BackgroundSmokers undergoing surgery are at a higher risk of complications than non-smokers. Preoperative evaluation by an anesthesiologist could provide an excellent opportunity to promote smoking cessation. Previous surveys of anesthesiologists have found that self-reported smoking cessation counseling rates have room for improvement, but no study has surveyed patients to obtain more accurate estimates.MethodsA single-center study was conducted from January 2010 to June 2010 in a tertiary teaching hospital. A telephone survey was conducted, which included all adult cigarette smokers who visited the preoperative anesthesia clinic. The survey recorded anesthesiologist-delivered interventions to help patients quit smoking before surgery. At the end of the study period, the self-reported smoking cessation counseling of the anesthesiologist was evaluated by questionnaire.ResultsOne thousand one hundred and sixty-five patients were evaluated, of which 217 were current smokers with a median pack-year of 15 (interquartile range 5.25–30.00) and 34% were scheduled to undergo major surgery. With regard to preoperative interventions, most anesthesiologists (85%) asked about smoking status, although only 31% advised patients about the health risks of smoking and 23% advised patients to quit before surgery. Provision of assistance to help patients quit was provided in 3% of cases. By contrast, 75% of anesthesiologists stated that they frequently or almost always advised patients about the health risks of smoking.ConclusionsThis study shows significant discrepancies between direct patient surveys of preoperative smoking cessation counseling activities by anesthesiologists and the self-reported perceptions of the anesthesiologists. Future studies are urgently needed to evaluate the provision of educational materials and other interventions to improve smoking cessation counseling rates among anesthesiologists and to narrow these discrepancies.

subacute CyA treatment even al doses not modifying GFR, may cause proximal tubule Na+ transport impairment, resulting in increased rates of distal delivery and absorption of fluid load. Renal uptake of O2 may be increased and tubule glomerular feedback should be expected to be activated. Absence of changes of GFR with furosemide is an early sign of CyA renal damage.

RESUMENPAPEL DEL TÚBULO EN LA VASOCONSTRICCIÓN RENAL INDUCIDA POR CICLOSPORINA Introducción: Ciclosporina es el primero de una familia de potentes inmunosupresores con capacidad anticalcineurínica que, sin embargo, presentan como limitación terapéutica una nefrotoxicidad que puede aparecer desde periodos tempranos. Los primeros datos funcionales sugerían la existencia de vasoconstricción renal, si bien estudios posteriores han mostrado un efecto tóxico directo de ciclosporina sobre el túbulo proximal.Materiales y Métodos: En este artículo se presenta un modelo porcino de nefrotoxicidad por ciclosporina a medio plazo, analizándose los cambios hemodinámicos intrarrenales y las funciones tubulares, así como la relación entre ambos.Resultados: Ciclosporina produce específicamente una internalización e inactivación de la Na + , K + -ATPasa basolateral del túbulo proximal, determinando el desplazamiento axial de la carga filtrada hacia regiones distales (asa de Henle), con transportes activos más intensos y no modificados por ciclosporina. El resultado es un aumento en la reabsorción fraccional distal de cloro que condiciona un estímu-lo del "feed-back" túbulo glomerular, vasoconstricción aferente pero no eferente, aumento de las resistencias renales y caída de la presión intraglomerular. Furosemida restaura parcialmente la situación basal. La consecuencia inmediata es un aumento en el consumo de O 2 por unidad de sodio trasportado. A nivel del túbulo colector no se observan cambios en la secreción de agua libre, pero la secreción de K + parece limitada, y no se corrige al aumentar la oferta distal de sodio con furosemida, ni con aldosterona, cuyos valores fueron más altos en los animales tratados con ciclosporina.Conclusión: En resumen, el efecto vasoconstrictor de ciclosporina sobre el riñón se debe en parte a una retroalimentación túbulo glomerular activada por el desplazamiento de solutos filtrados de sus sitios de reabsorción proximal a otros sitos más distales. Las dietas con alto contenido en sodio pueden aumentar el efecto deletéreo de ciclosporina sobre el filtrado glomerular.Palabras clave: Ciclosporina. Nefrotoxicidad. Furosemida. Na + , K + -ATPasa. ABSTRACT STUDY ON THE ROLE OF THE TUBULE IN RENAL VASOCONSTRICTION INDUCED BY CYCLOSPORINEIntroduction: Cyclosporine (CyA) has proved to induce cell apoptosis on cultured proximal tubule cells. However, there is no much data about the in vivo functional consequences of this injury or the long time observed CyA-induced renal vasoconstriction.Material and Methods: In a swine model of subacute CyA nephrotoxicity (10 mg/ Kg. d x 15 days), we performed a right nephrectomy, followed by left renal artery, vein and ureter catheterisation. After inducing water diuresis, three clearance periods of 15 minutes were performed before and after a furosemide 1 mg/kg infusion. Plasma and urine electrolytes, blood gas, acid excretion, plasma renin activity and aldosterone concentration, GFR, RPF, RBF, intra-renal vascular resistances, glomerular filtration pressure, distal Cl -d...