Pulmonary vascular disease – Phytochemicals and Antioxidants to prevent pulmonary arterial hypertension

Pulmonary arterial hypertension
Pulmonary arterial hypertension is a subgroup of a specific subgroup of pulmonary hypertension (PH) defined as a condition of slowly progressive disorder as a result of abnormally high blood pressure in the blood vessel, including pulmonary artery, pulmonary vein, or pulmonary capillaries, that carries blood from the heart to the lungs due to narrowing in diameter of most of the very small arteries throughout the lungs of that increased resistance to blood flow, leading to right heart failure and death. Because the phrase pulmonary arterial hypertension is long and pulmonary hypertension is a bit shorter the phrase. Pulmonary hypertension is often used in place of pulmonary arterial hypertension(a). According to statistic, approximately over 1,000 new cases of pulmonary arterial hypertension are diagnosed each year, in the United States alone.
V. Preventions
B. Phytochemicals and Antioxidants to prevent pulmonary arterial hypertension
Idiopathic pulmonary arterial hypertension (IPAH) is associated with lower levels of the pulmonary vasodilator nitric oxide (NO) and its biochemical reaction products (nitrite [NO(2) (-)], nitrate [NO(3) (-)]), in part, due to the reduction in pulmonary endothelial NO synthesis. According to the study by the Cleveland Clinic Foundation, in the testing of nitrotyrosine and antioxidants glutathione (GSH), glutathione peroxidase (GPx), catalase, and SOD were evaluated in IPAH patients and healthy controls, indicated that SOD and GPx activities were decreased in IPAH lungs (all p 0.2). SOD activity was directly related to exhaled NO (eNO) (R(2)= 0.72, p= 0.002), and inversely related to bronchoalveolar lavage (BAL) NO(3) (-) (R(2)=-0.73, p= 0.04). Pulmonary artery pressure (PAP) could be predicted by a regression model incorporating SOD, GPx, and NO(3) values (R(2)= 0.96, p= 0.01). These findings suggest that SOD and GPx are associated with alterations in NO and PAP in IPAH(31).
1. L-carnitine
In the study of a total of 66 pulmonary arterial hypertension patients (14 idiopathic, 36 congenital heart disease associated and 16 connective-tissue disease associated PAH, WHO heart functional class III, n = 38 or IV, n = 28) to investigate the efficacy of L-carnitine in patients with right-sided heart failure induced by pulmonary arterial hypertension (PAH), found that L-carnitine could improve short-term exercise capacity and WHO heart functional class in right-sided heart failure patients induced by PAH(32).
2. Retinoic acid
Retinoic acid has antimitogenic effects on smooth muscle cells. Studies on the systemic circulation suggest that it may reduce vascular thickening. In the study to study examine retinoid levels in plasma of patients with idiopathic pulmonary arterial hypertension and the effects of retinoic acid on human pulmonary artery smooth muscle cell growth, showed that Idiopathic pulmonary arterial hypertension patients have reduced retinoic acid levels, and retinoic acid treatment can elicit growth-inhibitory signals in pulmonary artery smooth muscle cells in vitro. Thus, retinoic acid may influence pulmonary vascular remodeling in humans(33).
3. Vitamin C
There is areport of 40-year-old female patient who developed severe pulmonary hypertension and life-threatening right-sided heart failure in association with dietary scurvy and iron deficiency. Supplementation with oral vitamin C and iron very likely contributed to her complete cure(34).
4. Genistein
Pretreatment with a phytoestrogen genistein has been shown to attenuate the development of pulmonary hypertension (PH). Because PH is not always diagnosed early. In the study to examine whether genistein could also reverse preexisting established PH and prevent associated right heart failure (RHF), found that Genistein restored PH-induced downregulation of estrogen receptor-β expression in the right ventricle and lung. In conclusion, genistein therapy not only rescues preexisting severe PH but also prevents the progression of severe PH to RHF(35).
5. Resveratrol
Resveratrol, a sirtuin-1 (SIRT1) pathway activator, can prevent the development of PH in a commonly used animal model, but it is unclear whether it can reverse established PH pathophysiology. Furthermore, atrophic ubiquitin ligases, such as atrogin-1 and MuRF-1, are known to be induced by SIRT1 activators but have not been characterized in hypertrophic vascular disease. Therefore, we hypothesized that monocrotaline (MCT)-induced PH would attenuate atrophy pathways in the PA while, conversely, SIRT1 activation (resveratrol) would reverse indices of PH and restore atrophic gene expression, according to the University of New Mexico Health Sciences Center(36).
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Sources
(a) http://pulmonaryhypertensionrn.com/ph-vs-pah/
(28) http://lib.bioinfo.pl/paper:21968645
(31) http://www.ncbi.nlm.nih.gov/pubmed/20443830
(32) http://www.ncbi.nlm.nih.gov/pubmed/20398563
(33) http://www.ncbi.nlm.nih.gov/pubmed/15699255
(34) http://www.ncbi.nlm.nih.gov/pubmed/22796843
(35) http://www.ncbi.nlm.nih.gov/pubmed/22753213
(36) http://www.ncbi.nlm.nih.gov/pubmed/22146233