scholarly journals Ultrastructural changes in the microvessels and perivascular space in cerebral infarction in the experiment

Morphologia ◽  
2021 ◽  
Vol 14 (4) ◽  
pp. 16-28
Author(s):  
O. O. Voloshanska ◽  
S. i. Tertyshnyi
Keyword(s):  
Cerebral Infarction ◽  
Basement Membranes ◽  
Perivascular Space ◽  
Ultrastructural Changes ◽  
Intracellular Regeneration ◽  
Common Cause ◽  
Cell Contacts ◽  
Perivascular Edema ◽  
Intercellular Contacts ◽  
The Brain

Background. Ischemic stroke is the second most common cause of death after coronary heart disease and the most common cause of disability worldwide. Much of the recent basic research on stroke is concerned with the mechanisms underlying the dysfunction and adaptation of the neurovascular block, which includes the blood-brain barrier structures, microglia, neurons, and the extracellular matrix of the basement membrane. Isolated studies of recent years have been devoted to the issues of morphology and in particular the ultrastructure of the brain in ischemic injury. Meanwhile, only morphological studies can reveal the peculiarities of the response of cellular structures to the influence of various adverse factors. Objective – to investigate ultrastructural changes in the vessels of the brain and perivascular space in experimental ischemic heart attack. Methods. Experimental cerebral infarction was reproduced on 15 white Wistar rats by injection of a suspension of barium sulfate in sterile saline in a ratio of 1: 3 in the amount of 0.1 -0.3 ml. Three animals formed a control group. The material was collected in terms of: up to 3, 9, 12 days and more than 12 days from the beginning of the experimental action, followed by standard processing of the material for electron microscopy. Results. In the early stages of ischemic brain damage perivascular edema, destructive changes of capillaries with destruction of basement membranes are registered. Some microvessels undergo irreversible changes with deformation of the vascular lumen, pyknosis and lysis of endothelial nuclei, destruction and vacuolation of cytoplasmic structures, microvacuolation and edema of mitochondria with partial destruction of cristae and enlightenment of the mitochondrial matrix. In the endothelium with signs of coagulation processes in the cytoplasm and nucleus, changes in cell contacts were observed. Structural changes of vessels are combined with changes of perivascular processes of astrocytes. On days 9 and 12, the structure of the endothelium, perivascular astrocytes, and intercellular contacts are restored. Hyperplasia of intracytoplasmic structures, increase in mitochondria and length of cytoplasmic network are noted. In the cells of the perivascular environment and in the cytoplasm of pericytes a significant number of phagolysosomes is detected, in the long term in the perifocal areas of irreversible ischemic changes around the vessels is reparative astrogliosis. Conclusion. Ultrastructural changes of the microcirculatory part in the perifocal areas of ischemic lesions within 3 days are characterized by perivascular edema and destructive changes in the endothelium of capillaries and pericytes, damage to basement membranes, changes in cell contacts. After 9-12 days in the endothelium, the processes of intracellular regeneration increase, the ultrastructure of intercellular contacts is restored. A significant number of phagolysosomes is registered in the cells of the perivascular environment and in the cytoplasm of pericytes, and reparative astrogliosis is detected in the perifocal areas of irreversible ischemic changes around the vessels.

PATHOHISTOLOGICAL CHANGES IN PIGS WITH MYCOPLASMOSIS

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
N. B. Kolych ◽  
◽  
N. V. Hudz ◽  
Keyword(s):  
Mucous Membrane ◽  
Alveolar Wall ◽  
Soft Or ◽  
Diffuse Infiltration ◽  
Small Areas ◽  
Perivascular Edema ◽  
Mucous Membranes ◽  
The Right ◽  
The Brain ◽  
Dark Pink

