Severe Cerebral Ischemia Research Articles

Influence of endothelial dysfunction caused by estrogen deficiency on the severity of cerebral ischemia in rats

The aim of this study was to assess the effect of endothelial dysfunction caused by a decrease in the estrogen level on the severity of cerebral ischemia.
 Methods. Endothelial dysfunction was caused by extirpation of the uterus with appendages and was confirmed by counting circulating endothelial cells and evaluating stimulated and basal secretion of nitric oxide. Focal cerebral ischemia was modeled by intravasal occlusion of the middle cerebral artery. The severity of ischemia was assessed according to the scales of neurological deficit (Combs & D’Alecy and McGraw), in the Rotarod test and in terms of the volume of necrosis.
 Results. Estrogen deficiency resulted in an increase in the circulating endothelial cells by 88%, as well as a decrease in stimulated and basal nitric oxide secretion by 17.1% and 14.7% respectively. Focal cerebral ischemia in animals with endothelial dysfunction caused by estrogen deficiency resulted in greater cerebral damage, resulting in an increase in the level of neurological deficit on the Combs & D’Alecy and McGraw scales for 7 days, a decrease in the retention time on the rotating rod by 32%, as well as an increase in the infarct volume by 89% relative to the group of animals without sexual hormones failure.
 Conclusion. It has been shown that endothelial dysfunction caused by estrogen deficiency complicates the severity of cerebral ischemia, causing a more pronounced neurological and motor deficit, and contributes to an increase in the size of infarct volume.

MEDIATORS OF ENDOTHELIAL DYSFUNCTION IN CEREBRAL ISCHEMIA IN PREMATURE INFANTS

N preterm infants with cerebral ischemia, the blood level of such mediators of endothelial dysfunction (MED), as endothelin-1, nitric oxide, angiotensin II, homocysteine, neurotrophic factors, tissue type plasminogen activator and von Willebrand factor was quantified. The established patterns of changes in the blood level of these mediators, depending on the degree of prematurity and severity of cerebral ischemia, reflect the severity of impairment of the functional state of the endothelial system. The quantitative data on the blood MED level in premature infants can be considered as criteria for the assessment of the degree of endothelial dysfunction, as in choosing modes for adequate timely correction of cerebrovascular disorders in newborns.

Allogeneic adipose-derived mesenchymal stem cell sheet that produces neurological improvement with angiogenesis and neurogenesis in a rat stroke model.

Stem cell therapy is a promising strategy for the treatment of severe cerebral ischemia. However, targeting sufficient grafted cells to the affected area remains challenging. Choosing an adequate transplantation method for the CNS appears crucial for this therapy to become a clinical reality. The authors used a scaffold-free cell sheet as a translational intervention. This method involves the use of cell sheet layers and allows the transplantation of a large number of cells, locally and noninvasively. The authors evaluated the effectiveness of allogeneic adipose tissue-derived mesenchymal stem cell sheets in a rat model of stroke. The animals, subjected to middle cerebral artery occlusion, were randomly divided in two groups: one in which a cell sheet was transplanted and the other in which a vehicle was used (n = 10/group). Over a period of 14 days after transplantation, the animals' behavior was evaluated, after which brain tissue samples were removed and fixed, and the extent of angiogenesis and infarct areas was evaluated histologically. Compared to the vehicle group, in the cell sheet group functional angiogenesis and neurogenesis were significantly increased, which resulted in behavioral improvement. Transplanted cells were identified within newly formed perivascular walls as pericytes, a proportion of which were functional. Newly formed blood vessels were found within the cell sheet that had anastomosed to the cerebral blood vessels in the host. The transplantation approach described here is expected to provide not only a paracrine effect but also a direct cell effect resulting in cell replacement that protects the damaged neurovascular unit. The behavioral improvement seen with this transplantation approach provides the basis for further research on cell sheet-based regenerative treatment as a translational treatment for patients with stroke.

