The dynamics of the brain heat fields of rats in the late postresuscitation period during stress]

By thermoencephaloscopy method the temperature relief of the rats cerebral cortex was studied after the clinical death and reanimation. The rehabilitation of the animals neurological status was completed in 1-2 days. In the remote postresuscitation period (up to 2 months), expressed disturbances were revealed of the background thermomaps and of thermal reactions of the cerebral hemispheres, evoked by the stress influence. Pathologic mosaics of thermal characteristics was revealed in conditions of relative rest and disturbance of dynamics of the brain temperature reactions and the character of interhemispheric asymmetries at stress influence. Individual character is pointed out of postreanimative pathology, which is manifest both in the background thermomaps and after the functional load. The results of the studies suggest the importance of individual approach in rehabilitation therapy of postreanimative disease.     

Early postresuscitation centralization of the blood circulation

Experiments on cats were made to study the cardiac output and its main fractions supplying blood to the epi- and subdiaphragmal parts of the body during the postresuscitation period. The phenomenon of early postresuscitation centralization of circulation was established, correlating with the gravity of the sustained terminal state in the severity and duration.     

Effects of carnosine on systemic hemodynamics and myocardial metabolism in rats in the early postresuscitation period]

It was demonstrated in experiments on male rats that acute lethal blood loss and subsequent resuscitation after 4- and 6-min clinical death induce lipid peroxidation processes, decreased antioxidant enzyme activity, cause activation of anaerobic glycolysis in the myocardium. This metabolic heart impairment causes hemodynamic instability in postresuscitation period. 25 mg/kg of carnosine injected during resuscitation decreased functional-metabolic heart impairments and hemodynamic disarrangement as well as early postresuscitation lethality. The authors attribute positive carnosine effect to its significant antioxidant activity.     

Structural aspects of the functional activity of the cerebral cortex synapses in the early postresuscitation period

The numeral density of the revealed with the help of PTA-plane and twisted asymmetric and symmetric interneuronal contacts of the sensomotor brain cortex of rats after 6 minutes mechanical asphyxia has been studied. It was revealed that in 90 minutes and 6 hours the relative contacts of the concave synapses will be increased progressively. This reaction has the compensatory-adaptive character and ensures the restoration of the integrative activity of the brain during the early postresuscitation period.     

Ultrastructure of the cerebral cortex and hippocampus of rats in the early postresuscitation period following total ischemia

The rat frontal brain cortex and CAr hippocampal region were studied on the 4th day after 10-min complete ischemia. It has been established that the number of "dark" osmiophilic neurons was increased. The reparative, destructive and adaptive processes in cells were observed. The most prominent destructive changes were found in CAr hippocampal region, they can be associated with the microcirculatory disturbances. The hypertrophic thread-like mitochondria appear in the nervous and glial cells, with the quantity of lipofuscin granules increasing. Lipofuscin and hypertrophic mitochondria are thought to provide energy exchange in the brain cells during the postischemic period, forming one of the mechanisms of intracellular adaptation to hypoxia.     

Toxic activity of the blood plasma in the early postresuscitation period

The time course of blood plasma toxicity was studied in dogs in the early postresuscitation period 10 minutes after clinical death because of acute hemorrhage. The duration of dying, the rate of the recovery of the main vitally important body functions were discovered to affect the rate of accumulation in the blood of substances with different molecular weights. There were 3 phases in blood plasma toxicity accumulation. The first phase is marked by the overflow of blood vessels with low-molecular substances, the second one by relative lessening of the content of low-molecular metabolites and an increase in the content of medium-molecular substances. The second phase is in agreement with the maximal rise of blood plasma toxicity. The third phase that develops by the 60th minute of the postresuscitation period is characterized by reduction of the peak activity of all substances under study and by overt toxicity with relative normalization of the main body functions.     

Morphologic changes of the pancreas in hemorrhagic shock and the postresuscitation period

The canine pancreas (20) in the terminal period of hemorrhagic shock and postresuscitation period was studied histologically and electronmicroscopically. There were detected ultrastructural signs of the plasmatic membranes of pancreatocytes and membranes of secretory granules with "leakage" of pancreatic ferments in the interstitial tissue. The incretion of pancreatic ferments in the vascular bed is conditioned by the elevation of proteolytic activity of blood serum in hemorrhagic shock and postresuscitation period.     

Plastic restructuring of cerebral cortex synapses in the postischemic period

Using the technique for the cerebral tissue contrasting with phosphoric-tungsten acid, synaptic architectonics of the molecular layer of the rat sensomotor cortex has been studied for 30 days of recirculation after 5 minutes' stop of the systemic circulation resulted from an acute hemorrhage. Gradation of the synapses per groups is performed according to the height of compact projections of the presynaptic network. Dynamics of the synaptic compactness changes with different height is stated to differ essentially during the postischemic period. A conclusion is made that in reconstruction of the synaptic architectonics of the neocortex during the postischemic period a leading role belongs to the change of state of specialized paramembranous microfilamentous compact projections of the presynaptic network. They make a part of the neuronal cytoskeleton and are included into a single integral complex--the system of subcytoskeleton and are included into a single integral complex--the system of subsynaptic units.     

