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Electroencephalographic evidence of cortical network disruption preceding overt cardioinhibition during tilt-induced reflex syncope.

OBJECTIVE: Reflex syncope is a common cause of transient loss of consciousness. However, the early cerebral mechanisms underlying cardiovascular changes remain poorly understood. Our objective was to investigate early cerebral changes by quantitatively analyzing EEG activity preceding overt cardioinhibition during tilt-induced reflex syncope. METHODS: EEG recordings from patients undergoing tilt testing were retrospectively analyzed. Patients who experienced reflex syncope were compared to those who did not. Spectral and functional connectivity analyses were performed across baseline, pre-cardioinhibition, and syncopal phases. RESULTS: Prior to the onset of cardioinhibitory pathological reflex, a significant increase in theta-band spectral power was observed in the right temporal region, accompanied by a widespread increase in functional connectivity within the same frequency band. These findings suggest the involvement of brain networks before cardioinhibition. CONCLUSIONS: EEG changes in the theta band (power and functional connectivity) were observed before overt cardioinhibition during tilt-induced reflex syncope. SIGNIFICANCE: Our findings support the hypothesis of cortical processing preceding cardioinhibition in reflex syncope. EEG may represent a valuable complementary tool for improving the understanding and diagnosis of these events.

Humans

Multi-organ gene expression analysis and network modeling reveal regulatory control cascades during the development of hypertension in female spontaneously hypertensive rat.

Hypertension is a multifactorial disease with stage-specific gene expression changes occurring in multiple organs over time. The temporal sequence and the extent of gene regulatory network changes occurring across organs during the development of hypertension remain unresolved. In this study, female spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats were used to analyze expression patterns of 96 genes spanning inflammatory, metabolic, sympathetic, fibrotic, and renin-angiotensin (RAS) pathways in five organs, at five time points from the onset to established hypertension. We analyzed this multi-dimensional dataset containing ~15,000 data points and developed a data-driven dynamic network model that accounts for gene regulatory influences within and across visceral organs and multiple brainstem autonomic control regions. We integrated the data from female SHR and WKY with published multiorgan gene expression data from male SHR and WKY. In female SHR, catecholaminergic processes in the adrenal gland showed the earliest gene expression changes prior to inflammation-related gene expression changes in the kidney and liver. Hypertension pathogenesis in male SHR instead manifested early as catecholaminergic gene expression changes in brainstem and kidney, followed by an upregulation of inflammation-related genes in liver. RAS-related gene expression from the kidney-liver-lung axis was downregulated and intra-adrenal RAS was upregulated in female SHR, whereas the opposite pattern of gene regulation was observed in male SHR. We identified disease-specific and sex-specific differences in regulatory interactions within and across organs. The inferred multi-organ network model suggests a diminished influence of central autonomic neural circuits over multi-organ gene expression changes in female SHR. Our results point to the gene regulatory influence of the adrenal gland on spleen in female SHR, as compared to brainstem influence on kidney in male SHR. Our integrated molecular profiling and network modeling identified a stage-specific, sex-dependent, multi-organ cascade of gene regulation during the development of hypertension.

Animals

Postganglionic sympathetic activity with correlation to heart rhythm and central cortical rhythms.

1. Renal sympathetic nerve activity, ECG and parieto-occipital EEG were recorded in dogs anaesthetized with chloralose. The carotid sinus nerves were cut. Autocovariance functions and power spectra for these variables were computed. 2. During cooling of the vagus nerves, the integrated renal sympathetic activity exhibited rhythms which were correlated to the delta-theta rhythm of the EEG. This rhythm was also present with the vagus nerves functionally intact, but a cardiac rhythm was dominant. 3. Blood pressure-dependent neurones in the lower brain stem reticular formation have both cardiac and central cortical rhythms. This provides a hint that these neurones might be involved in the sympathetic tone generating network.

Animals

Basis for synchronization of sympathetic and phrenic nerve discharges.

The basis for the relationship between the discharges in the external cartized cats that were vagotomized, paralyzed, and artificially ventilated. Ive discharge (with the period of the cycle of phrenic nerve activity) is extrinsically imposed on central sympathetic networks by elements of the brainstem respiratory oscillator. However, a number of observations made in the present study contradict this view. First, changes in respiratory rate were accompanied by dramatic shifts in the phase relations between sympathetic and phrenic nerve discharge. Second, slow oscillations of sympathetic and phrenic nerve discharge were not always locked in a 1:1 relation. Third, the slow sympathetic rhythm persisted when respiratory rhythmicity disappeic components of sympathetic and phrenic nerve activity are generated by in

Animals