Progesterone treatment in rats after severe global cerebral ischemia promotes hippocampal dentate gyrus neurogenesis and functional recovery

ABSTRACT Objective: Rats treated with progesterone (P4) after ischemia show an adequate functional performance despite a significant loss of hippocampal pyramidal neurons, suggesting that P4 could favour a permissive microenvironment for cerebral plasticity mechanisms. The possibility of P4 treatment promoting the survival of newly generated hippocampal neurons, in relation to the performance of ischemic rats in a spatial learning task, was assessed in this study. Methods: Adult male rats were subjected to a severe global cerebral ischemia episode (30 min) and treated with P4 or its vehicle at 15 min, 2, 6, 24, 48 and 72 h of reperfusion. From day 4 to 8 post-ischemia 5-bromo-2-deoxyuridine (BrdU) was administered to label proliferating cells. Twenty-one days post-ischemia, the rats were exposed to the Morris water maze to assess behavioral parameters of spatial learning and memory. Subsequently, the brain was perfusion-fixed and immunofluorescence procedures were performed to quantify the number of new mature neurons (BrdU+/NeuN+) in the dentate gyrus (DG) of the hippocampus. Results: Rats subjected to severe global cerebral ischemia and treated with P4 had a significantly better performance in spatial learning-memory tests, than those treated with vehicle, and a significantly higher number of new mature neurons (BrdU+/NeuN+) in the DG. Conclusion: These findings show that post-ischemia P4 treatment, following an episode of severe global cerebral ischemia, promotes the survival of newly generated hippocampal neurons in the DG, which may be one of the mechanisms of cerebral plasticity induced by the hormone, that underlie a successful functional performance in learning and memory tests.

Abstract TP124: Nicotine Alters Brain Energy Metabolism and Exacerbates Ischemic Brain Damage

Background: Smoking-derived nicotine (N) and oral contraceptives (OC) are known to synergistically magnify the risk and severity of cerebral ischemia in females. The underlying pathological mechanism remains elusive. Our studies have shown that N toxicity is exacerbated by OC via altered mitochondrial function, which involved a defect in activity of cytochrome c oxidase, the terminal enzyme of the electron transport chain. However, the effects of impaired mitochondrial function on brain metabolism remain to be investigated. To understand the impact in brain metabolisms, in the current study we investigated the global metabolomic profile of brains of adolescent and adult female rats exposed to N +/- OC. Methods: Six and twelve weeks old Sprague-Dawley female rats were randomly (n = 8/group) exposed to either saline, N (4.5 mg/kg) +/- OC for 16-21 days. At the end of the treatment, brain tissue was harvested for metabolomic analysis (performed by Metabolon Inc.) The metabolomic profile was complemented with western blot analysis and enzyme activity measurements. Results: Pathway enrichment analysis showed significant changes in energy metabolism (glycolysis and TCA cycle) and neurotransmitters in both adolescent and adult rats exposed to N, OC and N+OC in relation to saline treatment. The changes were more pronounced in adolescent rats with a significant decrease in glucose, glucose 6-phosphate, fructose-6-phosphate along with a significant increase in pyruvate in N and N+OC exposed groups when compared to saline (p<0.05), suggesting alterations in the glycolytic pathway. Western blot analyses of glycolytic enzymes support the observed metabolic changes. Conclusion: Nicotine and N+OC exposure increased brain glycolysis in an age-dependent manner. Since glucose metabolism is critical for brain physiology, altered glycolysis deteriorates neural function thus exacerbating ischemic brain damage. Moreover, significant decrease in the neuroactive peptide GABA was observed in young female rats treated with N+OC when compared to saline group. Discerning the exact effects of N +/- OC on overall brain metabolism and the molecular mechanisms affecting mitochondrial function at different ages will open a new window for future therapeutic intervention.

Are glutamate transporters neuroprotective or neurodegenerative during cerebral ischemia?