Iron Deposition after Transient Forebrain Ischemia in Rat Brain

In this study, we investigated the iron deposition in the cerebral cortex, hippocampus CA1 area and corpus striatum pars dorsolateralis in a rat model of cerebral ischemia. Forebrain ischemia was induced by four-vessel occlusion for 20 min. Using iron histochemistry, regional changes were examined from 1 to 8 weeks of postischemic recirculation. Neuronal death was demonstrated in pyramidal cells of the hippocampal CA1 area and in the dorsolateral part of the corpus striatum, which are known as areas most vulnerable to ischemia. Iron deposition in hippocampal CA1 area was coupled to delayed pyramidal cell death. Perl's reaction with DAB intensification revealed of the 1 week iron deposits in the CA1 area, which gradually increased and formed clusters by 8 weeks. In the corpus striatum, strong iron staining was observed in injured cellular layer pars dorsolateralis 1 week after recirculation. Granular iron was deposited in the cytoplasm of pyramidal cells in layers III and V of the frontal cortex after 2 weeks of recirculation. In contrast to the hippocampus and striatum, the cerebral cortex did not develop severe neuronal cell death and atrophy immediately after the ischemic insult, which suggest that the neuronal cell death in the cerebral cortex occurs extremely late.     

Metabolic Changes in Cerebral Cortex, Hippocampus, and Cerebellum During Sustained Bicuculline-Induced Seizures

Abstract— The objective of the present experiments was to study metabolic correlates to the localization of neuronal lesions during sustained seizures. To that end, status epilepticus was induced by i.v. administration of bicuculline in immobilized and artificially ventilated rats, since this model is known to cause neuronal cell damage in cerebral cortex and hippocampus but not in the cerebellum. After 20 or 120 min of continuous seizure activity, brain tissue was frozen in situ through the skull bone, and samples of cerebral cortex, hippocampus, and cerebellum were collected for analysis of glycolytic metabolites, phosphocreatine (PCr), ATP, ADP, AMP, and cyclic nucleotides. After 20 min of seizure activity, the two “vulnerable” structures (cerebral cortex and hippocampus) and the “resistant” one (cerebellum) showed similar changes in cerebral metabolic state, characterized by decreased tissue concentrations of PCr, ATP, and glycogen, and increased lactate concentrations and lactate/ pyruvate ratios. In all structures, though, the adenylate energy charge remained close to control. At the end of a 2-h period of status epilepticus, a clear deterioration of the energy state was observed in the cerebral cortex and the hippocampus, but not in the cerebellum. The reduction in adenylate energy charge in the cortex and hippocampus was associated with a seemingly paradoxical decrease in tissue lactate levels and with failure of glycogen resynthesis (cerebral cortex). Experiments with infusion of glucose during the second hour of a 2-h period of status epilepticus verified that the deterioration of tissue energy state was partly due to reduced substrate supply; however, even in animals with adequate tissue glucose concentrations, the energy charge of the two structures was significantly lowered. The cyclic nucleotides (cAMP and cGMP) behaved differently. Thus, whereas cAMP concentrations were either close to control (hippocampus and cerebellum) or moderately increased (cerebral cortex), the cGMP concentrations remained markedly elevated throughout the seizure period, the largest change being observed in the cerebellum. It is concluded that although the localization of neuronal damage and perturbation of cerebral energy state seem to correlate, the results cannot be taken as. evidence that cellular energy failure is the cause of the damage. Thus, it appears equally probable that the pathologically enhanced neuronal activity (and metabolic rate) underlies both the cell damage and the perturbed metabolic state. The observed changes in cyclic nucleotides do not appear to bear a causal relationship to the mechanisms of damage.     

ABRA在正常成年大鼠大脑皮质和海马区的表达

目的观察ABRA(Actin binding Rho activator)在成年大鼠大脑皮质和海马中的表达。方法制备成年大鼠脑的冰冻切片,采用共聚焦免疫荧光技术和免疫荧光强度测量检测ABRA在大鼠大脑皮质和海马区的表达。结果 ABRA在神经元的胞核、胞浆、突起内可见,其中胞核着色最强。在大脑皮质,ABRA阳性的神经元胞体和突起广泛分布于皮质的分子层、外颗粒层、外锥体细胞层、内颗粒层、内锥体细胞层、多形细胞层,其免疫荧光强度分别为129.22±16.94、125.39±29.83、117.67±22.50、105.85±17.65、103.90±18.00、100.23±20.38,ABRA阳性细胞率分别为0.51±0.01、0.69±0.02、0.64±0.03、0.58±0.05、0.65±0.09、0.63±0.01。在海马,ABRA均匀分布于海马各部,阳性神经元集中于锥体细胞层,而其阳性突起弥散分布于海马分子层和多形层。海马锥体细胞层、分子层、多形层免疫荧光强度分别为141.19±35.48、53.19±10.38、43.32±9.59,ABRA阳性细胞率分别为0.62±0.04、0.27±0.07、0.25±0.03。结论 ABRA广泛表达于大鼠大脑皮质和海马各层,提示ABRA可能在大鼠这些部位的神经细胞功能活动方面起重要作用。     

