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Thursday, 28 November 2013

Pulmonary vascular disease – Diet to prevent 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
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
A. Diet to prevent pulmonary arterial hypertension
1. Dietary nitrate
According to the study by the Queen Mary University of London, dietary nitrate (vegetables, fruit, and processed meats) and to a lesser extent dietary nitrite, elicit pulmonary dilatation, prevent pulmonary vascular remodeling, and reduce the right ventricular hypertrophy characteristic of PH. This favorable pharmacodynamic profile depends on endothelial NO synthase and xanthine oxidoreductase -catalyzed reduction of nitrite to NO. Exploitation of this mechanism (ie, dietary nitrate/nitrite supplementation) represents a viable, orally active therapy for PH(28).
2. Fish oil
In the study of the effects of dietary polyunsaturated fats on chronic hypoxic pulmonary hypertension were assessed in rats fed fish oil, corn oil, or a lower fat, “high-carbohydrate” diet (regular) beginning 1 mo before the start of hypoxia (0.4 atm, n = 30 for each), showed that fish oil diet increased lung eicosapentaenoic acid 50-fold and depleted lung arachidonic acid 60% (P less than 0.0001 for each). Lung thromboxane B2 and 6-ketoprostaglandin F1 alpha levels were lower, and platelet aggregation, in response to collagen, was reduced in rats fed fish oil. Chronically hypoxic rats fed fish oil had lower mortality rates than the other hypoxic rats. They also had lower blood viscosity, as well as less right ventricular hypertrophy and less peripheral extension of vascular smooth muscle to intra-acinar pulmonary arteries (P less than 0.05 for each). The mechanism by which dietary fish oil decreases pulmonary hypertension and vascular remodeling during chronic hypoxia remains uncertain(29).
3. Dietary phytoestrogens
In the study totest the hypothesis that phytoestrogenic compounds in the diet contributed to the female cardioprotectionfour groups of female rats were studied: sham-operated (Sham) and fistula (Fist) rats fed a diet with [P(+)] or without [P(-)] phytoestrogens. Eight weeks postfistula, systolic and diastolic cardiac function was assessed by using a blood-perfused, isolated heart preparation. High-phytoestrogen diet had no effect on body, heart, and lung weights, or cardiac function in Sham rats., showed that hypothesized that phytoestrogenic compounds in the diet contributed to the female cardioprotection(30).
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Sources
(a) http://pulmonaryhypertensionrn.com/ph-vs-pah/
(28) http://lib.bioinfo.pl/paper:21968645
(29) http://www.ncbi.nlm.nih.gov/pubmed/2732158
(30) http://www.ncbi.nlm.nih.gov/pubmed/15961607