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INTRODUCCIÓN: En el retratamiento endodóntico, la remoción de gutapercha es esencial para lograr una adecuada limpieza y conformación del conducto. Los instrumentos D-Race/I Race y XP-endo Finisher R (FKG) son sistemas mecanizados usados para la desobturación del conducto. OBJETIVO: Comparar, ex vivo, la remoción de gutapercha del conducto radicular con el sistema D-Race/I Race, con la obtenida con el instrumento suplementario XP-endo Finisher R y xilol, en premolares. MATERIAL Y MÉTODO: Se seleccionaron 10 premolares con un solo conducto obturados con gutapercha y sellador AH26. Para la desobturación, la muestra se dividió en Grupo A: sin xilol y Grupo B: con Xilol. En ambos grupos se utilizaron los sistemas D-Race/I Race; irrigando con hipoclorito de sodio a cada cambio de instrumento. Posteriormente, se usó XP-endo Finisher R. Se tomaron tres radiografías: la primera, con la obturación del conducto; la segunda luego de usar D Race/I Race y la tercera, posteriormente a XP-endo Finisher R. Se midieron las áreas radiopacas de los conductos con el Software Image Pro-Plus v6. Los datos se evaluaron mediante análisis de varianza con medidas repetidas. En todos los casos el nivel de significación fue p

The neuronal (GlyT2) and glial (GlyT1) glycine transporters, two members of the Na(+)/Cl(-)-dependent neurotransmitter transporter superfamily, differ by many aspects, such as substrate specificity and Na(+) coupling. We have characterized under voltage clamp their reactivity toward the membrane impermeant sulfhydryl reagent [2-(trimethylammonium)-ethyl]-methanethiosulfonate (MTSET). In Xenopus oocytes expressing GlyT1b, application of MTSET reduced to the same extent the Na(+)-dependent charge movement, the glycine-evoked current, and the glycine uptake, indicating a complete inactivation of the transporters following cysteine modification. In contrast, this compound had no detectable effect on the glycine uptake and the glycine-evoked current of GlyT2a. The sensitivities to MTSET of the two transporters can be permutated by suppressing a cysteine (C62A) in the first extracellular loop (EL1) of GlyT1b and introducing one at the equivalent position in GlyT2a, either by point mutation (A223C) or by swapping the EL1 sequence (GlyT1b-EL1 and GlyT2a-EL1) resulting in AFQ <--> CYR modification. Inactivation by MTSET was five times faster in GlyT2a-A223C than in GlyT2a-EL1 or GlyT1b, suggesting that the arginine in position +2 reduced the cysteine reactivity. Protection assays indicate that EL1 cysteines are less accessible in the presence of all co-transported substrates: Na(+), Cl(-), and glycine. Application of dithioerythritol reverses the inactivation by MTSET of the sensitive transporters. Together, these results indicate that EL1 conformation differs between GlyT1b and GlyT2a and is modified by substrate binding and translocation.

A neurotransmitter transporter can potentially mediate uptake or release of substrate, and its stoichiometry is a key factor that controls the driving force and thus the neurotransmitter flux direction. We have used a combination of electrophysiology and radio-tracing techniques to evaluate the stoichiometries of two glycine transporters involved in glycinergic or glutamatergic transmission. We show that GlyT2a, a transporter present in glycinergic boutons, has a stoichiometry of 3 Na+/Cl-/glycine, which predicts effective glycine accumulation in all physiological conditions. GlyT1b, a glial transporter, has a stoichiometry of 2 Na+/Cl-/ glycine, which predicts that glycine can be exported or imported, depending on physiological conditions. GlyT1b may thus modulate glutamatergic synapses by increasing or decreasing the glycine concentration around N-methyl-D-aspartate receptors (NMDARs).

Fast inactivating Shaker H4 potassium channels and nonconducting pore mutant Shaker H4 W434F channels have been used to correlate the installation and recovery of the fast inactivation of ionic current with changes in the kinetics of gating current known as "charge immobilization" (Armstrong, C.M., and F. Bezanilla. 1977. J. Gen. Physiol. 70:567-590.). Shaker H4 W434F gating currents are very similar to those of the conducting clone recorded in potassium-free solutions. This mutant channel allows the recording of the total gating charge return, even when returning from potentials that would largely inactivate conducting channels. As the depolarizing potential increased, the OFF gating currents decay phase at -90 mV return potential changed from a single fast component to at least two components, the slower requiring approximately 200 ms for a full charge return. The charge immobilization onset and the ionic current decay have an identical time course. The recoveries of gating current (Shaker H4 W434F) and ionic current (Shaker H4) in 2 mM external potassium have at least two components. Both recoveries are similar at -120 and -90 mV. In contrast, at higher potentials (-70 and -50 mV), the gating charge recovers significantly more slowly than the ionic current. A model with a single inactivated state cannot account for all our data, which strongly support the existence of "parallel" inactivated states. In this model, a fraction of the charge can be recovered upon repolarization while the channel pore is occupied by the NH2-terminus region.

