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对未麻醉的上丘去大脑大鼠孤束核微量注射谷氨酸的心血管反应。

Cardiovascular responses to microinjections of glutamate into the nucleus tractus solitarii of unanesthetized supracollicular decerebrate rats.

作者信息

Dhruva A, Bhatnagar T, Sapru H N

机构信息

Section of Neurological Surgery, MSB H-586, New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103-2757, USA.

出版信息

Brain Res. 1998 Aug 10;801(1-2):88-100. doi: 10.1016/s0006-8993(98)00550-2.

Abstract

In anesthetized rats, microinjections of excitatory amino acids (EAAs) into the nucleus tractus solitarii (nTS), in a region located immediately rostral to the calamus scriptorius (CS), have been generally reported to elicit depressor and bradycardic responses. On the other hand, in conscious freely moving rats, similar microinjections have been reported to elicit pressor and bradycardic responses. These divergent results have been attributed to the effect of anesthetics. A reinvestigation of the effects of EAAs into the nTS in unanesthetized animals became necessary in order to resolve this controversy. The microinjection technique used in freely moving conscious rats suffers from several technical limitations; for example, microinjections cannot be delivered stereotaxically. In order to avoid these limitations, the present experiments were carried out in unanesthetized supracollicular decerebrate rats. A systematic mapping of nTS in these rats, using microinjections of the solutions of EAAs in artificial cerebrospinal (aCSF) fluid, confirmed that depressor and bradycardic responses are elicited from all the sites in the nTS extending from the CS to a level about 1 mm rostral to it. Pressor responses were elicited by microinjections of l-glutamate (l-Glu) only from the chemoreceptor projection site (a region of the commissural subnucleus, 0.1-0.5 mm caudal to the CS, 0-0.5 mm lateral to the midline and 0.4-0.5 mm deep from the medullary surface). The pressor responses elicited from the aforementioned site were accompanied with bradycardia; this response may be due to diffusion of l-Glu to the dorsal motor nucleus of vagus because the bradycardia disappeared when the depth of the microinjection was reduced to 0.3, instead of 0.5 mm, from the dorsal medullary surface. When urethane was administered intravenously in unanesthetized decerebrate rats, the responses to microinjections of l-Glu remained unchanged, i.e., depressor and bradycardic responses were elicited from all the sites in the nTS extending from the CS to a level about 1 mm rostral to it and pressor and tachycardic responses were elicited from the chemoreceptor projection site. These observations indicated that there is no anesthetic-induced qualitative alteration of the cardiovascular responses to microinjections of EAAs into the nTS.

摘要

在麻醉大鼠中,一般报道称,将兴奋性氨基酸(EAA)微量注射到孤束核(nTS)中紧邻书写叶(CS)头侧的区域,会引发降压和心动过缓反应。另一方面,在清醒自由活动的大鼠中,类似的微量注射据报道会引发升压和心动过缓反应。这些不同的结果归因于麻醉剂的作用。为了解决这一争议,有必要对未麻醉动物中EAA注入nTS的效应进行重新研究。在清醒自由活动的大鼠中使用的微量注射技术存在一些技术限制;例如,微量注射不能通过立体定位进行。为了避免这些限制,本实验在未麻醉的上丘去大脑大鼠中进行。通过将EAA溶液微量注射到人工脑脊液(aCSF)中,对这些大鼠的nTS进行系统定位,证实从CS延伸至其头侧约1毫米水平的nTS所有部位均能引发降压和心动过缓反应。仅从化学感受器投射部位(联合亚核的一个区域,位于CS尾侧0.1 - 0.5毫米、中线外侧0 - 0.5毫米以及延髓表面深0.4 - 0.5毫米处)微量注射L - 谷氨酸(L - Glu)能引发升压反应。从上述部位引发的升压反应伴有心动过缓;这种反应可能是由于L - Glu扩散至迷走神经背核,因为当微量注射深度从延髓背表面的0.5毫米减至0.3毫米时,心动过缓消失。当在未麻醉的去大脑大鼠中静脉注射乌拉坦时,对L - Glu微量注射的反应保持不变,即从CS延伸至其头侧约1毫米水平的nTS所有部位均引发降压和心动过缓反应,而从化学感受器投射部位引发升压和心动过速反应。这些观察结果表明,对于将EAA微量注射到nTS所引发的心血管反应,不存在麻醉剂诱导的定性改变。

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