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Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.
Respiratory Disease
Respiratory Disease is defined as medical conditions, affecting the breathing organ and tissues including Inflammatory lung disease, Obstructive lung diseases, Restrictive lung diseases, Respiratory tract infections, trachea, bronchi, bronchioles, alveoli, the nerves and muscles breathing, etc,.
Pulmonary vascular disease: Pulmonary arterial hypertension
Pulmonary vascular disease is defined as a condition of blood flow to the lung’s artery is blocked suddenly due to a blood clot somewhere in the body, including pulmonary embolism, chronic thromboembolic disease, pulmonary arterial hypertension, pulmonary veno-occlusive disease, pulmonary arteriovenous malformations, pulmonary edema, etc.
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.
The Prevention: Phytochemicals
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
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