glutathione sjogren's syndrome Oxidative stress in autoimmune rheumatic diseases Selective activation of antioxidant resources

In occlusion/occlusion-like syndromes affecting both periphery and brain (portal hypertension, caval hypertension, intracranial hypertension), BPC-157 simultaneously normalized blood pressure disturbances, healed gastrointestinal and liver lesions, minimized brain lesions and hemorrhage, prevented thrombosis, and preserved neurological function

Nitrates such as nitroglycerin (NTG) are enzymatically broken down in the vascular wall by both glutathione S-transferase (GST) and mitochondrial aldehyde dehydrogenase isoform 2 (MtADH2) to release the vasodilator substance nitric oxide (NO)(Figure 6)(Zhang et al, 2009) Enzymatic conversion of NTG to NO is greater in venous smooth muscle compared to arterial smooth muscle, which may account for the venoselectivity of NTG at low doses (Bauer & Fung, 1999) Venodilation results in decreased preload (decreased ventricular chamber size, end diastolic volume, fiber tension) = decreased work by the heart Decreased preload & work of the heart results in decreased O , an effect which reduces ischemia (Figure 1) 2 demand Reduction of afterload (arterial resistance), a desirable therapeutic effect produced at higher doses can also produce reflex tachycardia (an unwanted side effect) Other possible contributors to the mechanism of action for nitroglycerin are under investigation, and include: Redistribution of Coronary Blood Flow Nitrates can selectively increase collateral blood flow to ischemic areas (e.g

PMID: 121 HuangPL

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