired t-test was performed to evaluate the changes in amplitude values during CSD, ajhp.120120-QUAN-57 between control and during the three pathological conditions tested. Results are presented as Mean ?SEM and a value of p