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El núcleo del tracto solitario comisural (NTSc) es el centro de relevo de las fibras aferentes procedentes de los baro y quimiorreceptores carotídeos, por lo que modula la presión arterial y la glucemia ante los estímulos en dichos receptores. La estimulación anóxica con cianuro de sodio (NaCN) en los cuerpos carotídeos produce una respuesta hiperglucemiante. La somatostatina (SS) inhibe la secreción de la hormona del crecimiento y del glucagón lo que produce un efecto hipoglucemiante. La SS y sus receptores en el NTS tienen un efecto inhibidor. Se postula que la somatostatina modula la respuesta hiperglucemiante después de la estimulación de los quimiorreceptores carotídeos (QRC) con NaCN. En este trabajo, la infunsión de SS en el NTSc 4 min antes del estímulo anóxico de los QRC, disminuyó el reflejo hiperglucemiante y la retención de glucosa cerebral a los 10 min del estímulo anóxico. Se concluye que la SS en el NTSc modula la respuesta hiperglucemiante y la retención de glucosa cerebral post-estimulación anóxica de los cuerpos carotídeos en ratas.The commissural nucleus of the solitary tract (NTSc) is the relay center of the afferents fibers from the carotid baro and chemoreceptors, so that modulates blood pressure and blood sugar to stimuli in these receptors. Anoxic stimulation with sodium cyanide (NaCN) in the carotid bodies produces a hyperglycemic response. Somatostatin (SS) inhibits secretion of growth hormone and glucagon producing a hypoglycemic effect. The SS and its receptors in the NTS have an inhibitory effect. It is postulated that somatostatin modulates the hyperglycaemic response after stimulation of carotid chemoreceptors (QRC) with NaCN. In this work, the SS infusion into NTSc 4 min before the anoxic stimulation of the QRC, decreased the hyperglycemic reflex and cerebral glucose retention after 10 min of anoxic stimulus. We conclude that SS modulates the NTSc hyperglycemic response and brain glucose retention post-anoxic stimulation of the carotid bodies in rats.

Highlights: [•] Carotid chemoreceptor stimulation increases arterial glucose and Fos-ir in the cNTS. [•] NO in cNTS modulates carotid chemoreceptor hyperglycemic reflex and c-Fos expression. [•] NO signaling, and cNTS neurons activation, plays key roles in glucose homeostasis. [ABSTRACT FROM AUTHOR]

The concentrations of glucose and insulin were determined with high precision at half minute intervals in arterial and deep forearm vein blood after a bolus injection of glucose (4 g), followed by a constant i. v. infusion (200 mg/min), in four healthy subjects. The values for the deep vein were corrected for the transit time, which was determined by injection of Cardio-green. Arterial glucose peaked at the end of the bolus injection, venous glucose 1 1/2 min later. Arterial insulin reached its maximum later than glucose, after 2 1/2-4 min. The venous insulin reached its maximum later and was much lower than the arterial level, in two cases only around 50% of the arterial concentration. It is concluded that early after glucose administration there is a considerable extraction of both glucose and insulin by the forearm. Since the insulin extraction was quite variable venous insulin concentrations cannot be used for the assessment of early insulin response to glucose. [ABSTRACT FROM AUTHOR]