RESUMO

BACKGROUND AND OBJECTIVES: Fentanyl addition is a common practice when administering spinal anesthesia. Intrathecal fentanyl has been associated to increased postoperative pain and increase morphine consumption, but considered to be related to acute opioid tolerance. This prospective, randomized, blind study evaluates the effect of intrathecal fentanyl in the development of secondary hyperalgesia, measured with Von Frey filaments, in patients undergoing anterior cruciate ligament repair. METHODS: 46 patients having anterior cruciate ligament repair, received intrathecal hyperbaric bupivacaine 13.5 mg with fentanyl 20 mcg or no fentanyl addition. Light touch pain threshold was measured with von Frey filaments before anesthesia, at 6 and 24 hours post anesthesia in the non-operated thigh and in the forearm. Visual analogue pain scores and morphine consumption were also measured at the same time. RESULTS: Baseline thresholds to mechanical stimuli were similar in both groups. In the forearm, analysis showed a decreased threshold for the non-fentanyl group at 24 h p = 0.036. In the lower extremity, control and treatment group showed lower thresholds (secondary hyperalgesia) p = 0.002 but no difference between them p = 0.795. VAS score and morphine consumption did not differ among groups. CONCLUSIONS: Spinal fentanyl added to hyperbaric bupivacaine showed no evidence of an augmented state of hyperalgesia after ACL repair, neither by pain threshold modification nor clinical outcomes. On the contrary, at 24 h, fentanyl may have a protective effect at levels above the spinal block.

ANTECEDENTES Y OBJETIVOS: El uso de fentanilo es una práctica común en la administración de anestesia espinal. Su aplicación se ha asociado a un aumento del dolor post operatorio y a un aumento en el uso de morfina; por otro lado, se ha vinculado a una tolerancia aguda a opioides. El siguiente estudio prospectivo, randomizado y ciego, evalúa los efectos del fentanilo intratecal en la aparición de hiperalgesia secundaria, medida a través de filamentos Von Frey, en pacientes operados de ligamento cruzado anterior. METODOLOGÍA: Se incluyeron a 46 pacientes operados de ligamento cruzado anterior (LCA) con una dosis intratecal de bupivacaína hiperbárica de 13,5 mg; con y sin la adición de fentanilo de 20 mcg. Se midió el umbral del dolor mecánico, a través de filamentos Von Frey, antes de la anestesia, a las 6 y 24 horas postanestesia en el muslo no operado y en el antebrazo. Al mismo tiempo, se midió la puntuación del dolor en la escala verbal numérica (EVN) y el consumo de morfina. RESULTADOS: Los umbrales basales ante la estimulación mecánica resultaron similares en ambos grupos. En el antebrazo, el análisis mostró una disminución del umbral en el grupo de pacientes sin fentanilo, a las 24 h, p = 0,036 comparado con uso de fentanilo. En el muslo, el grupo control y tratamiento mostró umbrales más bajos (hiperalgesia secundaria) p = 0,002; no obstante, no se mostraron diferencias entre ellos. No se mostraron diferencias entre las puntuaciones de la EVN y el consumo de morfina en los dos grupos. CONCLUSIÓN: No hay evidencia que la adición de fentanilo espinal, a la dosis de bupivacaína hiperbárica, haya contribuido a un aumento en la hiperalgesia tras la reparación del LCA, medido por la modificación del umbral del dolor, ni en los resultados clínicos. Al contrario a las 24 h fentanilo puede tener un efecto protector de la hiperalgesia secundaria sobre el nivel del bloqueo espinal.

Assuntos

RESUMO

BACKGROUND: A variety of stimuli are involved in the pathogenesis of parathyroid gland hyperplasia in renal failure. Recently, it was shown that blocking the signal from the endothelin-1 (ET-1) receptor (ET(A)R/ET(B)R) by a non-selective receptor antagonist, bosentan, reduced parathyroid cell proliferation, parathyroid gland hyperplasia and parathyroid hormone (PTH) levels in normal rats on a calcium deficient diet. Our goal was to determine whether in 5/6 nephrectomized (NPX) rats with developing or established hyperparathyroidism, the endothelin receptor blocker, bosentan, reduced the increase in parathyroid cell proliferation, parathyroid gland hyperplasia and PTH values. METHODS: High (HPD, 1.2%) or normal phosphorus diets (PD) (NPD, 0.6%) were given to 5/6 NPX rats for 15 days (NPX(15)). In each dietary group, one-half the rats were given bosentan (B) i.p. 100 mg/kg/day. The four groups of rats were: (1) NPX(15)-1.2% P; (2) NPX(15)-1.2% P+B; (3) NPX(15)-0.6% P; and (4) NPX(15)-0.6% P+B. In a second study in which hyperparathyroidism was already established in 5/6 NPX rats fed a HPD for 15 days, rats were divided into two groups in which one group was maintained on a HPD and the other group was changed to very low PD (VLPD, <0.05%) for an additional 15 days. In each dietary group, one-half the rats were given bosentan i.p. 100 mg/kg-day. The four groups of rats were: (1) NPX(30)-1.2% P; (2) NPX(30)-1.2% P+B; (3) NPX(30)-0.05% P and (4) NPX(30)-0.05% P+B. Parathyroid cell proliferation was measured by proliferating cell nuclear antigen (PCNA) staining and ET-1 expression by immunohistochemical techniques. RESULTS: In the study of developing hyperparathyroidism, bosentan reduced ET-1 expression in the parathyroid glands of rats on the NPD and HPD (P<0.05). But only in rats on the NPD did bosentan result in a reduced increase in parathyroid gland weight (P<0.05). In the study of established hyperparathyroidism, in which 5/6 NPX rats were given a HPD for 15 days, bosentan started on day 15 reduced (P<0.05) ET-1 expression in rats maintained for 15 additional days on the HPD or the VLPD. On the VLPD, parathyroid gland weight was less (P<0.05) than that in rats on the HPD sacrificed at 15 or 30 days. Bosentan did not reduce parathyroid cell proliferation or parathyroid gland weight in rats maintained on the HPD or further reduce these parameters beyond that obtained with dietary phosphorus restriction. PTH values were lowest in the VLPD group, intermediate in the NPD group, and highest in the HPD group, but in none of the three groups did bosentan decrease PTH values. CONCLUSIONS: In azotemic rats with developing hyperparathyroidism, bosentan resulted in a reduced increase in parathyroid gland weight when dietary phosphorus content was normal. Despite a reduction in ET-1 expression in rats on a HPD with developing or established hyperparathyroidism, bosentan did not reduce the increase in parathyroid cell proliferation, parathyroid gland growth or PTH values. Thus, ET-1 blockade with bosentan did not prevent parathyroid gland growth in the azotemic rat.

Assuntos