Agenesia tuboovárica unilateral y masa intraperitoneal calcificada / Unilateral tuboovarian agenesis and calcified intraperitoneal mass

El hallazgo de ausencia unilateral de ovario y trompa es extremadamente raro. Existen dos posibles etiologías: ausencia congénita o torsión subaguda, necrosis y autoamputación. Presentamos un caso en el que en el transcurso de una laparoscopia se objetiva la ausencia de anejo derecho y el hallazgo de una masa ovoidea calcificada libre intraperitoneal sin relación con otras malformaciones genitales o urológicas. Revisamos la bibliografía existente y proponemos como etiopatogenia la torsión subaguda, necrosis, autoamputación del anejo y su posterior calcificación, así como el manejo laparoscópico en el contexto de una unidad de cirugía sin ingreso (AU)

Intercepción postcoital / Postcoital interception

La intercepción postcoital se viene utilizando como medida contraceptiva secundaria de forma habitual desde hace años. La generalización de su uso podría disminuir la tasa de interrupciones de embarazos no deseados. En este trabajo se pretende revisar algunos conceptos sobre el manejo práctico de este tipo de tratamientos, incluyendo el uso de Levonorgestrel para esta indicación, recientemente introducido en nuestro país. (AU)

Modulation of kappa-opioid receptor mediated tolerance in the guinea-pig ileum by chronic co-administration of dihydropyridines.

The influence of the L-type Ca2+ channel modulators nimodipine (a Ca2+ blocker) and BAY K 8644 (a Ca2+ activator) on the expression of tolerance to the inhibitory effects of kappa- and mu-opioid agonists in the guinea-pig ileum from guinea-pigs rendered tolerant to the kappa-opioid receptor agonist U-50,488H was investigated. Tolerance to U-50,488H was induced by its administration (15 mg/kg twice a day) for 4 days. Control groups received saline at the same time schedule. Chronic infusion of guinea-pigs with nimodipine (2 micrograms/microliters/h for 7 days) or BAY K 8644 (0.5 microgram/microliters/h for 7 days), did not cause any modification of the height of contractions induced by electrical stimulation of the myenteric plexus-longitudinal muscle (MPLM) preparation from naïve guinea-pigs. The Ca2+ antagonist nimodipine increases the potency of U-50,488H (selective kappa agonist) to reduce the amplitude of neurogenic contractions of the MPLM strip in naïve animals, whereas the Ca2+ activator BAY K 8644 induced the opposite effect. However, the effect of DAMGO (selective mu agonist) was not modified in guinea-pigs infused with nimodipine or BAY K 8644. Tolerance to the inhibitory effects of both U-50,488H and DAMGO was observed following administration of U-50,488H for 4 days and was revealed as a rightward shift of the concentration-response curves for the two agonists. Chronic infusion of guinea-pigs with nimodipine concurrently with chronic U-50,488H, markedly attenuated the expression of selective tolerance to U-50,488H as well as the cross-tolerance between U-50,488H and DAMGO. By the contrary, the magnitude of tolerance to U-50,488H and to DAMGO was enhanced by concomitant infusion of BAY K 8644. The results suggest that, in the GPI, kappa-opioid receptor may be functionally linked to the dihydropyridine sensitive Ca2+ channel: The blockade of the channel increased whereas its activation reduced the potency of U-50,488H. In chronic experiments, nimodipine prevented the expression of tolerance to U-50,488H and the cross-tolerance between U-50,488H and DAMGO, whereas BAY K 8644 produced the opposite effect. These results suggest that, in the GPI, selective tolerance to kappa-agonist as well as cross-tolerance between kappa- and mu-opioid agonists would involve activation of L-type Ca2+ channels, which could indicate that intracellular Ca2+ may be the final common pathway through which myenteric neurons adapt to the chronic opioid exposure.

Effect of chronic administration of dihydropyridine Ca2+ channel ligands on sufentanil-induced tolerance to mu- and kappa-opioid agonists in the guinea pig ileum myenteric plexus.

The present investigation was aimed at elucidating if the entry of Ca2+ plays a role in the development of tolerance to mu- and kappa-opioid agonists in the guinea pig ileum myenteric plexus. For this purpose, the influence of the L-type Ca2+ channel modulators nimodipine (Ca2+ blocker) and Bay K 8644 (Ca2+ activator) on the expression of tolerance to the inhibitory effects of mu- and kappa-opioid agonists in the ileum of guinea pigs rendered tolerant to sufentanil was investigated. Chronic perfusion of guinea pigs with nimodipine (2 micrograms/microliter/h for 7 days) or Bay K 8644 (0.5 microgram/microliter/h for 7 days) did not cause any modification of the height of contractions induced by electrical stimulation of the myenteric plexus-longitudinal muscle (MPLM) strip from naive animals. Tolerance to sufentanil (a selective mu-agonist) was induced by s.c. implantation of osmotic minipumps for 7 days, which deliver at 2 micrograms/microliter/h. Control groups received saline. Tolerance to sufentanil as well as to U-50,488H (selective kappa-agonist) was observed following chronic treatment with sufentanil and was revealed as a rightward shift of the concentration-response curves. Chronic perfusion of guinea pigs with the Ca2+ antagonist nimodipine concurrently with chronic sufentanil, markedly blocked the expression of tolerance to sufentanil, as well as the cross-tolerance between sufentanil and U-50,488H. On the contrary, when guinea pigs were perfused with the Ca2+ agonist Bay K 8644 concurrently with sufentanil, it enhanced the magnitude of tolerance to both sufentanil and U-50,488H. These results suggest that, in guinea pig ileum, chronic exposure to opioids may involve the activation of L-type Ca2+ channel, which would indicate that intracellular Ca2+ may be one of the final pathways through which myenteric neurons adapt to the chronic opioid exposure.