A pathological autopsy was performed on 6 corpses of piglets in the first week of life who died from mycoplasmosis. Examination of the visible mucous membranes revealed hyperemia of the mucous membrane of the nasal cavity and thymus. Simultaneous lesions of the pharyngeal, parotid, cervical, mandibular lymph nodes were noted. They were slightly enlarged, from dark pink to dark red. The heart is irregularly shaped due to the expansion of the right ventricle or the diffuse expansion of all departments. Lungs have doughy consistency, uneven color. In some cases, there are diffuse red areas covering the entire lobe of the lungs, in other cases, there is a defeat of small areas. The liver has a smooth surface, soft or pasty consistency, the parenchyma pattern is slightly smoothed in section. The color of the liver is different: dark red areas, without clear boundaries turn into creamy-clay. Flatulence was a characteristic feature of the stomach and intestines. Catarrhal enteritis was registered in animals, which manifested itself in the form of moderate hyperemia of the intestinal mucosa and serous membranes. Microscopically, there is a significant blood supply to the vessels in the lungs. Alveoli are half fall down, in the form of slit-like lumens. In areas of tissue infiltration by inflammatory infiltrate, the alveolar wall is thickened, alveocytes are in a state of turbid swelling and vacuolar dystrophy, they are impregnated with erythrocytes. Peribronchial pneumonia of lymphocytic character is observed. The liver is in a state of acute venous hyperemia. The central and intraparticle capillaries are sharply dilated and filled with blood in some lobes, and the hepatic beams are compressed accordingly. In the center of other lobes, diffuse infiltration of liver tissue by erythrocytes as a consequence of diapedesis is noted. Hepatocytes are in a state of granular dystrophy. Destructive changes are strongly expressed in the mucous membrane of the small intestine: desquamation of the epithelium, necrosis of epitheliocytes and villi, destruction of crypts. In the brain tissue, there is dilation of the lumens of large and small blood vessels, extracellular and perivascular edema, areas of reactive necrosis.

Ultrastructural changes of Basolateral Amygdaloid nuclei in the Sprague Dawley rats brain following exposure to naphthalene balls

2021 ◽  
Vol 12 (2) ◽  
pp. 1272-1275
Author(s):  
Angu Bala Ganesh K S V ◽  
Sujeet Shekhar Sinha ◽  
Kesavi Durairaj ◽  
Abdul Sahabudeen K
Keyword(s):  
Structural Changes ◽  
Corn Oil ◽  
Chromatin Condensation ◽  
Ultrastructural Changes ◽  
High Dose ◽  
Model Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
The Brain ◽  
Amygdaloid Nuclei

Naphthalene is a bicyclic aromatic constituent commonly used in different domestic and marketable applications comprising soil fumigants, lavatory scent disks and mothballs. Accidentally, workers, children and animals are exposed to naphthalene mothballs, so there is a need to study the pathology behind this chemical toxicity. The current study was carried out to assess the ultra structural changes of basolateral amygdaloid nuclei in the Sprague Dawley rats brain in association to naphthalene toxicity. The toxicity model group was administered with naphthalene (200 and 400mg) using corn oil as a vehicle for 28 days. The post delayed toxicity of naphthalene high dose ingestion was also assessed in rats. After the experimental period, the brain tissue was processed to observe the ultra structural changes using a transmission electron microscope. The alterations in cell organelles, nuclei damage, mitochondrial swelling, chromatin condensation suggested naphthalene induced damage in the neurons of the basolateral amygdala of the brain in the toxicity model group. These experimental trials provide information about the alert of mothball usage in the home and identify risks linked with accidental exposure and misuse.

Comparative changes in the blood-brain barrier and cerebral infarction of SHR and WKY rats

2007 ◽  
Vol 292 (5) ◽  
pp. R1881-R1892 ◽  
Author(s):  
Sharon Hom ◽  
Melissa A. Fleegal ◽  
Richard D. Egleton ◽  
Christopher R. Campos ◽  
Brian T. Hawkins ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Blood Brain Barrier ◽  
Infarct Volume ◽  
Brain Barrier ◽  
Ion Transporter ◽  
Transporter Proteins ◽  
Wky Rats ◽  
Blood Brain ◽  
Hypertension Development ◽  
The Brain

Hypertension is involved in the exacerbation of stroke. It is unclear how blood-brain barrier (BBB) tight-junction (TJ) and ion transporter proteins critical for maintaining brain homeostasis contribute to cerebral infarction during hypertension development. In the present study, we investigated cerebral infarct volume following permanent 4-h middle cerebral artery occlusion (MCAO) and characterized the expression of BBB TJ and ion transporter proteins in brain microvessels of spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto (WKY) rats at 5 wk (prehypertension), 10 wk (early-stage hypertension), and 15 wk (later-stage hypertension) of age. Hypertensive SHR show increased infarct volume following MCAO compared with WKY control rats. BBB TJ and ion transporter proteins, known to contribute to edema and fluid volume changes in the brain, show differential protein expression patterns during hypertension development. Western blot analysis of TJ protein zonula occludens-2 (ZO-2) showed decreased expression, while ion transporter, Na+/H+ exchanger 1 (NHE-1), was markedly increased in hypertensive SHR. Expression of TJ proteins ZO-1, occludin, actin, claudin-5, and Na+-K+-2Cl− cotransporter remain unaffected in SHR compared with control. Selective inhibition of NHE-1 using dimethylamiloride significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR.