Neuronal mechanisms for the perception of ambiguous stimuli

Ambiguous figures that may take on the appearance of two or more distinct forms have fascinated philosophers and psychologists for generations. Recently, several laboratories have studied the neuronal basis of perceptual appearance at the level of single neurons in the cerebral cortex. Experiments that integrate neuronal recording with analyses based on sensory detection theory reveal a remarkable degree of specificity in these neuronal responses. The new challenges are to understand how cognitive processes, such as attention and memory, interact with perception to generate these neuronal signals.     

The autologous intestinal microflora in the postresuscitation period after acute blood loss in rats

In this work the data obtained in the study of intestinal microbiocenosis in rats on the third day of the postresuscitation period after acute blood loss are presented. The quantitative and qualitative shifts of microflora at different biotopes, such as the wall of the small intestine, the parietal microflora of Peyer's patches, the contents and wall of the large intestine, have been characterized. Some specific features of dysbiotic changes have been revealed in comparison with the shifts of intestinal microflora in cases of dysbacteriosis caused by other reasons. The translocation of different microorganisms, including Bacterium bifidum and lactobacilli, into mesenteric lymph nodes, the liver, the spleen and the blood has been observed.     

The effect of low-intensity laser radiation on blood metabolic indices in the postresuscitation period]

The effect of He-Ne laser radiation (632.8 nm; 0.3 mW/cm parallel to oxygenation on metabolism indices of blood, taken in early postresuscitation period after discontinuation of hemorrhagic shock was studied in vitro. Compared to oxygenation alone, combined therapy resulted in more marked oxygen consumption of the blood, normalization of plasma antioxidant total activity, superoxydismutase erythrocyte catalase activity, the number of double connections in fatty acid chain of general lipids and membrane viscosity were elevated. Regular dependence of lipid peroxidation on a number of metabolic blood parameters is revealed.     

Transient focal cerebral ischemia upregulates immunoproteasomal subunits

This study was designed to determine whether focal cerebral ischemia alters the expression of the immunoproteasomal (i-proteasomal) subunits. Transient cerebral ischemia significantly increased the expression of the i-proteasomal subunits, 20S β1i (LMP2) and β5i (LMP7) in the parietal cortex and hippocampus. This alteration was associated with a remarkable increase in ubiquitinated proteins. It is likely that the postischemic induction of the i-proteasome plays an important role in coping with the damaged proteins and thus may have an important effect on neuronal survival and death.     

Comparative study of the epileptogenic effect of kainic acid injected into the cerebral cortex, hippocampus and amygdala in adult cats chronically implanted

Intracerebral injection of kainic acid in cerebral cortex, hippocampus or amygdala in cats chronically implanted showed that: 1) Hippocampus and amygdala presented a greater sensitivity than the cerebral cortex, while hippocampus presented a greater sensitivity than the amygdala to the generation of an epileptic focus. 2) Comparison of latency, mean duration of afterdischarges, and the mean time period to obtain the peak intensity of the afterdischarge in the three cited structures, showed that mean latency of the first afterdischarge was significantly shorter in hippocampus and amygdala compared with the cerebral cortex. Moreover the mean time period to reach the peak intensity of the afterdischarge was again shorter in the subcortical structures. 3) The epileptic foci both in hippocampus and amygdala were blocked by CNQX and muscimol. 4) The behavioral changes depended on the intensity of the epileptic process. Tonic-clonic convulsions appeared only when the motor cerebral cortex was involved. Finally, 5) kainic acid injections in hippocampus and amygdala elicited an intense neuronal destruction and gliosis of these structures. We conclude that intracerebral injection of low doses of kainic acid in cats represent a good model to study focal epileptic thresholds in the CNS.     

Central hemodynamics of dogs in the early postresuscitation period and the outcome of resuscitation

Variations in central hemodynamics of dogs were compared with the outcome of resuscitation of 18 dogs subjected to 12-minute reversible circulatory arrest because of ventricular fibrillation. Nine survived dogs with completely recovered neurological status during the first 10 minutes after resuscitation had moderate hypertension, the mean arterial pressure (MAP) being 175.0 + 8.9 mm Hg. In the dogs who died within 24-48 hours after resuscitation, the MAP did not rise during this period as compared to the initial level; 2 dogs developed excessive hypertension (MAP about 200 mm Hg). There were also found certain differences in other parameters of central hemodynamics. Moderate hypertension in the first 10 minutes of the postresuscitation period leads to rapid restoration of the adequate level of peripheral blood flow in organs and tissues, thus favouring survival of animals subjected to a long circulatory arrest.