The accumulation of glutamate (Glu) in the synaptic cleft during cerebral ischemia triggers the death of neurons, causing mental or physical handicap. However, the mechanisms of the alteration in Glu homeostasis and the imbalance between the release and clearance of Glu in ischemia are not yet completely understood. Additionally, the role of Glu transporters in regulating Glu concentration in the synaptic cleft is controversial. This review aims to provide readers with an in-depth understanding of Glu transporters in the early or later stages of ischemic events, or in mild or severe cerebral ischemia via alteration of Glu transporter expression, reversal of Glu transporters function, and trafficking between membrane and cytoplasm, to further clarify whether the Glu transporters are neuroprotective or neurodegenerative during cerebral ischemia. We provide the insights for deeper understanding of the mechanism of Glu transporters regulation after different periods and severities of cerebral ischemia.

МОРФОЛОГИЧЕСКОЕ СТРОЕНИЕ КОРЫ НАДПОЧЕЧНИКОВ У ДОНОШЕННЫХ НОВОРОЖДЕННЫХ С ВРОЖДЕННОЙ ЦИТОМЕГАЛОВИРУСНОЙ ИНФЕКЦИЕЙ

The aim was to study the structure of the adrenal cortex in 36 dead full-term newborns. The main group consisted of 16 newborns with congenital cytomegalovirus infection, clinically manifested by moderate and severe cerebral ischemia, predominance of hypertensive-hydrocephalic syndrome, pseudocysts of the vascular plexus, sub-perpendicular and subarachnoid hemorrhages, monocytosis, vesiculosis, pneumonia, hepatitis and meningoencephalitis. The comparison group consisted of 20 dead newborns from mothers who did not have infectious diseases during pregnancy, as well as moderate and severe somatic and obstetric pathology. Birth trauma, intranatal and postnatal hypoxia were the main cause of their death. The evaluation of the pathomorphological picture of the adrenal cortex included a description of the general plan of the structure, the severity of alterative changes in glandulocytes, the number of adenomatous-like structures and their morphological forms, the reaction of loose fibrous connective tissue. It was found out that in suprarenal glands in children of the main group unlike the comparison group there was often detected a breach of the strands of granulocytes, there were found pronounced alterative changes in the cells; there were revealed large adenomatous-like structures in the lumen of which eosinophilic mass was often found and there was observed strongly-pronounced plethora of vessels. Only in the main group there were determined areas of thinning of the cortical substance of the glands, several adenomatous-like formations and anatomical forms containing in their lumen red blood cells and erythroblasts, as well as large hemorrhages. These structural changes indicated inhibition of adrenal cortex formation and prolonged antenatal stimulation of steroidogenesis under the influence of congenital cytomegalovirus infection leading to a decrease in glucocorticoid function of the suprarenal glands in children after birth.

ПАТОМОРФОЛОГИЧЕСКАЯ ХАРАКТЕРИСТИКА БРОНХОЛЕГОЧНОГО АППАРАТА У ПОГИБШИХ НОВОРОЖДЕННЫХ С ВРОЖДЕННОЙ ЦИТОМЕГАЛОВИРУСНОЙ ИНФЕКЦИЕЙ

The aim of the research was to study a morphological structure of airway and respiratory parts of lungs in 36 full-term newborns who died at the 2-5th day of life. The main group included 16 died newborns with the inborn cytomegalovirus infection who were diagnosed with moderate to severe cerebral ischemia with hypertension-hydrocephalic syndrome, pseudocysts of the blood vessels plexus, subependymal and subarachnoid haemorrhages, monocytosis, vesiculitis, pneumonia, hepatitis and meningocephalitis against intrauterine hypoxia and chronic subcompensated placental insufficiency. The comparison group consisted of 20 newborns whose mothers during the gestation period did not have acute respiratory viral infections, moderate and severe somatic and obstetrical pathology. The cause of their death was a birth trauma, intranatal and postnatal hypoxia. Describing lungs the following morphologic features were emphasized: 1) the changes of the general composition of the organ; 2) the state of the lumen of the large, medial and small bronchi; 3) the reaction of the epithelial lining, conjunctive tissue and the blood channel of the bronchial tree and aero-hematic barrier. As a result of the studies it was found out that in the newborns of the main group in comparison with the children of the comparison group in the lumen of large bronchi there was a rare case of mucus, there were often found erythrocytes and desquamated epithelial cells. Only infected children were found to have leucocytes. More intensified were alterative processes in epithelial cells; there were often found cells of the bronchial epithelium without ciliary structures, desquamation of highly differential ciliary and goblet cells, cell elements with a small hyperchromic nucleus and light cytoplasm in the cambial layer, sharply expressed vascular congestion, proliferative changes in the bronchial epithelium as well as hydropic-hemorrhagic and aspiration syndromes. Pneumonia and signs of the virus metamorphosis were diagnosed only in the main group.

