scholarly journals The Role of Inducible Nitric Oxide Synthase Following Spinal Cord Injury in Rat

2005 ◽  
Vol 20 (4) ◽  
pp. 663 ◽  
Author(s):  
Eun Kyoung Kwak ◽  
Jung Wan Kim ◽  
Ku Seong Kang ◽  
Yoon Hee Lee ◽  
Quan Hong Hua ◽  
...  
2009 ◽  
Vol 111 (4) ◽  
pp. 818-825 ◽  
Author(s):  
Akiko Ishikawa ◽  
Atsuo Mori ◽  
Nobuyuki Kabei ◽  
Akihiro Yoshitake ◽  
Takeshi Suzuki ◽  
...  

Background By using a U-shaped lumen catheter, the authors examined the effects of epidural cooling on spinal cord injury after aortic cross-clamping (ACC), with a focus on changes of spinal cord blood flow and expression of inducible nitric oxide synthase. Methods Sixteen pigs were randomized into two groups: Control group (n = 8) or Cooling group (n = 8). In the latter, epidural cooling started at 30 min (baseline) before 45 min of ACC and persisted for the next 30 min of reperfusion period. Spinal cord blood flow and somatosensory-evoked potentials were assessed during peri-ACC period. At 48 h, we evaluated hind limb function by using Tarlov score and expression of inducible nitric oxide synthase on spinal cord using immunohistochemistry. Results After ACC, spinal cord blood flow dropped to a similar extent in both groups. During the reperfusion period, spinal cord blood flow increased up to 113% (103-124%), median (interquartile range), level transiently and decreased to 32% (22-47%) level versus baseline in the Control group, whereas it increased and remained at 92% (86-97%) level in the Cooling group. Simultaneously, somatosensory-evoked potentials showed that onset of loss time was delayed and recovery time was shortened in the Cooling group. Tarlov scores in the Cooling group were significantly higher and accompanied by normal-appearing motor neurons and significantly greater expression of inducible nitric oxide synthase on spinal cord versus the Control group. Conclusions This study shows that epidural cooling during ACC minimized the risk of spinal cord injury, possibly by preventing delayed hypoperfusion and upregulating inducible nitric oxide synthase expression.


2017 ◽  
Vol 18 (2) ◽  
pp. 245 ◽  
Author(s):  
Dominic Maggio ◽  
Amanpreet Singh ◽  
J. Iorgulescu ◽  
Drew Bleicher ◽  
Mousumi Ghosh ◽  
...  

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  

1998 ◽  
Vol 158 (6) ◽  
pp. 1883-1889 ◽  
Author(s):  
ARNOLD S. KRISTOF ◽  
PETER GOLDBERG ◽  
VICTOR LAUBACH ◽  
SABAH N. A. HUSSAIN

2007 ◽  
Vol 103 (3) ◽  
pp. 1045-1055 ◽  
Author(s):  
Juliann G. Kiang ◽  
Phillip D. Bowman ◽  
Xinyue Lu ◽  
Yansong Li ◽  
Brian W. Wu ◽  
...  

Hemorrhage has been shown to increase inducible nitric oxide synthase (iNOS) and deplete ATP levels in tissues and geldanamycin limits both processes. Moreover, it is evident that inhibition of iNOS reduces caspase-3 and increases survival. Thus we sought to identify the molecular events responsible for the beneficial effect of geldanamycin. Hemorrhage in mice significantly increased caspase-3 activity and protein while treatment with geldanamycin significantly limited these increases. Similarly, geldanamycin inhibited increases in proteins forming the apoptosome (a complex of caspase-9, cytochrome c, and Apaf-1). Modulation of the expression of iNOS by iNOS gene transfection or siRNA treatment demonstrated that the level of iNOS correlates with caspase-3 activity. Our data indicate that geldanamycin limits caspase-3 expression and protects from organ injury by suppressing iNOS expression and apoptosome formation. Geldanamycin, therefore, may prove useful as an adjuvant in fluids used to treat patients suffering blood loss.


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