Impact of age on cardiovascular function, inflammation, and oxidative stress in experimental asphyxial cardiac arrest

2017 ◽  
Vol 62 (1) ◽  
pp. 49-62 ◽  
Author(s):  
N. Secher ◽  
L. Østergaard ◽  
E. Tønnesen ◽  
F. B. Hansen ◽  
A. Granfeldt
2020 ◽  
Vol 35 (4) ◽  
pp. 286-295
Author(s):  
Yoonsoo Park ◽  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Bora Kim ◽  
Hyun-Jin Tae ◽  
...  

2018 ◽  
Vol 28 (9) ◽  
pp. 819-836 ◽  
Author(s):  
Simon J. Wilson ◽  
Mark R. Miller ◽  
David E. Newby

2020 ◽  
Vol 52 (7S) ◽  
pp. 815-815
Author(s):  
Cassie Williamson-Reisdorph ◽  
Katie S. Christison ◽  
Shae C. Gurney ◽  
Kathryn G.S. Tiemessen ◽  
Joseph A. Sol ◽  
...  

2019 ◽  
Vol 320 ◽  
pp. 112983 ◽  
Author(s):  
Jeong Hwi Cho ◽  
Hyun-Jin Tae ◽  
In-Shik Kim ◽  
Minah Song ◽  
Hyunjung Kim ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Bianca P. Campagnaro ◽  
Agata L. Gava ◽  
Silvana S. Meyrelles ◽  
Elisardo C. Vasquez

Mouse models provide powerful tools for studying the mechanisms underlying the dysfunction of the autonomic reflex control of cardiovascular function and those involved in cardiovascular diseases. The established murine model of two-kidney, one-clip (2K1C) angiotensin II-dependent hypertension represents a useful tool for studying the neural control of cardiovascular function. In this paper, we discuss the main contributions from our laboratory and others regarding cardiac-autonomic imbalance and baroreflex dysfunction. We show recent data from the angiotensin-dependent hypertensive mouse demonstrating DNA damage and oxidative stress using the comet assay and flow cytometry, respectively. Finally, we highlight the relationships between angiotensin and peripheral and central nervous system areas of cardiovascular control and oxidative stress in the 2K1C hypertensive mouse.


2011 ◽  
Vol 39 (2) ◽  
pp. 335-343 ◽  
Author(s):  
Karen H. Walson ◽  
Minke Tang ◽  
Ashley Glumac ◽  
Henry Alexander ◽  
Mioara D. Manole ◽  
...  

Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.


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