Brain ischemic preconditioning protects against moderate, not severe, transient global cerebral ischemic injury.

Ischemic preconditioning (IPC) in the brain increases ischemic tolerance to subsequent ischemic insults. In this study, we examined whether IPC protects neurons and attenuates microgliosis or not in the hippocampus following severe transient global cerebral ischemia (TCI) in gerbils. Gerbils were assigned to 8 groups; 5- and 15-min sham operated groups, 5-min and 15-min TCI operated groups, IPC plus 5- and 15-min sham operated groups, and IPC plus 5- and 15-min TCI operated groups. IPC was induced by subjecting animals to 2-min transient ischemia 1day before 5-min TCI for a typical transient ischemia and 15-min TCI for severe transient ischemia. Neuronal damage was examined by cresyl violet staining and Fluoro-Jade B histofluorescence staining. In addition, microglial activation was examined using immunohistochemistry for Iba-1 (a marker for microglia). Delayed neuronal death and microgliosis was found in the CA1 alone in the 5-min TCI operated group at 5days post-ischemia, and, in the 15-min TCI operated group, neuronal death and microgliosis was shown in all CA areas (CA1-3) and the dentate gyrus. IPC displayed neuroprotection and attenuated microglial activation in the 5-min TCI operated group. However, in the 15-min TCI operated group, IPC did not show neuroprotection and not attenuate microglial activation. Our present findings indicate that IPC hardly protect against severe transient cerebral ischemic injury.

МОРФОЛОГИЧЕСКОЕ СОСТОЯНИЕ ПЕЧЕНИ У НОВОРОЖДЕННЫХ С ВРОЖДЕННОЙ ЦИТОМЕГАЛОВИРУСНОЙ ИНФЕКЦИЕЙ

The aim of the study was to study the morphological structure of the liver in newborns with congenital cytomegalovirus infection. The material for the study was the liver of 36 full-term newborns who died on the 2nd-5th day of life from birth trauma, intranatal and postnatal hypoxia. The main study group included 16 full-term newborns with congenital cytomegalovirus infection. The comparison group included 20 newborns from mothers without any viral infections, as well as moderate, severe somatic diseases and obstetric pathology during pregnancy, and these babies died at the 2nd-5th day of life from birth trauma, intrapartum and postnatal hypoxia. The main cause of death of children of early neonatal age was intrauterine infection which was clinically manifested by moderate or severe cerebral ischemia with hypertension-hydrocephalic syndrome, pseudocysts of the vascular plexus, subependymal and subarachnoid hemorrhages, monocytosis, vesiculosis, pneumonia, hepatitis and meningoencephalitis and antenatal hypoxia caused by the development of subcompensated placental insufficiency. When describing the liver, the attention was drawn to the following macroscopic and pathohistological changes in the organ: 1) the condition of the capsule of the organ; 2) the change of the general plan of a structure; 3) the reaction of the bloodstream of the liver: 4) the condition of the portal tracts; 5) the state of the lumen of the bile ducts and its epithelium. The material was fixed in 10% neutral formalin, dehydrated in alcohols and poured into paraffin. For observational microscopy, histological sections 5-7 μm thick were stained with Böhmer hematoxylin and eosin. Morphological examination of the liver in the newborns of the main group showed an increase in the frequency of detection of subcapsular hematomas, pronounced congestion of sinusoids, foci of lymphohistiocytic infiltration of the connective tissue of the portal tracts, small-focal proliferation of Kupffer cells, alterative and proliferative changes in the epithelium of the bile ducts, as well as cells with viral metamorphosis. The revealed structural changes in the morphological structure of the liver in full-term newborns indicate the development of pronounced dyscirculatory, alterative and inflammatory changes in the liver of cytomegalovirus genesis.