scholarly journals A case of severe acute respiratory syndrome coronavirus 2 with acute thrombotic cerebral infarction and generalized thrombosis

2021 ◽  
pp. 405-408
Author(s):  
Sylvia Nikolaeva Genova ◽  
Nikolaeva Genova ◽  
Mina Miroslavova Pencheva ◽  
Alexander Georgiev Ivanov
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Cerebral Infarction ◽  
Viral Pneumonia ◽  
Autopsy Case ◽  
Full Spectrum ◽  
Histological Changes ◽  
Large Size ◽  
Thrombotic Complications ◽  
Coronavirus Infection ◽  
The Brain

The full spectrum of coronavirus disease 2019 (COVID-19) has not been fully described yet. COVID-19 is associated with a high risk of thrombotic complications such as venous thromboembolism and cerebrovascular disease. Here, we report an autopsy case of a 55-year-old woman diagnosed with severe viral pneumonia complicated by acute cerebral infarction and venous and arterial thrombosis in different organs. The patient died due to severe acute respiratory syndrome coronavirus 2. Macroscopically and histologically, in addition to viral pneumonia and diffuse hemorrhages, fibrin clots were found in arteries and venous vessels of medium and large size in the brain, lungs, and pancreas. Propagation of cerebrovascular thrombosis has led to extensive cerebral infarction. The dating of this infarction, according to the macroscopical findings and the histological changes, was between 24 and 48 h before death. This case confirms the hypothesis on the risk of generalized arterial and venous thromboses in coronavirus infection.

scholarly journals A ROLE OF POLYMORPHONUCLEAR LEUKOCYTES AND COMPLEMENT IN NEPHROTOXIC NEPHRITIS

1965 ◽  
Vol 122 (1) ◽  
pp. 99-116 ◽  
Author(s):  
Charles G. Cochrane ◽  
Emil R. Unanue ◽  
Frank J. Dixon
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Basement Membranes ◽  
Ultrastructural Changes ◽  
Glomerular Injury ◽  
Large Numbers ◽  
Secondary Stage ◽  
Vascular Beds ◽  
Nephrotoxic Nephritis ◽  
Glomerular Damage

In acute nephrotoxic nephritis, polymorphonuclear leukocytes (polymorphs) accumulated in large numbers in the glomeruli in the first 12 hours. The endothelial cells were dislodged by the polymorphs which then came to lie immediately adjacent to the glomerular basement membranes. Ultrastructural changes in neither polymorphs nor basement membranes were observed. Depletion of polymorphs in both rats and rabbits prevented the development of proteinuria. This occurred when doses of nephrotoxic globulin were employed that produced proteinurias of as much as 1800 mg/kg/24 hours in intact rabbits, or enough to yield near maximal immediate proteinuria in intact rats. In addition, measurable glomerular damage was frequently averted until the onset of the secondary stage of NTN. Controls indicated that the polymorph depleted animals exhibited minimal non-specific changes in the blood, that the ability of their vascular beds to react to stimuli was not affected, and that deposition of nephrotoxic antibody and C' in the glomeruli was not inhibited. Elimination of polymorphs from the circulation was only partially effective in preventing glomerular damage when large doses of nephrotoxic globulin were used. This indicated that under these circumstances, a polymorph independent glomerular injury may also take place in first stage nephrotoxic nephritis. An indirect role of C', i.e., the accumulation of polymorphs, in bringing about glomerular injury in first stage nephrotoxic nephritis was apparent. When rabbit nephrotoxic globulin was injected into rats depleted of C', or when duck nephrotoxic globulin that fixed C' poorly was injected into normal rats, C' failed to bind with the antibody along glomerular basement membranes and polymorphs did not accumulate.

Ultrastructural changes in the penumbra zone of the local cerebral infarction in rats

2021 ◽  
Vol 172 (11) ◽  
pp. 643-649
Author(s):  
N. Chlikadze ◽  
◽  
M. Arabuli ◽  
I. Lazrishvili ◽  
N. Mitagvaria ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Ultrastructural Changes

General concepts of hypothalamus-pituitary anatomy

2011 ◽  
pp. 71-81
Author(s):  
Ignacio Bernabeu ◽  
Monica Marazuela ◽  
Felipe F. Casanueva
Keyword(s):  
Median Eminence ◽  
Third Ventricle ◽  
Optic Chiasm ◽  
Perivascular Space ◽  
Ependymal Cells ◽  
The Third ◽  
Long Time ◽  
Central Grey Matter ◽  
Imaginary Line ◽  
The Brain

