Efecto de Lachesis trigonocephalus sobre dopamina cerebral en la rata / Lachesis trigonocephalus effect on dopamine in the rat brain

La dopamina (DA) estimula el factor liberador de hormona luteinizante (LHR), incrementa la hormona luteinizante (LH) e induce ovulación. El precursor inmediato, la L-dopa, ha sido usado para inducir la ovulación y en el síndrome amenorrea-galactorrea, pero esta droga produce varios efectos indeseables. Por esta razón pareció conveniente investigar drogas capaces de elevar la DA cerebral con menos efectos colaterales. La acción del veneno de la serpiente Lachesis trigonocephalus sobre la DA cerebral fue estudiada en ratas Wistar. Treinta y nueve animales recibieron el veneno a una dinamización de 1 x 10-24 = 12CH en etanol al 22.5%. La droga fue administrada per os con un catéter a la dosis de 0.25 ml, con intervalos de 8 horas, durante 10 días. Treinta y tres ratas sirvieron como controles y recibieron la misma dosis de etanol sin la droga. El grupo control mostró un nivel medio de 998 ± 43 ng/g (X ± SE) y los animales que recibieron la droga 1136 ± 57 ng/g (P < 0.05). La concentración de noradrenalina (NA) fue de 528 ± 29 ng/g en el grupo control y de 452 ± 16 ng/g en el grupo que recibió Lachesis (P < 0.025). Los niveles de adrenalina no mostraron cambios significativos con la droga...

Dopamine (DA) stimulates hormone luteinizing liberator (LHR), increases hormone luteinizer (LH) and induces ovulation. L-Dopa, its immediate precursor, has been used to induce ovulation and in the amenorrhea-galactorrhea syndrome, but this drug produces several undesirable effects. It was therefore considered convenient to investigate drugs which can raise Brain DA with less side effects. The effect of Lachesis trigonocephalus snake poison was studied in rats. Thirty nine animals received the venom at a 1 x 10-24 dynamization (Lachesis trig. 12CH), in ethanol at 22.5%. The drug was administered per os through a catheter on a 0.25 ml dose, at 8 hour intervals during 10 days. Thirty three rats were used as controls and received the same dosage of ethanol without the drug. The control batch gave a mean level of 998 ± 29 ng/g (X ± SE) and animals which received the drug showed 1136 ± 57 ng/g (P < 0.025). The concentration of noradrenaline (NA) was 528 ± 29 ng/g in the group which received Lachesis trig. 12CH (P < 0.025). No significant variations of adrenaline levels were apparent with the drug...

Serum S100B Protein Levels in Patients with Panic Disorder: Effect of Treatment with Selective Serotonine Reuptake Inhibitors

OBJECTIVE: Altered serum S100B protein levels have been shown in several psychiatric disorders. Our aim was to investigate whether plasma S100B is different in patients with panic disorder (PD) when compared with controls. Our second aim was to investigate whether treatment with SSRIs have an effect on S100B levels in patients with PD. METHODS: The sample included 32 patients diagnosed with PD (21 women, 11 men) per DSM-IV criteria and 21 healthy controls (11 women, 10 men). S100B levels were measured with BioVendor Human S100B ELISA (Enzyme Linked Immunosorbent Assay) kit. RESULTS: 14 patients were not on drug treatment (43.8%) while 18 patients were taking various SSRIs. Median S100B value was 151.7 pg/mL (minimum-maximum: 120.4-164.7 pg/mL) in the control group, 147.4 pg/mL (minimum-maximum: 138.8-154.1 pg/mL) in the drug free group and 153.0 pg/mL (minimum-maximum: 137.9-164.7 pg/mL) in the treatment group. Kruskal-Wallis analysis showed a significant diffrerence among the three groups (z=9.9, df=2, p=0.007). Follow up Mann-Whitney-U tests indicated that while the control and the patients with treatment were not significantly different (z=-0.05, p=0.96), there were significant differences between the control group and untreated patients (z=-2.6, p=0.009) and treated and untreated patients (z=-3.0, p=0.003). CONCLUSION: Our results suggested that, serum S100B protein level might be decreased in untreated PD patients and that patients who were treated with SSRIs had similar S100B level to healthy controls.

Síndrome serotoninérgico / Serotonin syndrome

El síndrome serotoninérgico (SS) se caracteriza por la presencia de disfunción autonómica, deterioro neuromuscular y alteraciones en el estado mental. El diagnóstico es clínico y por laboratorio. El tratamiento es mediante medidas de apoyo a base de líquidos, hipotermia, benzodiacepinas y, cuando lo amerite, intubación y ventilación mecánica. El pilar de la intervención farmacológica es ciproheptadina, un antagonista central H1, con un antagonismo periférico 5-HT2A. El medicamento disponible sólo se puede administrar por vía oral, por lo que en enfermos críticos debe administrarse a través de sonda nasoyeyunal. El objetivo de este trabajo es presentar un caso de SS y revisar la literatura al respecto.

The serotonin syndrome (SS) is characterized by a spectrum of signs characterized by autonomic dysfunction, neuromuscular impairment, and alterations in mental status. The diagnosis of the serotonin syndrome is clinical and by laboratory evaluation. Treatment is with active cooling and benzodiazepines to control agitation, and intubation, especially in patients with severe hyperthermia and delirium. The mainstay of pharmacologic intervention is cyproheptadine, a centrally acting H1-antagonist, with a prominent peripheral 5-HT2A antagonism. The drug is only available orally, and if the patient is unable to swallow, the drug should be administered nasogastrically. The objective of this paper is report a case of Serotonin Syndrome and review the literature related to this disease.