Abstract 106: Collateral Circulation in Thrombectomy for Stroke Beyond 6 Hours: Dawn Collaterals

Background: Collaterals govern the pace and severity of cerebral ischemia, distinguishing fast or slow progressors and corresponding therapeutic opportunities. The fate of sustained collateral perfusion or collateral failure is poorly characterized without arterial revascularization. We characterized the nature and impact of collaterals in the late time window for thrombectomy established in DAWN. Methods: The DAWN Imaging Core Lab prospectively scored collateral grade on baseline CTA and DSA (endovascular arm only), blinded to all other data. CTA collaterals were graded with the Tan scale and DSA collaterals were scored by ASITN grade. Descriptive statistics characterized CTA collateral grade in all DAWN subjects and DSA collaterals in the endovascular arm. The relationship between collateral grade and day 90 outcomes was separately analyzed for each treatment arm. Results: Collateral circulation to the ischemic territory was evaluated on CTA (n=144; median 2, 0-3) and DSA (n=57; median 2, 1-4) before thrombectomy in 161 DAWN subjects (mean age 69.8 ± 13.6 years; 55.3% women; 91 endovascular therapy, 70 control). CTA revealed a broad range of collaterals (grade 3=100%, n=64; 2=50-99%, n=45; 1=0-49%, n=31; 0=0%, n=4). DSA also showed a diverse range of collateral grades (grade 4, n=4; 3, n=22; 2, n=27; 1, n=4). Across treatment arms, baseline demographics, clinical variables except AF (41.6% endovascular vs. 25.0%, p=0.04) and CTA collateral grades were balanced. More robust CTA collateral grade was linked with lower baseline NIHSS (r=-0.25; p=0.003), smaller core infarct volumes (r=-0.36, p<0.001) and better day 90 mRS 0-2 clinical outcomes (r=0.20, p=0.019), but was unrelated to time from symptom onset or last known well to thrombectomy. Higher DSA collateral grade was linked with lower baseline NIHSS (r=-0.32; p=0.015), but sample size limited other potential associations. Interestingly, collateral grades on CTA and DSA were highly correlated (r=0.88, p<0.001). Conclusions: DAWN subjects enrolled at 6-24 hours after onset with small infarct cores had a wide range of collateral grades on both CTA and DSA. In this late time window, better collaterals manifest milder stroke severity at baseline, smaller infarct cores and better clinical outcomes.

Predictive power of abnormal electroencephalogram for post-cerebral infarction depression.

Electroencephalography is a sensitive indicator for measuring brain condition, and can reflect early changes in brain function and severity of cerebral ischemia. However, it is not yet known whether electroencephalography can predict development of post-cerebral infarction depression. A total of 321 patients with ischemic stroke underwent electroencephalography and Hamilton Depression Rating Scale assessment to analyze the relationship between electroencephalography and post-cerebral infarction depression. Our results show that electroencephalograms of ischemic stroke patients with depression exhibit low-amplitude alpha activity and slow theta activity. In contrast, electroencephalograms of ischemic stroke patients without depression show fast beta activity and slow delta activity. These findings confirm that low-amplitude alpha activity and slow theta activity can be considered as independent predictors for post-cerebral infarction depression.