The hypothalamus is the part of the diencephalon associated with visceral, autonomic, endocrine, affective, and emotional behaviour. It lies in the walls of the third ventricle, separated from the thalamus by the hypothalamic sulcus. The rostral boundary of the hypothalamus is roughly defined as a line through the optic chiasm, lamina terminalis, and anterior commissure, and an imaginary line extending from the posterior commissure to the caudal limit of the mamillary body represents the caudal boundary. Externally, the hypothalamus is bounded rostrally by the optic chiasm, laterally by the optic tract, and posteriorly by the mamillary bodies. Dorsolaterally, the hypothalamus extends to the medial edge of the internal capsule (Fig. 2.1.1) (1). The complicated anatomy of this area of the central nervous system (CNS) is the reason why, for a long time, little was known about its anatomical organization and functional significance. Even though the anatomy of the hypothalamus is well established it does not form a well-circumscribed region. On the contrary, it is continuous with the surrounding parts of the CNS: rostrally, with the septal area of the telencephalon and anterior perforating substance; anterolaterally with the substantia innominata; and caudally with the central grey matter and the tegmentum of the mesencephalon. The ventral portion of the hypothalamus and the third ventricular recess form the infundibulum, which represents the most proximal part of the neurohypophysis. A bulging region posterior to the infundibulum is the tuber cinereum, and the zone that forms the floor of the third ventricle is called the median eminence. The median eminence represents the final point of convergence of pathways from the CNS on the peripheral endocrine system and it is supplied by primary capillaries of the hypophyseal portal vessels. The median eminence is the anatomical interface between the brain and the anterior pituitary. Ependymal cells lining the floor of the third ventricle have processes that traverse the width of the median eminence and terminate near the portal perivascular space; these cells, called tanycytes, provide a structural and functional link between the cerebrospinal fluid (CSF) and the perivascular space of the pituitary portal vessels. The conspicuous landmarks of the ventral surface of the brain can be used to divide the hypothalamus into three parts: anterior (preoptic and supraoptic regions), middle (tuberal region), and caudal (mamillary region). Each half of the hypothalamus is also divided into a medial and lateral zone. The medial zone contains the so-called cell-rich areas with well-defined nuclei. The scattered cells of the lateral hypothalamic area have long overlapping dendrites, similar to the cells of the reticular formation. Some of these neurons send axons directly to the cerebral cortex and others project down into the brainstem and spinal cord.

The Challenging Data of Neuroscience and the Challenges Mounted from That Data

2020 ◽  
pp. 207-261
Author(s):  
Michael S. Moore
Keyword(s):  
Moral Agency ◽  
Mental States ◽  
Privileged Access ◽  
Common Cause ◽  
The Brain

The suppositions about the psychology of moral agency are challenged by neuroscience in four ways: first, by denying that the choices of persons can be uncaused (and thus “free” in this contra-causal sense); second, by denying that the choices of persons actually cause the actions that are chosen, such actions rather being epiphenomenal with such actions, co-effects of some common cause in the brain; third, by denying that the minds of persons are anything but the brute, dumb firing of two valued switches in the brains of such persons, a mere mechanism or machine; fourth, by denying that persons have the kind of privileged access to their own mental states that gives persons the knowledge needed for control and for responsibility. Two responses to these four challenges are previewed, a response denying the truth of these claims and a response denying the relevance of these claims to responsibility. The attempt to sidestep these challenges known as “cheap compatibilism” is also reviewed and rejected.

Malformation of the Brain, Skull, and Spine

2021 ◽  
pp. 1057-1070
Author(s):  
Lily C. Wong-Kisiel
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Developmental Delay ◽  
Abnormal Development ◽  
Gene Expressions ◽  
Common Cause ◽  
Genetic Causes ◽  
The Central Nervous System ◽  
The Brain ◽  
Central Nervous System Malformation

Abnormal development of the central nervous system is a common cause of developmental delay and epilepsy. An understanding of central nervous system malformation begins with an overview of normal embryology. Genetic advances in embryogenesis have unfolded a complex orchestration of gene expressions in place of the traditional developmental epochs (induction, neurulation, proliferation, migration, organization, synaptogenesis, and myelination). Causes of malformation of the central nervous system are multifactorial. Genetic causes, vitamin excess or deficiency, infections, or teratogens any time during pregnancy may disturb the preprogrammed mechanisms.

Sign in / Sign up

Export Citation Format

Share Document