Important interaction between urethral taste bud-like structures and Onuf's nucleus following spinal subarachnoid hemorrhage: A hypothesis for the mechanism of dysorgasmia / Interacción importante entre las estructras de tipo papila gustativa de la uretra y el núcleo de Onuf tras hemorragia subaracnoidea espinal: una hipótesis para el mecanismo de la disorgasmia

Background: We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not.Methods: The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm3, for the SHAM, and .7cm3 homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm3 and the results analyzed statistically.Results: The mean degenerated neuron densities of taste bud-like structures, Onuf's nucleus and pudendal ganglia were estimated as 2±1/mm3, 5±1/mm3, 6±2/mm3 in GI; 12±4/mm3, 35±9/mm3, 188±31/mm3, in GII and 41±8/mm3, 215±37/mm3, 1321±78/mm3, in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p<.0001). (AU)

Antecedentes: Hemos postulado previamente que la sensación orgásmica puede producirse a través de las recientemente descubiertas estructuras de tipo papila gustativa de los genitales. La interacción entre el nervio pudendo y el núcleo de Onuf puede ser importante para desarrollar información orgásmica. El objetivo del estudio fue estudiar si el daño isquémico a la red núcleo-ganglios pudendos de Onuf tras una hemorragia subaracnoidea espinal (HSA) puede causar o no una degeneración de las estructuras de tipo papila gustativa.Métodos: El estudio fue realizado en 22 conejos fértiles que se dividieron en 3 grupos: control (GI; n=5), placebo (GII; n=5) y de etudio (GIII; n=12). Se inyectaron 0,7cc de solución isotónica a los miembros del grupo placebo, y 0,7cc de sangre homóloga en los espacios subaracnoideos espinales a nivel de S2, al grupo de estudio. Al cabo de 2 semanas se examinaron histopatológicamente el núcleo de Onuf, los ganglios pudendos y las estructuras de tipo papila gustativa de la uretra. Se calcularon por mm3 las densidades de las neuronas degeneradas del núcleo de Onuf, los ganglios pudendos y las estructuras atróficas de tipo papila gustativa, analizándose estadísticamente los resultados.Resultados: Las densidades medias de las neuronas degeneradas de las estructuras de tipo papila gustativa, el núcleo de Onuf y los ganglios pudendos se calcularon como 2±1, 5±1, 6±2/mm3 en GI; 12±4, 35±9, 188±31 en GII y 41±8, 215±37, 1321±78/mm3, en GIII. La neurodegeneración inducida de HSA en el núcleo de Onuf, los ganglios pudendos y la atrofia de las papilas gustativas fue significativamente diferente entre los grupos GI/GII (p<0,005); GII/GIII (p<0,0005) y GI/GIII (p<0,0001). (AU)

New Histopathologic Evidence for the Parasympathetic Innervation of the Kidney and the Mechanism of Hypertension Following Subarachnoid Hemorrhage.

BACKGROUND: The Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). METHODS: A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. RESULTS: Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. The mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 ±â€Š2.0 mm, 1.87 ±â€Š0.19; 65.0 ±â€Š12.0 mm, 1.91 ±â€Š0.34; and 986.0 ±â€Š112.0 mm, 2.32 ±â€Š0.89, consecutively. Blood pressure was measured as 94.0 ±â€Š10.0 mmHg in control group, 102.0 ±â€Š12.0 mmHg in SHAM; 112.0 ±â€Š14.0 mmHg in middle (n = 9); and >122.0 ±â€Š10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). CONCLUSION: The degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.