mmune inflammatory response and sympathetic nervous system activation plays an important
role in the occurrence and development of chronic heart failure (CHF) [1,2] ,But its activation mechanism and the relationship between central and peripheral
levels of activation are not clear. There is evidence to show that CHF central renin
angiotensin angiotensin system (RAS) over enhancement, central Pro inflammatory cytokines
(PIC) increased expression, and promote the activity of the sympathetic nervous system
over enhancement, but the second not mediated CHF state week immune inflammatory reaction
is uncertain [3,4]. In this study, the CHF model of myocardial ischemia was made by ligation of the
left anterior descending branch of the left coronary artery, and the central and peripheral
sympathetic activity and immune inflammatory response were observed at different time
points after ligation. And through the intervention of the central level of RAS, to
observe whether the coronary artery ligation in rats can reduce the level of immune
inflammatory reaction and sympathetic nervous system activity, and improve the cardiac
function. To provide new ideas and basis for the prevention and treatment of CHF.
weeks and plasma catecholamine, PIC levels were compared with the sham operated rats,
coronary artery ligation rats plasma NE levels with time prolonged significantly increased,
e non significant difference; coronary artery node ligation group plasma pic levels
were also increased with time and increased significantly (Figure 1). 2). 3). IV. Discussion Chronic heart failure (CHF) is a serious hazard to human health,
but the treatment effect is not good enough. Urgent need to explore the mechanism
of CHF disease progression in order to find a more effective treatment. There is an
interaction between sympathetic nervous system and immune system activation in the
CHF state. In the past, most of the researches are based on the activation of sympathetic
nervous system and immune system, which is an effective method for the treatment of
CHF. Less research about the interaction between sympathetic nervous system and immune
system in CHF, especially the change of the peripheral activity of a certain factor.
Studies have shown that CHF myocardial ischemia and infarction by autonomic nerve
afferent signals reach the central, thereby inducing central pic increased generation
[5,8], and central pic and ROS [2; 7]; mutual effect of 8] and RAS [9] system in control of sympathetic activity, inhibition of central pic can reduce the
CHF of the sympathetic nervous system excitability [6,7].However, it is not clear whether CHF and RAS in the PIC state of cardiovascular central
nuclei, such as the nucleus of the hypothalamus (PVN) and the rostral medulla (RVLM),
mediate the inflammatory response. In this study, the CHF model of myocardial ischemia
was made by ligation of the left anterior descending branch of the left coronary artery,
and the central and peripheral sympathetic activity and immune inflammatory response
were observed at different time points after ligation. Compared with the sham operated
rats, coronary artery ligation rats plasma NE levels with time prolonged significantly
increased, e non significant difference was found; coronary artery ligation rats plasma
pic levels also with time prolonged increased significantly; coronary artery ligation
group rat paraventricular nucleus (PVN), Yin cord rostral ventrolateral (RVLM) TNF
alpha and IL-1 beta level from 3 days to 6 weeks were significantly increased, but
between each time point without significant difference. Further, we use via mini osmotic
pumps to the bilateral lateral ventricle for 6 weeks to give AT1 receptor blocker
losartan intervention central RAS, observe whether it can reduce the coronary artery
ligated rats the level of peripheral inflammatory reaction and the activity of the
sympathetic nervous system, improve heart function; Results suggest that heart failure
rat sympathetic nerve activity level was significantly enhanced and peripheral plasma
TNF alpha, IL-1 beta and NE levels were significantly increased (P < 0.05), and given
the AT1 receptor blockade losartan via mini osmotic pumps to the bilateral lateral
ventricle administration intervention RAS in central nervous system after the excessive
proliferation of strong sympathetic nerve activity level decreased significantly and
peripheral TNF alpha, IL-1 beta and NE levels were decreased (P < 0.05). That heart
failure rat central RAS inhibition can reduce the peripheral excessive inflammatory
reaction and the activity of the sympathetic nervous system, also found that the intervention
after cardiac function was significantly improved, and the model group were significant
differences (P < 0.05), suggesting that the cardiac function as with inhibition of
Ras in central nervous system, thereby reducing the CHF when the excitement of the
sympathetic system and outer peripheral immune inflammation. This study is expected
to explain the mechanism of the interaction between the sympathetic nervous system
and the immune system, and provide a new idea and basis for the prevention and treatment
of CHF. In addition, this study on heart failure rats given AT1 receptor blockade
losartan via mini osmotic pumps to the bilateral lateral ventricle administration
intervention central Ras levels found the pivot pic levels were also significantly
decreased, the interaction between the two and peripheral inflammation, sympathetic
nerve activity regulation of network access and the specific mechanism still need
further study.