Cardiovascular Properties of a Nitric Oxide Releasing Rofecoxib Analogue: Beneficial Anti-hypertensive Activity and Enhanced Recovery in an Ischemic Reperfusion Injury Model

ChemMedChem ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. 1365-1368 ◽  
Author(s):  
Atul Bhardwaj ◽  
Sri N. Batchu ◽  
Jatinder Kaur ◽  
Zhangjian Huang ◽  
John M. Seubert ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Enhanced Recovery ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Injury Model ◽  
Nitric Oxide Releasing ◽  
Hypertensive Activity

scholarly journals Pengaruh Lidokain Intravena Terhadap Kadar Superoxide Dismutase 1 (Sod-1) Paru Kelinci Dengan Lung Ischemic Reperfusion Injury Model

2015 ◽  
Vol 7 (3) ◽  
pp. 146
Author(s):  
Mohammad Arief Kurniawan ◽  
Johan Arifin ◽  
Taufik Eko Nugroho
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Injury Model

Latar belakang : Angka kejadian komplikasi paru paska operasi non jantung dibandingkan dengan komplikasi jantung yaitu 2,7% dan 2,5%. Penyebab hal ini adalah stres oksidatif, ketidakseimbangan radikal oksigen dan endogenous scavenging system.Lidokain  menghambat saluran natrium dan, mengurangi masukan kalsium intraseluler, mengurangi produksi Reactive Oxygen Species (ROS) dan modulasi bioenergetika mitokondria, sehingga diharapkan lidokain mampu meningkatkan kadar antioksidan alami di dalam sel.Superoxide Dismutase-1 (SOD-1) adalah salah satu antioksidan alami didalam sel yang berperan dalam melindungi organ dari anion superoksida yang berbahaya dengan mengubah anion yang dihasilkan dari cedera setelah ischaemia-reperfusion.Tujuan : Mengetahui efek lidokain intravena terhadap kadar Superoxide Dismutase 1 (SOD-1) paru kelinci dengan lung ischemic reperfusion injury model.Metode : Desain eksperimental laboratorik, 16 kelinci dibagi menjadi dua kelompok secara acak. Kelompok kontrol mendapat perlakuan lung ischemic reperfusion injury dan kelompok perlakuan dilakukan lung ischemic reperfusion injurydan mendapat injeksi lidokain 1,5mg/kgBB/jam intravena secara kontinyu kemudian diukur kadar SOD-1 jaringan paru kedua kelompok. Uji normalitas menggunakan uji Shapiro Wilk dilanjutkan uji beda Independent T-test.Hasil : Kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injurydan mendapat lidokain lebih tinggi secara signifikan (p=0,01) dibandingkan dengan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injuryKesimpulan : Pemberian lidokain kontinyu intravena dapat meningkatkan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injury. 

scholarly journals Protective Role of Ramipril and Candesartan against Myocardial Ischemic Reperfusion Injury: A Biochemical and Transmission Electron Microscopical Study

2016 ◽  
Vol 2016 ◽  
pp. 1-7
Author(s):  
Mohamed Saleem Thattakudian Sheik Uduman ◽  
Rajitha Bodd Reddy ◽  
Priyanka Punuru ◽  
Gopinath Chakka ◽  
Gauthaman Karunakaran
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Protective Role ◽  
Global Ischemia ◽  
Protective Mechanism ◽  
Myocardial Tissue ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Transmission Electron

The present study was designed to investigate the role of combined administration of Ramipril and Candesartan againstin vitromyocardial ischemic reperfusion injury in rat. Male Wistar albino rats were divided into five groups (n=6) and treated with saline (10 mL/kg), Ramipril (2 mg/kg), Candesartan (1 mg/kg), and the combination of both drugs, respectively 24 h before induction of global ischemia (5 min of stabilization, 9 min of global ischemia, and 12 min of reflow). Combination of Ramipril and Candesartan when compared to the monotherapy significantly increased the levels of superoxide dismutase, reduced glutathione, catalase, and nitric oxide and decreased the levels of thiobarbituric acid reactive substances. In addition, the superior protective role of combination of Ramipril and Candesartan on ischemia induced myocardial damage was further confirmed by well preserved myocardial tissue architecture in light microscopy and transmission electron microscopy analysis studies. The combination was proved to be effective in salvaging the myocardial tissue against ischemic reperfusion injury when compared to the monotherapy of individual drugs and further investigations on protective mechanism of drugs by increasing the nitric oxide level at molecular levels are needed.

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