Functional magnetic resonance signal changes in neural structures to baroreceptor reflex activation.
J Appl Physiol (1985)
; 96(2): 693-703, 2004 Feb.
Article
en En
| MEDLINE
| ID: mdl-14565965
ABSTRACT
The sequence of neural responses to exogenous arterial pressure manipulation remains unclear, especially for extramedullary sites. We used functional magnetic resonance imaging procedures to visualize neural responses during pressor (phenylephrine) and depressor (sodium nitroprusside) challenges in seven isoflurane-anesthetized adult cats. Depressor challenges produced signal-intensity declines in multiple cardiovascular-related sites in the medulla, including the nucleus tractus solitarius, and caudal and rostral ventrolateral medulla. Signal decreases also emerged in the cerebellar vermis, inferior olive, dorsolateral pons, and right insula. Rostral sites, such as the amygdala and hypothalamus, increased signal intensity as arterial pressure declined. In contrast, arterial pressure elevation elicited smaller signal increases in medullary regions, the dorsolateral pons, and the right insula and signal declines in regions of the hypothalamus, with no change in deep cerebellar areas. Responses to both pressor and depressor challenges were typically lateralized. In a subset of animals, barodenervation resulted in rises and falls of blood pressure that were comparable to these resulting from the pharmacological challenges but different regional neural responses, indicating that the regional signal intensity responses did not derive from global perfusion effects but from baroreceptor mediation of central mechanisms. The findings demonstrate widespread lateralized distribution of neural sites responsive to blood pressure manipulation. The distribution and time course of neural responses follow patterns associated with early and late compensatory reactions.
Buscar en Google
Bases de datos:
MEDLINE
Asunto principal:
Presión Sanguínea
/
Imagen por Resonancia Magnética
/
Núcleo Solitario
/
Barorreflejo
Idioma:
En
Revista:
J Appl Physiol (1985)
Año:
2004
Tipo del documento:
Article
País de afiliación:
Estados Unidos