КЛИНИКО-УЛЬТРАЗВУКОВАЯ И МОРФОЛОГИЧЕСКАЯ ХАРАКТЕРИСТИКА ЦЕРЕБРАЛЬНОЙ ИШЕМИИ ТЯЖЕЛОЙ СТЕПЕНИ У НОВОРОЖДЕННЫХ С ВНУТРИУТРОБНОЙ МОНО- И МИКСТ-РЕСПИРАТОРНОЙ ВИРУСНОЙ ИНФЕКЦИЕЙ

The contents of the tumor necrosis factor-alpha (TNF-α) in the serum of the umbilical blood as well as ultrasound and morphologic composition of liquor ways of the brain at severe cerebral ischemia was studied in 103 full-term newborns. The first group included 30 newborns from mothers with a physiologic course of pregnancy (subgroup A) and 20 dead newborns with antenatal anamnesis with uncomplicated virus infection, severe somatic pathology and late gestosis in their mothers during gestation (subgroup B); the second one included 28 newborns with severe cerebral ischemia against intrauterine parainfluenza infection (parainfuenza of 1 and 3 type), and 18 of them died at 3-6th day. The third group consisted of 25 newborns with severe cerebral ischemia against antenatal mixed-respiratory virus infection (parainfluenza of 1 and 3 types and influenza A(H3N2), and 16 of them died at the 2-4 days). It was found out that in the patients of the third group the contents of TNF-α increased till 62.7±2.14 pg/L (in the first and second groups it was 17.6±1.53 pg/L, p1<0.001 and 34.6±2.04 pg/L, respectively, p1<0.001). High values of pro-inflammatory cytokine were caused by the development of system inflammation reaction as a result of direct and mediated influence of some respiratory viruses. In the third group periventricular ischemia was found statistically oftener in 88% of newborns and brain immaturity in 48% of children (in the second group it was 32.1 and 10.7% of newborns, respectively); under pathomorphological study there were revealed big haematomas, subarachnoid haemorrhages, full-blown hyperemia and haematomas in the vascular plexus, karyorhexis, severe perivascular and pericellular edema, vasculitis as well as big focuses of atelectasis, aspirating pneumopathy and pneumonia. This suggested an important role of antenatal mixed-respiratory virus infection and pro-inflammatory cytokines in the improvement of penetrance of blood vessels wall under severe cerebral ischemia in newborns.

Therapeutic effect of enterprise stent-assisted embolization for very small ruptured intracranial aneurysms.

Enterprise stent has been widespread used in wide-necked intracranial aneurysms and good efficacy has been achieved, but there are few reports on its applications in very small ruptured intracranial aneurysms in literatures. This study aimed to evaluate the safety and efficacy of Enterprise stent-assisted coiling embolization of very small ruptured intracranial aneurysms.We retrospectively reviewed the clinical and imaging data from 37 patients with very small ruptured intracranial aneurysms who had SAC using Enterprise stents performed from February 2012 to July 2016 in our department. Data collected and analyzed included patient demographics, morphologic features of the aneurysm, treatment results, and follow-up results. Clinical outcomes were evaluated by the Glasgow Outcome Scale (GOS).Enterprise stents were successfully implanted in all 37 patients with very small ruptured intracranial aneurysms. Of the 37 individuals, 28 patients exhibited complete occlusion at Raymond grade I, 5 patients exhibited occlusion at Raymond grade II, and 4 patients at Raymond grade III. Procedure-related complications occurred in 3 of 37 patients (8.1%), including 1 case of intraprocedure aneurysm rupture who died from cerebral herniation caused by severe postoperative cerebral ischemia during the hospital stay, and the other 2 complications were acute in-stent thrombosis, and occlusion of parent artery caused by falling-off internal carotid artery plaque, respectively. A total of 36 patients underwent postoperative clinical follow-up visits for 6 to 24 months of which 31 patients recovered (GOS ≥ 4). One patient had hemiplegic paralysis, and no rehemorrhage was found. A total of 25 patients underwent follow-up digital subtraction angiography (DSA) at 3–21 months postintervention, in whom there were 22 cases with complete occlusion, 2 cases with recurrence of aneurysm neck, and 1 case with in-stent restenosis, but there was no patient with neurologic deficits.The Enterprise stent-assisted coiling embolization can be a safe and effective technique for treatment of very small ruptured intracranial aneurysms.