Cross-tolerance between kappa and mu opioid agonists in the guinea pig ileum myenteric plexus.

The aim of the present investigation was to determine whether chronic activation of kappa opioid receptor induces development of tolerance of kappa (specific tolerance) and to mu (cross-tolerance) agonists in the guinea pig ileum myenteric plexus-longitudinal muscle strip. trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1- pyrrolidynyl)ciclohexyl]-benzeneacetamide (U-50,488H) a selective kappa agonist, morphine (prototype of a mu agonist) and DAMGO (a selective mu agonist) were chosen. Tolerance to the kappa agonist was induced by chronic administration of the kappa agonist (15 mg/kg i.p. twice a day for 4 days). The guinea pigs were killed on day 5. Tolerance to U-50,488H was observed after its chronic administration and was revealed as a rightward shift of the concentration-response curve. In addition, we observed a decrease in the maximum response and in the slope. Preparations from chronically U-50,488H-treated guinea pigs were also tolerant to the inhibitory effects of both the mu-selective agonist DAMGO and morphine. That is, there was cross-tolerance to the mu agonists. The development of tolerance to DAMGO and morphine was characterized by a rightward shift of the concentration-response curve, a decrease in maximum response and a decrease in the slope, although the degree of tolerance appeared to be less than that observed to U-50,488H. These data suggest that tolerance at the myenteric plexus level may be associated with a functional change in the myenteric neurons that is unrelated to the individual receptor system.

Cross-tolerance between mu- and kappa-opioid agonists in the guinea pig ileum myenteric plexus.

The present investigation was aimed at elucidating if chronic activation of mu opioid receptor induces development of tolerance to mu (specific tolerance) and kappa agonists (cross-tolerance) in the guinea pig ileum myenteric plexus-longitudinal muscle strip. Morphine (prototype of mu agonist), [D-Ala2,N-MePhe4,Gly-ol5]enkephalin (DAMGO) and sufentanil (selective mu-agonists) and U-50,488H (selective kappa agonist) were selected. Tolerance to morphine was induced by subcutaneous implantation of morphine pellets (75 mg per pellet) for 7 days. Tolerance to sufentanil was induced by subcutaneous implantation of osmotic minipumps for 7 days, which deliver at a rate of 2 micrograms/microliters/hr. Control groups received placebo pellets or minipumps of vehicle. Tolerance to morphine and DAMGO was observed after chronic treatment with morphine or sufentanil and was revealed as a rightward shift of the concentration-response curve. In addition, a decrease in maximal response was observed. Preparations from morphine-pelleted guinea pigs were also tolerant to the kappa-selective agonist trans-(+-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidynyl)- cyclohexyl]benzeneacetamide (U-50,488H); that is, there was cross-tolerance to the kappa agonist. The development of tolerance to U-50,488H was characterized by a parallel rightward shift of the concentration-response curve, but the maximal response was unchanged. Sufentanil-tolerant tissues were also tolerant to the inhibitory effects of U-50,488H (cross-tolerance). These data indicate that alterations occur during chronic mu opioid administration that are not receptor specific and suggest that tolerance would be associated with a functional change in the myenteric neurons that is unrelated to individual receptor system.

Influence of temperature on the effects of mu-, delta- and kappa-opioid receptor agonists in the guinea-pig ileum myenteric plexus.

Electrically stimulated guinea-pig ileum myenteric plexus-longitudinal muscle was used to determine if changes in temperature alter the inhibitory effects of DAGO ([D-Ala2,N-MePhe4,Gly5-ol]enkephalin, mu-agonist), DPDPE ([D-Pen2,-Pen5] enkephalin, delta-agonist) and U-50,488H (trans-3,4-dichloro)-N-methyl-N-[2-(1- pyrrolidynyl)cyclohexyl]benzeneacetamide methane sulfonate, kappa-agonist). The potency (expressed as the concentration which produces 50% inhibition, IC50) of DAGO and DPDPE was significantly (P < 0.05) decreased at 30 degrees C (8.8 +/- 2.7 x 10(-9) and 8325.2 +/- 1070 x 10(-9) M), when compared to the potency at 37 degrees C (3.8 +/- 0.3 x 10(-9) and 6298.6 +/- 320 x 10(-9) M). Higher temperature (40 degrees C) did not modify the potency of DAGO or DPDPE compared to that at 37 degrees C. However, the potency of U-50,488H was significantly (P < 0.01) increased at 40 degrees C (0.7 +/- 0.0 x 10(-9) M) versus 37 degrees C (2.4 +/- 0.9 x 10(-9) M) or 30 degrees C (2.5 +/- 0.3 x 10(-9) M). The kappa-agonist was more potent than DAGO or DPDPE at 30 or 40 degrees C. These data demonstrate that changes in temperature can alter the potency of opioid agonists.