scholarly journals Particulate matter exposure induces persistent lung inflammation and endothelial dysfunction

2008 ◽  
Vol 295 (1) ◽  
pp. L79-L85 ◽  
Author(s):  
Eiji Tamagawa ◽  
Ni Bai ◽  
Kiyoshi Morimoto ◽  
Claire Gray ◽  
Tammy Mui ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Endothelial Dysfunction ◽  
Total Dose ◽  
Systemic Inflammation ◽  
Lung Inflammation ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Vascular Events ◽  
Acute And Chronic Exposure

Epidemiologic and animal studies have shown that exposure to particulate matter air pollution (PM) is a risk factor for the development of atherosclerosis. Whether PM-induced lung and systemic inflammation is involved in this process is not clear. We hypothesized that PM exposure causes lung and systemic inflammation, which in turn leads to vascular endothelial dysfunction, a key step in the initiation and progression of atherosclerosis. New Zealand White rabbits were exposed for 5 days (acute, total dose 8 mg) and 4 wk (chronic, total dose 16 mg) to either PM smaller than 10 μm (PM10) or saline intratracheally. Lung inflammation was quantified by morphometry; systemic inflammation was assessed by white blood cell and platelet counts and serum interleukin (IL)-6, nitric oxide, and endothelin levels. Endothelial dysfunction was assessed by vascular response to acetylcholine (ACh) and sodium nitroprusside (SNP). PM10 exposure increased lung macrophages ( P < 0.02), macrophages containing particles ( P < 0.001), and activated macrophages ( P < 0.006). PM10 increased serum IL-6 levels in the first 2 wk of exposure ( P < 0.05) but not in weeks 3 or 4. PM10 exposure reduced ACh-related relaxation of the carotid artery with both acute and chronic exposure, with no effect on SNP-induced vasodilatation. Serum IL-6 levels correlated with macrophages containing particles ( P = 0.043) and ACh-induced vasodilatation ( P = 0.014 at week 1, P = 0.021 at week 2). Exposure to PM10 caused lung and systemic inflammation that were both associated with vascular endothelial dysfunction. This suggests that PM-induced lung and systemic inflammatory responses contribute to the adverse vascular events associated with exposure to air pollution.

scholarly journals Paradoxical absence of a prothrombotic phenotype in a mouse model of severe hyperhomocysteinemia

Blood ◽  
2012 ◽  
Vol 119 (13) ◽  
pp. 3176-3183 ◽  
Author(s):  
Sanjana Dayal ◽  
Anil K. Chauhan ◽  
Melissa Jensen ◽  
Lorie Leo ◽  
Cynthia M. Lynch ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Carotid Artery ◽  
Inferior Vena ◽  
Vena Cava ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Vascular Events ◽  
Cerebral Arterioles ◽  
Increased Susceptibility

Abstract Hyperhomocysteinemia confers a high risk for thrombotic vascular events, but homocysteine-lowering therapies have been ineffective in reducing the incidence of secondary vascular outcomes, raising questions regarding the role of homocysteine as a mediator of cardiovascular disease. Therefore, to determine the contribution of elevated homocysteine to thrombosis susceptibility, we studied Cbs−/− mice conditionally expressing a zinc-inducible mutated human CBS (I278T) transgene. Tg-I278T Cbs−/− mice exhibited severe hyperhomocysteinemia and endothelial dysfunction in cerebral arterioles. Surprisingly, however, these mice did not display increased susceptibility to arterial or venous thrombosis as measured by photochemical injury in the carotid artery, chemical injury in the carotid artery or mesenteric arterioles, or ligation of the inferior vena cava. A survey of hemostatic and hemodynamic parameters revealed no detectible differences between control and Tg-I278T Cbs−/− mice. Our data demonstrate that severe elevation in homocysteine leads to the development of vascular endothelial dysfunction but is not sufficient to promote thrombosis. These findings may provide insights into the failure of homocysteine-lowering trials in secondary prevention from thrombotic vascular events.

scholarly journals A prospective study on urinary microalbuminuria as surrogate marker of vascular endothelial dysfunction, in patients of ischemic stroke

2017 ◽  
Vol 4 (3) ◽  
pp. 778
Author(s):  
Yogendra Jamra ◽  
Dharmendra Jhawar ◽  
Rajneesh Patidhar
Keyword(s):  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Serum Creatinine ◽  
Creatinine Clearance ◽  
Surrogate Marker ◽  
Normal Serum ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Vascular Events ◽  
Normal Serum Creatinine