Open and Endovascular Management of Severe Cerebral Ischemia in Takayasu's Arteritis

Severe cerebral ischemia in patients with Takayasu's arteries was caused by occlusion of most supra-aortic arteries. Arterial revascularization is necessary to decrease the incidence of stroke and improve the quality of life but may be complicated with multiple occlusive lesions and inflammation condition of this disease. This study was to assess options and long-term outcomes of surgical and endovascular treatment. Twenty-nine patients with severe cerebral ischemic symptoms underwent surgical or endovascular treatment from January 1991 to July 2015. Demographic characteristics, surgical and endovascular procedures, and follow-up outcomes were reviewed. Risk factors associated with primary patency of surgical treatment and assisted primary patency of endovascular treatment was identified by Cox regression analyses. There were 29 patients with a median age of 24 (range 9-37years), 9 in active and 20 in inactive phase. Seventeen patients underwent a variety of bypass procedures. Fourteen endovascular procedures were performed in 12 patients. No death occurred within 30days after both procedures. Complications within 30days after bypass included stroke in 1 patient, infection in 2 patients, and heart failure in 1 patient. Nine patients developed brain hyperperfusion after bypass. Transient hemiplegic paralysis occurred in 1 patient during dilation of the carotid artery. During a median follow-up time of 41months, primary and secondary patency rate of bypass at 1 and 3years was 93.75% and 100% and 87.5% and 100%, respectively. Assisted primary and secondary patency rate of endovascular treatment at 1 and 3years was 85.71% and 92.86% and 68.18% and 75.66%, respectively. There was no independent risk factor associated with either primary patency of surgical treatment or assisted primary patency of endovascular treatment. Disease activity was independent risk factor associated with combined rate of primary patency of surgical treatment and assisted primary patency of endovascular treatment (HR: 0.17, 95% CI: 0.03-0.93, P=0.04). Bypass is the preferred treatment in majority of patients with good long-term patency, even has a higher propensity for postoperative complications. Endovascular treatment should be preserved for short lesions in inappropriate or high-risk surgical patients but needs more reintervention and close monitoring of lesion for better outcomes. Long-term patency of surgical and endovascular treatment is related with disease activity. Combination of surgical or endovascular treatment and medical therapy may improve the efficacy of interventions.

Some health aspects of children born with different types of intrauterine growth restriction during the early neonatal period

Aim. To evaluate some health aspects of children born with different types of intrauterine growth restriction during the early neonatal period.Methods. Clinical and anamnestic, physical, laboratory, electrophysiological, ultrasound and statistical methods were used. Children’s past medical history, development during early neonatal period, physical development, functioning of autonomic nervous system and cardiovascular system were assessed.Results. It was revealed that development of different types of intrauterine growth restriction is related to father and mother’s age at the time of pregnancy, women’s body mass before pregnancy, and time of pregnancy complication development (abortion risk, pre-eclampsia, arterial hypertension, Rh-immunization, edema). Fetuses with asymmetric type of intrauterine growth retardation had survived hypoxia more often (by 4.87 times). Children with symmetrical type of intrauterine growth retardation were more often born by C-section (by 2.66 times), with smaller anthropometric measurements, with more frequent and severe hypotrophy, moderate and severe cerebral ischemia and mild intracranial hemorrhage, cryptorchidism, kidney diseases, atrial septal defects, muscular ventricular septal defects, open arterial duct, and depleted reserves. Children with asymmetric type of intrauterine growth retardation more often had hypoglycemia, jaundice, polycythemia, restricted adaptation reserves, myocardial metabolic disorders, anterior mitral valve leaflet prolapse, posthypoxic changes similar to hypertrophic cardiopathy.Conclusion. Revealed features of past medical history, development during early neonatal period of life, physical development, functioning of autonomic nervous system and cardiovascular system in different types of children’s intrauterine growth restriction can promote formulation of criteria for early diagnosis of adaptive and reserve disorders and identification of dispensary groups.

