Cardiac Dysfunction in a Mouse Vascular Dementia Model of Bilateral Common Carotid Artery Stenosis.
Cardiac Dysfunction in a Mouse Vascular Dementia Model of Bilateral Common Carotid Artery Stenosis.
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DOI：
10.3389/fcvm.2021.681572
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发表时间：
2021
影响因子：
3.6
通讯作者：
Venkat P
中科院分区：
文献类型：
--
作者：
An L;Chopp M;Zacharek A;Shen Y;Chen Z;Qian Y;Li W;Landschoot-Ward J;Liu Z;Venkat P
背景：心脏功能与认知功能相关。此前，我们发现中风和创伤性脑损伤会引起小鼠心脏功能障碍。 In this study, we investigate whether bilateral common carotid artery stenosis (BCAS), a model that induces vascular dementia (VaD) in mice, induces cardiac dysfunction.方法：对成年晚期（6-8 个月）C57BL/6J 小鼠进行假手术（n = 6）或 BCAS（n = 8）。 BCAS 是通过在两条颈总动脉周围应用微线圈（内径 0.16 毫米）来进行的。 BCAS 后 21-28 天进行脑血流量和认知功能测试。 BCAS 后 29 天对清醒的小鼠进行超声心动图检查。 BCAS 后 30 天处死小鼠。分离心脏组织用于免疫组织化学评估和实时PCR测定。 Results: Compared to sham mice, BCAS in mice significantly induced cerebral hypoperfusion and cognitive dysfunction, increased cardiac hypertrophy, as indicated by the increased heart weight and the ratio of heart weight/body weight, and induced cardiac dysfunction and left ventricular (LV) enlargement, indicated by a decreased LV ejection fraction (LVEF) and LV fractional shortening (LVFS), increased LV dimension (LVD), and increased LV mass.认知缺陷与心脏缺陷显着相关。 BCAS mice also exhibited significantly increased cardiac fibrosis, increased oxidative stress, as indicated by 4-hydroxynonenal and NADPH oxidase-2, increased leukocyte and macrophage infiltration into the heart, and increased cardiac interleukin-6 and thrombin gene expression. Conclusions: BCAS in mice without primary cardiac disease provokes cardiac dysfunction, which, in part, may be mediated by increased inflammation and oxidative stress.
Background: Cardiac function is associated with cognitive function. Previously, we found that stroke and traumatic brain injury evoke cardiac dysfunction in mice. In this study, we investigate whether bilateral common carotid artery stenosis (BCAS), a model that induces vascular dementia (VaD) in mice, induces cardiac dysfunction. Methods: Late-adult (6–8 months) C57BL/6J mice were subjected to sham surgery (n = 6) or BCAS (n = 8). BCAS was performed by applying microcoils (0.16 mm internal diameter) around both common carotid arteries. Cerebral blood flow and cognitive function tests were performed 21–28 days post-BCAS. Echocardiography was conducted in conscious mice 29 days after BCAS. Mice were sacrificed 30 days after BCAS. Heart tissues were isolated for immunohistochemical evaluation and real-time PCR assay. Results: Compared to sham mice, BCAS in mice significantly induced cerebral hypoperfusion and cognitive dysfunction, increased cardiac hypertrophy, as indicated by the increased heart weight and the ratio of heart weight/body weight, and induced cardiac dysfunction and left ventricular (LV) enlargement, indicated by a decreased LV ejection fraction (LVEF) and LV fractional shortening (LVFS), increased LV dimension (LVD), and increased LV mass. Cognitive deficits significantly correlated with cardiac deficits. BCAS mice also exhibited significantly increased cardiac fibrosis, increased oxidative stress, as indicated by 4-hydroxynonenal and NADPH oxidase-2, increased leukocyte and macrophage infiltration into the heart, and increased cardiac interleukin-6 and thrombin gene expression. Conclusions: BCAS in mice without primary cardiac disease provokes cardiac dysfunction, which, in part, may be mediated by increased inflammation and oxidative stress.
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影响因子：
20.1
作者：
Ismahil MA;Hamid T;Bansal SS;Patel B;Kingery JR;Prabhu SD
通讯作者：
Prabhu SD
影响因子：
4.7
作者：
Ihara M;Tomimoto H
通讯作者：
Tomimoto H
影响因子：
1.9
作者：
Darwish H;Mahmood A;Schallert T;Chopp M;Therrien B
通讯作者：
Therrien B
脑和认知脆弱的相交的脑肾素 - 血管紧张素系统。
影响因子：
4.3
作者：
Cosarderelioglu C;Nidadavolu LS;George CJ;Oh ES;Bennett DA;Walston JD;Abadir PM
通讯作者：
Abadir PM
影响因子：
3.7
作者：
Higaki A;Mogi M;Iwanami J;Min LJ;Bai HY;Shan BS;Kukida M;Kan-No H;Ikeda S;Higaki J;Horiuchi M
通讯作者：
Horiuchi M