External Ba2+ speeds the OFF gating currents (IgOFF) of Shaker K+ channels but only upon repolarization from potentials that are expected to open the channel pore. To study this effect we used a nonconducting and noninactivating mutant of the Shaker K+ channel, ShH4-IR (W434F). External Ba2+ slightly decreases the quantity of ON gating charge (QON) upon depolarization to potentials near -30 mV but has little effect on the quantity of charge upon stepping to more hyperpolarized or depolarized potentials. More strikingly, Ba2+ significantly increases the decay rate of IgOFF upon repolarization to -90 mV from potentials positive to approximately -55 mV. For Ba2+ to have this effect, the depolarizing command must be maintained for a duration that is dependent on the depolarizing potential (> 4 ms at -30 mV and > 1 ms at 0 mV). The actions of Ba2+ on the gating current are dose-dependent (EC50 approximately 0.2 mM) and are not produced by either Ca2+ or Mg2+ (2 mM). The results suggest that Ba2+ binds to a specific site on the Shaker K+ channel that destabilizes the open conformation and thus facilitates the return of gating charge upon repolarization.

We undertook a comparative study on the effects of dobutamine and placebo on hemodynamic parameters, O2 transport (DO2), O2 consumption (VO2, and acid lactic production during peripheral arterial surgery under general anesthesia with enflurane at a constant inspiratory concentration (1.2%). This study involved 18 patients older than 65 years (9 patients allocated in the dobutamine group and 9 in the placebo group). The hemodynamic course was monitorized by means of noninvasive methods such as the aortic output measured by continuous transoesophageal echo-Doppler. After introduction of enflurane into the circuit aortic output decreased by 39% in dopamine group and 36% in placebo. Total systemic vascular resistances increased by 52% in dopamine and by 48% in placebo treatment. DO2 showed a decrease of 39% in dopamine and 38% in placebo group. There were no appreciable differences in VO2 among the two groups. Recovery of hemodynamic parameters and DO2 was only observed in the dopamine group when the drug was perfused at a rate of 4 +/- 1.2 micrograms/kg/min. Dobutamine induced a transient increase of VO2 up to 225% of the baseline value. During the postanesthetic period VO2 and blood acid lactic were significantly higher in the dopamine than in the placebo group (192%, p less than 0.01 and 33%, p less than 0.05, respectively). The course of hemodynamic parameters, DO2, VO2, and blood acid lactic of dobutamine group appear to demonstrate that dobutamine perfusion reverts myocardial depression and improves cellular perfusion during general anesthesia with enflurane.

In order to test the therapeutic action of nicergoline during peroperative arterial hypertension, an intravenous perfusion of 5 mcg/kg/mn average dose was given to 15 patients which presented a peroperative increase of Systolic Blood Pressure (SBP) greater than 30% when compared with preanaesthetic corresponding value. The haemodynamic evolution was monitored, using non invasive method (except for central venous pressure, CVP). Particularly Aortic Blood Flow (ASF) was measured by ultrasonic means using specially designed intraoesophageal probe and flow meter including A-Scan and Doppler Velocity meter. SBP increased in 43% during hypertensive peak (initial level mean 129, +/- 12.6 mmHg; hypertensive peak, mean 185 +/- 16.80 mmHg; p less than 0.001). Ten minutes after the beginning of nicergoline perfusion, SBP showed a significative decrease (mean 141.4 +/- 11.20 mmHg, +9%). At the end of operation the SBP was nearly to average initial value (mean 135, +/- 11.85 mmHg; +4.5%). Diastolic Blood Pressure and Mean Blood Pressure presented similar variations. ABF decreased significatively during hypertensive peak (Initial ABF value means 3.49, +/- 0.99 l/mn, hypertensive peak ABF value means 2.68, +/- 0.54 l/mn, -25%, p less than 0.01). Nicergoline perfusion induced a partial recovery of ABF (mean 3.23 +/- 0.56 l/mn, +8%, p less than 0.05). This one was confirmed at the end of operation (mean 3.6 +/- 0.56 l/mn; -4% N.S.). Heart rate did not change significantly during monitoring period. From this results is seems that nicergoline perfusion induces a protection of hypertensive patients during peroperative decompensation.

A new non-invasive haemodynamic monitoring technique was investigated on twenty female patients submitted to gynaecological laparoscopy under general anaesthesia. Continuous aortic output was measured with an echo-Doppler oesophageal probe specially developed by the authors. Peritoneal insufflation was performed with an average of 4 +/- 0.750 l CO2 at an average insufflation rate of 0.666 l X min-1; intraperitoneal pressure increased on average by 11.57 +/- 1.60 mmHg during insufflation. Aortic output changes were related to changes in the patient's position. In initial horizontal dorsal decubitus position, average aortic output was 2.83 +/- 0.642 l X min-1. Trendelenburg position (28 +/- 2 degrees) induced a transient 9.54% increase (p less than 0.05), while a return to the horizontal position was marked by an 11.3% increase (p less than 0.01) of the aortic output. No significant change was observed during insufflation and exsufflation (-2.13 and -5.3% respectively). Mean arterial pressure rose by 16.4% after insufflation (initial values: 90 +/- 15.08 mmHg; p less than 0.01). Total vascular systemic resistances were significantly higher at the end of insufflation (2.999 +/- 376 dyn X cm X s-5; + 18.04%; p less than 0.05). Heart rate did not change significantly. Aortic output monitoring with this non-invasive, easy-to-handle technique enabled early detection of haemodynamic changes during laparoscopy. These changes frequently preceded significant blood pressure or heart rate variations.