Background: Presence of overt proteinuria has been independently linked to greater stroke risk. The objectives of this study were to determine the relationship between the for ischemic stroke and albuminurea as a marker for vascular events. Microalbuminuria, is an early marker of both kidney disease and endothelial dysfunction, may be associated with global vascular risk, but the nature and relationship between microalbuminuria and incident ischemic stroke has not been clearly defined. The purpose of this study was to assess the association of microalbuminuria and ischemic stroke.Methods: Study enrolled 150 admitted patients of acute ischemic stroke. The patients were assessed by questionnaire, microalbuminuria, creatinine clearance after detailed history taking and thorough clinical examination.Results: The combined common risk factors were HTN (80%), diabetes (33%) and smoking (53%). The hypertensive patients had 8 times higher risk of microalbuminuria as compared to normotensive patients (95% 1.8-31.0 p<0.05). Among diabetes patients had risk of microalbuminuria 30 times higher compared to euglycemic patients (95% CL 9.6-78.8 p<0.01). The smoker patients had 8 times risk of microalbuminuria (CL 95%-1.2-22.8 p<0.16). However, the patients who had dyslipidemia had risk of microalbuminuria 1.07 times who have normal lipid level, but it was statistically insignificance (98% CL 0.8-4.1 p>0.05). The 38 patients out of 46 patients who had microalbuminuria has high normal serum creatinine with creatinine clearance (45-59 mL/min/1.73 m2. (82% versus. 4.4% 30.44 mL/min/173m2). The risk of microalbuminuria was higher in patients who had high normal serum creatinine (1.4 mg/dL) with creatinine clearance of 45-59 mL/min/1.73 m2 versus normal serum creatinine 0.8 mg/dL.Conclusions: The finding of the study, show the microalbuminuria is an independent risk factor for vascular endothelial dysfunction, in patient of diabetes early renal dysfunction and HTN, extrapolating the vascular event (ischemic stroke).

scholarly journals Periodontitis is associated with systemic inflammation and vascular endothelial dysfunction in patients with lacunar infarct

2018 ◽  
Vol 90 (5) ◽  
pp. 465-474 ◽  
Author(s):  
Yago Leira ◽  
Manuel Rodríguez‐Yáñez ◽  
Susana Arias ◽  
Iria López‐Dequidt ◽  
Francisco Campos ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Systemic Inflammation ◽  
Lacunar Infarct ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction

scholarly journals ASSOCIATION OF ARTERIAL STIFFNESS WITH MARKERS OF VASCULAR ENDOTHELIAL DYSFUNCTION AND SYSTEMIC INFLAMMATION IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE

2018 ◽  
Vol 1 (67) ◽  
pp. 31-36 ◽  
Author(s):  
Екатерина Кулик ◽  
Ekaterina Kulik ◽  
Валентина Павленко ◽  
Valentina Pavlenko ◽  
Светлана Нарышкина ◽  
...  
Keyword(s):  
High Risk ◽  
Endothelial Dysfunction ◽  
Arterial Stiffness ◽  
Systemic Inflammation ◽  
Group Analysis ◽  
Chronic Obstructive ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Severe Copd

In order to analyze the relationship between the indices of arterial stiffness and the markers of vascular endothelial dysfunction and systemic inflammation, 69 patients with severe COPD and high-risk (GOLD 2013) during an exacerbation were examined. The stiffness of the vascular wall was determined with the help of an automatic sphygmograph and a sphygmomanometer "VaSera VS-1000". For the study, the carotid-femoral pulse wave velocity (PWV-aorta), right and left cardiovascular vascular index (R/L-CAVI) were chosen. Determination of the indices of systemic inflammation and vascular damage was carried out in the blood serum by the method of enzyme immunoassay. Analysis of the quantitative characteristics of arterial stiffness in patients with severe COPD and high risk revealed that in general in the group the studied indices were significantly higher than those of healthy individuals. The mean age of the vessels in the group of patients exceeded the biological age by 11.5% and amounted, on average, to 68.46-1.22 years. The in-group analysis revealed that concentrations of biomarkers of systemic inflammation and endothelial dysfunction were higher in COPD patients with R-CAVI values greater than 9, compared with less than 9 in the R-CAVI group. In a separate correlation analysis, it was found that the increase in the basic indices of arterial stiffness was associated both with the level of the indicators of systemic inflammation, and with the biomarkers of endothelial dysfunction. The obtained interrelations show that the formation of excessive vascular stiffness in patients with severe COPD of high risk is associated with the activation of inflammatory mediators and endothelial dysfunction, mostly with high levels of high-sensitivity C-reactive protein, fibrinogen, endothelin-1, homocysteine and TNF-α, and that’s why the determination of these parameters of AS is recommended, first of all, to these patients. The registration of events that manifest interdependent changes in the processes of vascular bed remodeling, systemic inflammation and endothelial dysfunction will allow early detection of patients with increased cardiovascular risk and timely intensification of therapy in this category of patients

Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction

Cell Cycle ◽  
2021 ◽  
pp. 1-13
Author(s):  
Qian-Qian Zhu ◽  
Xi-Bin Pu ◽  
Tian-Chi Chen ◽  
Chen-Yang Qiu ◽  
Zi-Heng Wu ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
High Glucose ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction
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