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POSTNATAL MATURATION OF CARDIOVASCULAR REGULATORY SYSTEM

产后心血管调节系统的成熟

基本信息

批准号：
6682306
负责人：
Anthony Louis Sica
金额：
$ 30.7万
依托单位：
SUNY DOWNSTATE MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
1978
资助国家：
美国
起止时间：
1978-08-01 至 2007-11-30
项目状态：
已结题

项目摘要

DESCRIPTION (Verbatim from the application): The overall goal of this proposal is to provide physiological and anatomical indices of maturation within neural networks involved in cardiorespiratory (CV-RESP) regulation. We shall focus on brainstem circuit neurons that mediate the CV-RESP responses to hypercapnic stress because: (a) this circuit plays an essential role in the maintenance of blood/gas homeostasis and (b) evidence suggesting that maladaptive responses to hypercapnic stimulation may be involved in the pathogenesis of Sudden Infant Death Syndrome (SIDS).The swine model of early development will be used to test the hypothesis that CV-RESP responses to prolonged hypercapnia are: (a) age-related, (b) modulated by peripheral afferent inputs, and (c) mediated by central a2-adrenoceptors. We also hypothesize that the network response to hypercapnia involves area postrema, nucleus tractus solitarii, and their synaptic targets within sympathetic (SYMP) control regions of the lateral medullary reticular formation. We shall test our hypothesis that catecholaminergic cell areas of the piglet medulla, previously shown to be activated by (a) CO2 and (b) hypotension, play crucial roles in the coordinated response. Of special significance are a subset of epinephrinergic neurons located in the SYMP premotor region of the rostral ventrolateral medulla. The effects of prolonged hypercapnia on SYMP outflow from at least two different segmental levels will be recorded, simultaneously with phrenic (PHR) activity. lEG expression will be quantitated with respect to age and brain stem sites. Age-related alterations in physiologic and neqronal responses to hypercapnia will be assessed following blockade of central alpha-2 receptors. Peripheral denervation will determine the importance of peripheral afferent inputs versus central effects ofhypercapnia at different ages. The correlation between lEG expression and SYMP-PHR outflows should reveal whether age-related changes in CV-RESP brain circuits (suggesting periods of vulnerability), are also observed in SYMP-PHR outflows; thus explaining the absence of a linear pattern of maturation of CV responses with stress. These studies should identify apparent dissociation between level of lEG expression (neuronal activation), SYMP coherence (regulatory outflow) and CV-RESP responses to stress (critical developmental period). The results should help in our understanding of the most vulnerable period in the life of the child and the pathogenesis ('window of opportunity') of SIDS.

描述（来自申请的逐字）：本提案的总体目标是提供神经内成熟的生理和解剖学指标，参与心肺调节的网络（CV-RESP）。我们要聚焦介导CV-RESP对高碳酸血症反应的脑干回路神经元压力，因为：（a）这个电路在维持血液/气体稳态和（B）证据表明，高碳酸血症刺激可能参与了猝死的发病机制死亡综合征（SIDS）。将使用早期发育的猪模型来测试假设CV-RESP对长期高碳酸血症的反应是：（a）年龄相关，（B）由外周传入输入调节，和（c）由中枢α 2肾上腺素受体。我们还假设，网络对高碳酸血症涉及最后区，孤束核，以及它们的交感神经（SYMP）控制区内的突触靶点髓质网状结构。我们将检验我们的假设，先前显示的仔猪髓质的儿茶酚胺能细胞区域由（a）CO2和（B）低血压激活，在协调的反应具有特殊意义的是肾上腺素能神经元的一个子集位于延髓头端腹外侧区的SYMP运动前区。的长期高碳酸血症对至少两种不同的SYMP流出的影响将记录节段水平，同时记录膈神经（PHR）活动。将根据年龄和脑干部位对IEG表达进行定量。高碳酸血症引起的生理和呼吸反应的变化将在阻断中枢α-2受体后进行评估。外围去神经支配将决定外周传入输入与不同年龄高碳酸血症的中枢效应。IEG之间的关系表达和SYMP-PHR流出应揭示是否与年龄相关的变化，还观察到CV-RESP脑回路（提示脆弱期）在SYMP-PHR流出;从而解释了没有线性模式， CV反应与应激的成熟。这些研究应确定明显的 IEG表达水平（神经元活化）之间的分离，SYMP 一致性（调节流出）和CV-RESP对压力的反应（关键发展时期）。这些结果应该有助于我们理解儿童生命中的脆弱期和发病机制（“窗口期”）机会”）。

项目成果

期刊论文数量（21）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

仔猪传出膈活动功率谱与年龄相关的变化。

DOI：
10.1016/0006-8993(87)90439-2
发表时间：
1987
期刊：
Brain research
影响因子：
2.9
作者：
Cohen,HL;Gootman,PM;Steele,AM;Eberle,LP;Rao,PP
通讯作者：
Rao,PP

Unusual observations on hypermagnesemic levels and cardiorespiratory effects in neonatal swine.

对新生猪高镁血症水平和心肺影响的异常观察。

DOI：
发表时间：
1990
期刊：
Magnesium and trace elements
影响因子：
0
作者：
Rivera,LI;Gootman,PM;Brust,M;Condemi,G;Hundley,BW;Lin,RH;Cohen,HL;Gandhi,MR;Altura,BT;Gootman,N
通讯作者：
Gootman,N

Postnatal changes in cardiovascular regulation during hypoxia.

缺氧期间心血管调节的产后变化。