Capillary Wall Cells Research Articles

Assessment of cerebrovascular alterations induced by inflammatory response and oxidative–nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy

The rapid perfusion of cerebral arteries leads to a significant increase in intracranial blood volume, exposing patients with traumatic brain injury to the risk of diffuse brain swelling or malignant brain herniation during decompressive craniectomy. The microcirculation and venous system are also involved in this process, but the precise mechanisms remain unclear. A physiological model of extremely high intracranial pressure was created in rats. This development triggered the TNF-α/NF-κB/iNOS axis in microglia, and released many inflammatory factors and reactive oxygen species/reactive nitrogen species, generating an excessive amount of peroxynitrite. Subsequently, the capillary wall cells especially pericytes exhibited severe degeneration and injury, the blood–brain barrier was disrupted, and a large number of blood cells were deposited within the microcirculation, resulting in a significant delay in the recovery of the microcirculation and venous blood flow compared to arterial flow, and this still persisted after decompressive craniectomy. Infliximab is a monoclonal antibody bound to TNF-α that effectively reduces the activity of TNF-α/NF-κB/iNOS axis. Treatment with Infliximab resulted in downregulation of inflammatory and oxidative–nitrative stress related factors, attenuation of capillary wall cells injury, and relative reduction of capillary hemostasis. These improved the delay in recovery of microcirculation and venous blood flow.

Margination and diapedesis of inflammatory cells in the islets of langerhans in hamsters infected with the 139H strain of scrapie

The islets of Langerhans in hamsters infected with the 139H strain of scrapie contain large masses of red blood cells not surrounded by the usual arterial, venous or capillary wall cells. We have referred to these structures as "blood vessel cores" (BVCs). BVCs were almost always centrally located within the islets and surrounded by pancreatic B cells. Margination and diapedesis of inflammatory cells were observed at the BVC walls in 139H-infected hamsters. The cells consisted of the following types: single or clustered lymphocytes; and mixtures of lymphocytes and macrophages or neutrophils. Interaction observed between groups of inflammatory cells and B cells at the BVC walls and inside the islets of Langerhans indicated an inflammatory process. We refer to this interaction as the "linkage-reaction", and to the inflammatory cells as "linkage-inflammatory cells". These phenomena were not observed in other organs (adrenal, uterus, ovary, spleen, liver, kidney, oesophagus, trachea, intestine or pituitary) in 139H-affected hamsters or in the islets of Langerhans of animals infected with other scrapie strains (263K-infected hamsters; 139A-, ME7- and 22L-infected SJL mice). This appears to represent the first clear evidence of an inflammatory reaction in any organ in scrapie-infected animals.

Monte Carlo calculations of ion passages through brain endothelial nuclei during boron neutron capture therapy.

The Monte Carlo technique is used to examine the passage of ions from the (n, p) reaction in nitrogen and the (n, alpha) reaction in 10B through the nuclei of endothelial capillary wall cells of normal white matter. Contributions to the dose from different regions are evaluated, as is the distribution of doses to the nuclei for mean doses from 1 to 100 Gy. Calculation of mean dose to the nuclei is generalized for any neutron fluence and element concentration. The dose-averaged LETs for both reactions are found giving (for the particular conditions of the calculation); 60 keV/microns for the (n, p) reaction and 216 keV/micron for the (n, alpha) reaction in boron limited to the lumen, and 224 keV/micron for a uniform distribution of boron. From a consideration of 'minimal survival' and hit and dose distributions, evidence is presented which suggests that the RBE for the (n, alpha) reaction depends upon the distribution of the boron in the tissue, with the uniform distribution being less effective at cell killing than the boron restricted to the lumen for the same mean dose to the cell nuclei.

Immunochemical and immunohistochemical study of carbonic anhydrase II in adult rat cerebellum: A marker for oligodendrocytes

The use of specific antibodies to each of the two isoenzymes of carbonic anhydrase (CA I and CA II) shows that only CA II is intrinsic to nervous tissue, and all CA I detected is due to blood contamination. CA II is present in the cytosol as well as in the insoluble fraction of cerebellar homogenates. A small portion of the enzyme present in the sediment is a ‘cytosol’ enzyme trapped in membrane-limited structures but the majority appears to be membrane-bound. Immunohistology of CA II at the light and electron microscope levels and the use of double labelling technique with an astrocyte marker (glial fibrillary acidic protein) show that CA II is exclusively localized in cells with oligodendrocyte morphology and in their processes. Myelin appears to contain CA II only in the most peripheral lamella. Astrocytes, neurons and cells of capillary walls appear not to contain CA II. It can be concluded that carbonic anhydrase II serves as a marker for oligodendrocytes.

THE PROLIFERATIVE ACTIVITY OF MYOCARDIAL CAPILLARY WALL CELLS IN VARIOUSLY AGED SWIMMING‐EXERCISED RATS

Cellular proliferation was studied by incorporation of 3H-thymidine in the hearts of young, adult and old swimming-exercised rats. The proliferative activity was measured by scintillation counting. The swimming exercise induced a significant proliferation of capillary wall cells in the younger age groups, suggesting a neoformation of myocardial capillaries in these rats, whereas no cell proliferation was recorded in the old rats.

Proliferative activity of myocardial capillary wall cells in dipyridamole--treated rats.

The hearts of rats treated with dipyridamole were studied by light microscope autoradiography and measurement of tissue radioactivity after intravenous injection of 3H-thymidine. Total tissue radioactivity was significantly increased in the hearts of the dipyridamole-treated animals. Only capillary wall cells were labelled in the autoradiograms. The observations indicate a proliferation of capillary wall cells, suggesting a neoformation of myocardial capillaries during dipyridamole treatment.

EXPERIMENTAL CARDIAC HYPERTROPHY

Various forms of experimental cardiac hypertrophy were investigated by light and electron microscope autoradiography and measurements of myocardial tissue radioactivity after in vivo injections of 3H‐5‐uridine in rats. In the autoradiograms, the degree of labelling of striated muscle cells and capillary wall cells was estimated. A significant increase in 3H‐5‐uridine incorporation was recorded in the striated muscle cells of the left ventricle wall of rats with aortic stenosis, hypertension of short duration and of swimming exercised rats. In the latter case, an increased labelling was recorded also in the myocardial capillary endothelium. In the hypertrophying heart, the uridine was found in the striated muscle cell mitochondria in higher percentage than in the controls.

The proliferative activity of the myocardial tissue in various forms of experimental cardiac hypertrophy.

Various forms of experimental cardiac hypertrophy were investigated by light microscope autoradiography and measurements of tissue radioactivity after in vivo injections of 3H‐thymidine in rats. In the autaradiograms an attempt was made to distinguish between labelled vessel wall cells, connective tissue cells and heart muscle cells. A highly significant increase in the nuclear incorporation of 3H‐thymidine was recorded in both ventricle walls of rats with cardiac hypertrophy induced by swimming exercise. The increased incorporation was mainly confined to the nuclei of cells in the walls of the blood capillaries. A considerably smaller increase in the incorporation into capillary wall cells was recorded in the left ventricle wall of rats with cardiac hypertrophy secondary to prolonged arterial hypertension and aortic stenosis of 1–2 weeks1 duration. No increased incorporation of 3‐thymidine into the myocardial tissue was found in rats if their swimming exercise was followed by a period of rest, in rats with short‐term hypertension and in rats with aortic stenosis of 2 months' duration. The observations suggest a significant neoformation of myocardial blood vessels during swimming exercise, whereas any neoformation of myocardial blood vessels in arterial hypertension and aortic stenosis appears to be of minor degree.