NEWBORNS POSTHYPOXIC CARDIOPATHY: NEW TREATMENT OPTIONS

Objective of the research – to assess efficacy and safety of drug Elkar® 100 mg/ml for intravenous and intramuscular injection in treatment of newborns with posthypoxic cardiopathy. Patients were randomized into 2 groups, comparable in age, gestational age, severity of cerebral ischemia. The main group (n=43) in addition to standard therapy received Elkar® intravenously at a dose of 50–100 mg/kg/day, the comparison group (n=40) received only standard therapy for posthypoxic cardiopathy. The control group consisted of 20 children without clinically significant CNS and cardiovascular system (CVS) lesions. Elkar® contributed to a significant improvement in clinical status and optimization of postnatal CVS adjustment, manifesting as effective reduction of electrical instability and myocardial ischemia, heart rate recovery, systolic and diastolic function normalization, size of right heart chambers, reduced the diameter and hemodynamic significance of fetal functioning communications, restored vegetative regulation of heart rate and its circadian organization, helped to reduce rhythm pauses duration and arrhythmias representation. Elkar® intravenous use was satisfactorily tolerated by newborns and had no clinically significant adverse effects. The most rapid and complete regression of posthypoxic cardiopathy manifestations revealed after intravenous drug use at a dose of 80–100 mg/kg/day and continuing oral administration up to 1 month.

Staged Angioplasty for Vasculo-Behçet Disease with Severe Cerebral Ischemia

Staged Angioplasty for Vasculo-Behçet Disease with Severe Cerebral Ischemia

Combined Hemorrhagic Shock and Unilateral Common Carotid Occlusion Induces Neurological Injury in Adult Male Rats.

Background: Clinical assessment reveals that patients after surgery of cardiopulmonary bypass or coronary bypass experience postoperative cognitive dysfunction. This study aimed to investigate whether resuscitation after a hemorrhagic shock (HS) and/or mild cerebral ischemia caused by a unilateral common carotid artery occlusion (UCCAO) can cause brain injury and concomitant neurological dysfunction, and explore the potential mechanisms.Methods: Blood withdrawal (6 mL/100 g body weight) for 60 min through the right jugular vein catheter-induced an HS. Immediately after the termination of HS, we reinfused the initially shed blood volumes to restore and maintain the mean arterial blood pressure (MABP) to the original value during the 30-min resuscitation. A cooling water blanket used to induce whole body cooling for 30 min after the end of resuscitation.Results: An UCCAO caused a slight cerebral ischemia (cerebral blood flow [CBF] 70%) without hypotension (MABP 85 mmHg), systemic inflammation, multiple organs injuries, or neurological injury. An HS caused a moderate cerebral ischemia (52% of the original CBF levels), a moderate hypotension (MABP downed to 22 mmHg), systemic inflammation, and peripheral organs injuries. However, combined an UCCAO and an HS caused a severe cerebral ischemia (18% of the original CBF levels), a moderate hypotension (MABP downed to 17 mmHg), systemic inflammation, peripheral organs damage, and neurological injury, which can be attenuated by whole body cooling.Conclusions: When combined with an HS, an UCCAO is associated with ischemic neuronal injury in the ipsilateral hemisphere of adult rat brain, which can be attenuated by therapeutic hypothermia. A resuscitation from an HS regards as a reperfusion insult which may induce neurological injury in patients with an UCCAO disease.

Wavelet Analysis of Cerebral Microcirculation in Hypovolemic Shock.

Hypovolemic shock leads to severe cerebral ischemia and increases spectral amplitudes of cerebral blood flow oscillations in respiratory frequency range.