Amy Miner Ross, PhD, RN, CNS Associate Professor, Oregon Health & Science University (OHSU) School of Nursing, Portland Campus, Oregon. Christopher S. Lee, PhD, RN, FAHA, FAAN, FHFSA Carol A. Lindeman Distinguished Professor and Associate Professor, OHSU School of Nursing, Portland Campus, Oregon. Helmi Lutsep, MD Vice Chair and Dixon Term Professor, Department of Neurology; Associate Director, OHSU Stroke Center; and Chief, Neurology Service, VA Portland Health Care System, Oregon. Wayne M. Clark, MD Professor, Department of Neurology, and Director, Oregon Stroke Center at OHSU, OHSU School of Medicine, Portland.
J Cardiovasc Nurs. 2018 Jul/Aug;33(4):E3-E10. doi: 10.1097/JCN.0000000000000481.
Immunodeficiency in acute ischemic stroke (AIS) is thought to be a result of norepinephrine suppression of the lymphoid tissue. The possible differences in the distribution of lymphocytes after stroke may be due to differences in responsiveness of lymphocyte β-adrenergic receptors to their kinase (BARK-1).
The objective was to quantify the influence of lymphocyte BARK-1 on stroke-induced immunodeficiency in AIS patients.
A prospective clinical cohort study was conducted (N = 44). Measures included age, gender, race, risk factors for stroke, stroke severity, comorbidities, presence of infection, white blood cell counts and differential proportions, and lymphocyte BARK-1. Student t tests, effect sizes, and linear and logistic regressions were conducted to test the study objective. The study was approved by the Oregon Health & Science University Institutional Review Board.
There were significant changes in all white blood cells and differential proportions and in the National Institutes of Health Stroke Scale from admission to 48 hours after onset of stroke deficits. Higher BARK-1 influenced the lower lymphocyte proportion at 48 hours, independent of age, P < .0001. Furthermore, BARK-1 also was associated with an increase in the likelihood of having sustained or stroke-induced immunodeficiency at 48 hours: odds ratio, 2.41; 95% confidence interval, 1.10-5.25; P = .027, and odds ratio, 2.79; 95% confidence interval, 1.03-7.52; P = .043, respectively. In all backward stepwise selection of factors, BARK-1 was the only factor consistently retained in the models.
β-Adrenergic receptor kinase-1 has a significant quantifiable influence on lymphocyte proportion at 48 hours and on the classification of sustained stroke-induced immunodeficiency.
β-Adrenergic stimulation influences immunodeficiency in AIS.
急性缺血性脑卒中（AIS）患者的免疫功能缺陷被认为是去甲肾上腺素抑制淋巴组织的结果。卒中后淋巴细胞分布的差异可能是由于淋巴细胞β-肾上腺素能受体对其激酶（BARK-1）的反应性不同所致。
本研究旨在量化淋巴细胞 BARK-1 对 AIS 患者卒中后免疫缺陷的影响。
进行了一项前瞻性临床队列研究（N=44）。测量指标包括年龄、性别、种族、卒中风险因素、卒中严重程度、合并症、感染存在情况、白细胞计数和分类比例以及淋巴细胞 BARK-1。采用学生 t 检验、效应大小、线性和逻辑回归检验研究目的。该研究获得俄勒冈健康与科学大学机构审查委员会的批准。
从卒中发病到 48 小时，所有白细胞和分类比例以及国立卫生研究院卒中量表评分均发生显著变化。较高的 BARK-1 独立于年龄影响 48 小时时淋巴细胞比例降低，P＜0.0001。此外，BARK-1 还与 48 小时时持续或卒中诱导免疫缺陷的发生几率增加相关：比值比，2.41；95%置信区间，1.10-5.25；P=0.027，比值比，2.79；95%置信区间，1.03-7.52；P=0.043。在所有向后逐步选择因素中，BARK-1 是唯一始终保留在模型中的因素。
β-肾上腺素能受体激酶-1 对 48 小时时淋巴细胞比例以及持续卒中诱导免疫缺陷的分类有显著的量化影响。
β-肾上腺素能刺激影响 AIS 中的免疫功能缺陷。
