PATIENTS AND METHODS: Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used.
RESULTS: Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwentprofound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.
METHODS: Sodium nitrite (50mg/L) was given to angiotensin II-infused hypertensive C57BL/6J (eight to ten weeks old) mice for two weeks in the drinking water. Arterial systolic blood pressure was measured using the tail-cuff method. Vascular responsiveness of isolated aortae and renal arteries was studied in wire myographs. The level of nitrite in the plasma and the cyclic guanosine monophosphate (cGMP) content in the arterial wall were determined using commercially available kits. The production of reactive oxygen species (ROS) and the presence of proteins (nitrotyrosine, NOx-2 and NOx-4) involved in ROS generation were evaluated with dihydroethidium (DHE) fluorescence and by Western blotting, respectively.
RESULTS: Chronic administration of sodium nitrite for two weeks to mice with angiotensin II-induced hypertension decreased systolic arterial blood pressure, reversed endothelial dysfunction, increased plasma nitrite level as well as vascular cGMP content. In addition, sodium nitrite treatment also decreased the elevated nitrotyrosine and NOx-4 protein level in angiotensin II-infused hypertensive mice.
CONCLUSIONS: The present study demonstrates that chronic treatment of hypertensive mice with sodium nitrite improves impaired endothelium function in conduit and resistance vessels in addition to its antihypertensive effect, partly through inhibition of ROS production.
CASE PRESENTATION: A 23-year-old trauma patient with closed fracture of left femoral shaft and left humerus presented to our emergency department (ED). 11 h after admission to ED, patient became confused, hypoxic and hypotensive. He was then intubated for respiratory failure and mechanically ventilated. Transesophageal ultrasound revealed hyperdynamic heart, dilated right ventricle with no regional wall abnormalities and no major aorta injuries. Whole-body computed tomography was normal. During central venous cannulation of right internal jugular vein (IJV), we found free floating mobile hyperechoic spots, located at the anterior part of the vein. A diagnosis of fat embolism syndrome later was made based on the clinical presentation of long bone fractures and fat globulin in the blood. Despite aggressive fluid resuscitation, patient was a non-responder and needed vasopressor infusion for persistent shock. Blood aspirated during cannulation from the IJV revealed a fat globule. Patient underwent uneventful orthopedic procedures and was discharged well on day 5 of admission.
CONCLUSIONS: Point-of-care ultrasound findings of fat embolism in central vein can facilitate and increase the suspicion of fat embolism syndrome.