Intracerebral stimulation of the seventh cranial nerve in the rat: effects on cerebrospinal fluid pressure

The effets of the intracerebral stimulation of the seventh cranial nerve was studied in anesthetized, artificially ventilated rats, The stimulation was carried out at the genu level by inserting a micropipette according to known stereotaxic coordinates. In 9 experiments, the cerebrospinal fluids pressure increased significantly 0.92 to 1.05 cm H2O above basal level after the stimulation of the same point on the left and right sides of the brain, without changes in mean arterial blood pressure. This response was interpreted as a sudden increase in cerebral blood volume produced by the dilatation of cerebral blood vessels. The section of the right greater superficial petrosal nerve abolished the increase in cerebrospinal fluid pressure after stimulation of the right side, while the response to stimulation of the left side was similar to the one observed in control animals. Consequently, the neurogenic vasodilation produced by intracerebral stimulation of the seventh cranial nerve in the rat seems to be mediated by a functional Chorobski-Penfield pathway running with the greater superficial petrosal nerve

Endothelial role in alpha-adrenergic induced vasoconstriction in rat thoracic aorta

The effects of endothelial removal on vasoconstrictor responses elicited by phenilephrine (alpha-1 agonist), clonidine (alpha-2 agonist) and norepinephrine (alpha-1 and alpha-2 agomist) were studied on isolated rat thoracic aorta. The removal of vascular endothelium resulted in a significant reduction of the effective concentration 50% (EC 50) for norepinephrine from 9.12 x 10-9 M, without changes in the maximal response, which remained equal to the maximal concentration elicited by a solution of 70 mM K. Similary, the EC 50 for phenilephrine was significantly reduced from 2.19 x 10-8 M to 9.12 x 10-9 M, without changes in the maximal response. On the other hand, the maximal response to clonidine increased significantly in the arteries without andothelium from 5.5% to 35% of the maximal response to K, and the 50 was significantly reduced from 1.82 x 10-7 M to 1.10 x 10-7 . These result suggest that the presence of vascular endothelium increases the vasoconstriction induced by adrenergic, and that its action is predominantly manifested on alpha-2 dependent contractions, probably because these responses are highly dependent on extracellular calcium influx, which is modulated by the activity of the endothelial derived relaxing factor (EDRF)

Effects of conjugated estrogens on the vascular reactivity of the mesenteric vascular bed of the rat

Se estudiaron los efectos de los estrógenos conjugados sobre la reactividad vascular a KCl, epinefrina y norepinefrina en la red vascular mesentérica aislada de ratas macho, perfundida a flujo constante, donde los cambios en la presión media de perfusión reflejan cambios en la resistencia vascular. La perfusión con estrógenos conjugados (100 microng/ml) durante 45 minutos produce una reducción significativa del aumento de resistencia vascular inducido por epinefrina y norepinefrina, sin afectar la respuesta a KCl. Las curvas dosis-respuesta a la norepinefrina obtenidas durante la perfusión de 25 y 100 microng/ml de estrógenos muestran una desviación dosis-dependiente a la derecha, con reducción de la pendiente y de la respuesta máxima. Después de la perfusión con estrógenos, las curvas tienden a regresar a los valores controles sin modificaciones de la DE50. Se postula una acción de antagonismo no competitivo reversible de los estrógenos conjugados sobre los receptores adrenérgicos en esta preparación

Vascular effects of endotoxin in the rat.

La inyeccion endovenosa de endotoxina (5 mg/kg) en ratas produjo una hipotension arterial acompanada de un aumento transitorio en la resistencia vascular del miembro posterior denervado y perfundido con sangre a flujo constante. La perfusion del miembro con solucion de Krebs-Henseleit o con plasma de rata incubados con endotoxina no produjo variaciones significativas en la resistencia vascular. La perfusion con sangre completa incubada con endotoxina incremento significativamente la resistencia vascular. La interaccion de la endotoxina con un componente celular de la sangre fue investigada utilizando una preparacion de red vascular mesenterica de rata, aislada y perfundida a flujo constante. Se demostro que la endotoxina interactua con las plaquetas, produciendo agregacion y lisis, con posible liberacion de sustancias vasoactivas que incrementan en forma transitoria la resistencia vascular. Este efecto puede ser un factor de importancia en los mecanismos hemodinamicos que producen la fase hipotensiva inicial despues de la inyeccion endovenosa de endotoxina