Functional magnetic resonance signal changes in neural structures to baroreceptor reflex activation

Functional magnetic resonance signal changes in neural structures to baroreceptor reflex activation
复制标题

DOI:
10.1152/japplphysiol.00852.2003
复制
发表时间:
2004-02-01
影响因子:
3.3
通讯作者:
Harper, RM
Harper, RM
中科院分区:
医学2区
文献类型:
--
作者:
Henderson, LA;Richard, CA;Harper, RM

文献摘要

被引文献

相似文献

外源性动脉压操作的神经反应序列仍不清楚,特别是髓外部位。我们使用功能性磁共振成像程序,以可视化在升压(苯肾上腺素)和降压(硝普钠)的挑战,在七个异氟烷麻醉的成年猫的神经反应。抑制剂的挑战产生的信号强度下降,在多个心血管相关的网站在延髓,包括孤束核,尾侧和头端腹外侧延髓。信号降低也出现在小脑蚓部,下橄榄,背外侧脑桥,和右小脑。嘴部部位,如杏仁核和下丘脑,随着动脉压下降信号强度增加。相比之下,动脉压升高引起延髓区、脑桥背外侧和右丘脑信号增加较小,下丘脑区域信号下降,小脑深部区域无变化。对升压和降压刺激的反应通常是偏侧的。在一个动物亚组中,去压力神经支配导致血压的上升和福尔斯下降,与药理学挑战但不同的区域神经反应所导致的血压上升和下降相当,表明区域信号强度反应并非来自全局灌注效应,而是来自中枢机制的压力感受器介导。研究结果表明,广泛的偏侧分布的神经网站响应血压操纵。神经反应的分布和时间过程遵循与早期和晚期代偿反应相关的模式。
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.