We propose an extension of the detrended cross-correlation analysis (DCCA) for signals with highly inhomogeneous structure. The proposed approach evaluates two scaling exponents, one of which characterizes the detrended covariance, and the second exponent quantifies the effects of nonstationarity caused by the distribution of local fluctuations of signal profiles from the trend. Using simulated datasets produced by a system of coupled Lorenz models, we describe entrainment phenomena associated with chaotic synchronization and the role of nonstationarity in their description. The processing of experimental data related to cerebral blood flow in neighboring vessels of different size confirm the general conclusion of this study and shows the possible advantages of the proposed extension of the DCCA-method for diagnosing changes in cooperative dynamics in physiological systems, where the combined effects of dynamics, nonstationarity and noise may occur.
Chaos, Solitons & Fractals Volume 157, April 2022, 111972

Констрикторные реакции сосудов мозга, характерные для приступа мигрени, моделировали с помощью агониста 5HT2B/2C-рецепторов - мета-хлорфенилпиперазина (mCPP; 0,1 мг/кг, в вену). При многократном введении на протяжении всего опыта он вызывает кратковременное уменьшение локального мозгового кровотока и снижение артериального давления. Ацилгидразон (2,3,4-триметокси-N'-(8-метил-8-азабицикло[3.2.1.]октан-3-илиден)бензогидразид гидрохлорид; ЛК-933) в дозе 10 мг/кг значимо угнетает реакции локального мозгового кровотока и артериального давления, вызванные mCPP, т.е. обладает антисеротониновой цереброваскулярной активностью. ЛК-933 по выраженности эффекта не уступает тропоксину, но менее токсичен и превосходит его по продолжительности антисеротонинового действия. Вместе с тем ЛК-933, в отличие от тропоксина, проявляет отчетливую анксиолитическую активность в тесте приподнятого крестообразного лабиринта у мышей, сопоставимую с таковой для афобазола.

The aim of the present work was to test the hypothesis that early ischemic preconditioning provides effective protection of the brain against ischemic damage via effects on cerebral blood flow. Experiments were performed using male Wistar rats anesthetized with thiopental using two methods to produce ischemia: 1) ligation of the left common carotid and left middle cerebral arteries; 2) endovascular occlusion of the middle cerebral artery for 30 and 60 min. Preconditioning was modeled using two 5-min episodes of bilateral occlusion of the common carotid arteries with 5-min reperfusion periods. Infarct size was assessed by staining with triphenyltetrazolium chloride; major vessel blood flow was measured by Doppler ultrasonography, and ischemic zones were measured by staining with Evans blue. Preconditioning led to significant decreases in infarct size after ischemia for 30 and 60 min and after ischemia without reperfusion. Preconditioning had no effect on measures of major vessel blood flow in the middle cerebral artery, as indicated by Doppler ultrasonography data. The ischemic preconditioning group showed no decreases in ischemic zone size 5 min after occlusion of the left middle cerebral artery, while 30–40 min after the onset of ischemia there was a reduction in the ischemic zone in the preconditioning groups. Along with cytoprotective effects, ischemic preconditioning decreased ischemic zone size and had marked additional infarct-limiting effects in focal transient and permanent cerebral ischemia in rats.
Neuroscience and Behavioral Physiology: V.42, Issue 6 (2012), P. 643-650.