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应激状态下老年阿尔茨海默病照料者的血浆儿茶酚胺及淋巴细胞β2-肾上腺素能受体改变

Plasma catecholamine and lymphocyte beta 2-adrenergic receptor alterations in elderly Alzheimer caregivers under stress.

作者信息

Mills P J, Ziegler M G, Patterson T, Dimsdale J E, Hauger R, Irwin M, Grant I

机构信息

Department of Psychiatry, University of California, San Diego, USA.

出版信息

Psychosom Med. 1997 May-Jun;59(3):251-6. doi: 10.1097/00006842-199705000-00008.

Abstract

OBJECTIVE

The purpose of this study was to determine the effects of chronic stress on beta-adrenergic physiology in elderly spousal caregivers to Alzheimer patients.

METHODS

Thirty-seven elderly spousal caregivers and matched noncaregiver controls (mean age 73 years, SD = 6) were studied. Life stress categorization (presence of marked threat) covering the previous 6 months was determined using a semistructured interview based on the Psychiatric Epidemiological Research Inventory and the Life Events and Difficulties Schedule. beta 2-adrenergic receptor sensitivity (isoproterenol-stimulated cyclic AMP accumulation) and density were determined in lymphocytes.

RESULTS

Caregivers with high life stress had higher plasma norepinephrine levels (p < .04) but no change in plasma cortisol. For beta-receptor sensitivity, 30% of the variance was accounted for by high life stress rating, increased age, being male, and lower norepinephrine (p = .018); 17% of the variance in beta-receptor density was accounted for by plasma norepinephrine (p = .03).

CONCLUSIONS

The findings demonstrate that chronic high stress may be associated with changes in adrenergic physiology and may provide a mechanism through which chronic stress alters cellular immunity.

摘要

目的

本研究旨在确定慢性应激对老年阿尔茨海默病患者配偶照料者β-肾上腺素能生理的影响。

方法

对37名老年配偶照料者和相匹配的非照料者对照(平均年龄73岁,标准差 = 6)进行了研究。使用基于《精神疾病流行病学研究量表》和《生活事件与困难程度量表》的半结构化访谈,确定过去6个月的生活应激分类(存在明显威胁)。测定淋巴细胞中β2-肾上腺素能受体敏感性(异丙肾上腺素刺激的环磷酸腺苷积累)和密度。

结果

生活应激高的照料者血浆去甲肾上腺素水平较高(p <.04),但血浆皮质醇无变化。对于β受体敏感性,30%的变异可由高生活应激评分、年龄增加、男性以及较低的去甲肾上腺素水平解释(p =.018);血浆去甲肾上腺素可解释β受体密度17%的变异(p =.03)。

结论

研究结果表明,慢性高应激可能与肾上腺素能生理变化有关,并可能提供一种慢性应激改变细胞免疫的机制。

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