The Investigate The Mechanism And Interference Of Cerebrogenic Antonomic Cardiovascular Disturbances

Objective:The electrocardiographic repolarization changes,cardiac arrhythmias and raised plasma creatine kinase myocardial isoenzyme are frequently encountered after cerebral stroke. The cardiac damages in patients with cerebral stroke, interfere with either filling or emptying of the heart chambers,leads to diminished cardiac output and to reduced cerebral blood flow.Diminished cerebral blood flow results in cerebral ischemia and eventually enlarged cerebral infarction,and may be worsen the outcome of the primary disease.In addition, the cerebrogenic cardiac lesions may be a cause of sudden unexpected death in patients with stroke. The mechanism of this cardiac damages are not explained by concomitant ischemic cardiac disease.Augmentation of intracardiac sympathetic nerve activity and lesions of insular cortex and its subcortical center may be contribute to it, the changes of neurotransmitter and polypeptide may be also contribute to it, can theHRV and related parameters heritable in stroke?The pupose of the study was attempt to assess the relationship of lesion of insular cortex,subcortical center and autonomic cardiovascular disturbances. To investigate the changes of time-course of Neuropeptide Y and its possible utilities in stroke with autonomic cardiovascular disturbances and;To investigate the relationship of angiotensinogen gene polymorphisms and autonomic cardiovascular disturbances in stroke, these mechanism will be investigated in this study; To investigate the effect of treatment and its possible mechanisms of cerebellar fastigial nucleus stimulation (FNS) in stroke patients and rats with MCAo with autonomic cardiovascular disturbances.Method:1. The cardiac autonomic nervous activity were studied the relationship of HRV in different stroke groups by heart rate variability analysis system, and assessed the relationship of lesion of insular cortex,subcortical central and autonomic nervous cardiovascular disturbances by different electric intensity stimulating different cerebral regions of rats.2. NPY plasma levels were detected by radioimmunoassay in different stroke groups, and the changes in NPY over the insular cortex and amygdala were investigated at different times after middle cerebralartery occlusion (MCAo) using immunohistochemical staining.3. Angiotension-Converting Enzyme Gene polymorphisms and Heart Rate Variability in stroke using PCR method.4. The effect of FNS and its possible mechanisms were assessed on HRV.Results: 1. The effects of cerebral hemisphere stroke on cardiac autonomic nervous activity mainly correlated with destruction of right insular seems to cause cardiac parasympathetic hypofunction and sympathetic hyperfunction.Some measured components of HRV were significantly lower in insular cortex,amgydala,ventromedial hypothalamic nucleus,Dorsal motor nucleus of vagus compored with sensorimotor cortex(control) using electric stimulating them.2. Plasma NPY levels were significantly higher in stroke. Immunostaining for NPY demonstrated on increase that was localized to the insular cortex and amydala with a peak around 3days and a return to baseline levels by 10 days.3. ACE geneotype was correlated with pertubances of normal rhythmic HRV, And DD ACE genotype was associated with increased HRV in stroke .4. After FNS, some measured components of HRV were sighificantly higher in stroke, and the expression of NPY were downregulation in MCAo.Conclnsions: 1. The effects of cerebral hemisphere stroke on cordiac autonomic nervous activity mainly correlated with destruction of insular cortex and subcortical central regions adjacent to the insular cortex.2. The effects of cerebral hemisphere stroke on cardiac autonomic nervous activity correlated with NPY and heritage.3. FNS may be benefit to the treatment of autonomic nervous cardiovascular disturbances after cerebral ischemia.