Impairment of endothelium-dependent pulmonary-artery relaxation in chronic obstructive lung disease

Article Abstract:

A complex series of physiological events evolve from chronic obstructive lung disease. In conditions such as emphysema and cystic fibrosis, the alveoli (the tiny air sacs in the lungs) do not receive an adequate supply of oxygen. This inadequate oxygen supply (hypoxemia) causes increased pressure of the blood that passes from the heart to the lungs. If the condition persists, the right ventricle of the heart, which pumps blood to the lungs, will enlarge in an attempt to deal with the increased workload. This enlargement (hypertrophy) in response to the increased pulmonary blood pressure is called cor pulmonale, and may cause failure of the right ventricle. Why the inadequate oxygen supply in the alveoli should cause this series of events is far from certain, however. The potential role of the blood vessel endothelium in this process has been investigated. Blood vessels are composed of smooth muscle that contracts or relaxes as necessary to help control blood pressure. Lining the blood vessels is a thin layer of tissue called endothelium. The endothelial cells are more than a passive lining; they directly participate in the contraction and relaxation of the smooth muscle. Healthy arteries relax in response to nitric oxide produced by the endothelial cells; this relaxation was examined in specimens of arteries obtained from patients with chronic obstructive lung disease. The 22 patients in the study had undergone heart and lung transplants; blood vessels from the old lungs were used in the laboratory experiments. It was found that diseased arteries could relax normally in response to drugs that stimulated the smooth muscle directly. However, drugs such as acetylcholine, which affect the smooth muscle only indirectly, by eliciting a response from the endothelial cells, had less of a relaxing effect on the patients' arteries than on healthy arteries. Furthermore, when the arteries from the patients were treated with drugs to increase tension, the resulting tension was greater than that in healthy arteries; the difference appears to be due to the lack of a balancing relaxing influence from the endothelial cells. These results suggest that the pulmonary hypertension in patients with chronic obstructive lung disease may result from damage to the endothelium and loss of the proper amount of relaxing influence on the arteries. (Consumer Summary produced by Reliance Medical Information, Inc.)

Lung diseases, Obstructive, Chronic obstructive lung disease, Endothelium, Lung diseases, Pulmonary hypertension, Cor pulmonale, Endothelium-derived relaxing factors

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Regulatory functions of the vascular endothelium

Article Abstract:

Blood vessels are lined by sheetlike layers of endothelial cells, forming the vascular endothelium. This cell layer is an active physiological agent, with a variety of life-sustaining roles. These are reviewed, with particular emphasis on the production of prostacyclin, endothelium-derived relaxing factor (EDRF), now known to be nitric oxide, and endothelin-1. These compounds are produced by endothelial cells in response to constantly changing signals from the cells themselves, and to interactions between the endothelium and other cells in the circulation. They affect processes such as vasodilation (enlargement of the vessel's diameter) and attachment of platelets (cells essential for blood clotting) to the endothelium. Prostacyclin is a vasodilator and inhibits platelet aggregation. It is released by the endothelial cell in response to pulsatile pressure, or after the administration of certain drugs (calcium antagonists, dipyridamole, streptokinase). The ability of vessels to manufacture prostaglandin declines with age and in some diseases, which may contribute to atherosclerosis (deposition of plaques on arterial walls). Aspirin, through a complex feedback process, leads to an increase in prostacyclin production, and recent research has shown that low-dose aspirin is effective for treating several cardiovascular diseases. Fish oil, too, appears to ward off cardiovascular disease, because of biochemical action via related pathways. EDRF-nitric oxide has effects similar to those of prostacyclin on vasculature and platelets, and the two probably work together in a synergistic fashion. Both hormones are paracrine (having a local action) and cannot affect distant sites. EDRF-nitric oxide deficiency may contribute to hypertension, atherosclerosis, and diabetes. Endothelin-1 is one of at least three factors that constrict the blood vessel. Its levels are elevated after acute myocardial infarction (heart attack), and in hypertension, and it may play a role in acute renal (kidney) failure. The role of endothelial cell factors in normal physiology remains to be clarified, but it is clear that the vascular endothelium can no longer be considered merely a passive, partly permeable barrier between the blood and smooth muscle surrounding the vessel. (Consumer Summary produced by Reliance Medical Information, Inc.)

Vascular resistance, Vascular endothelium

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Platelet-endothelium interactions

Article Abstract:

The interaction between blood platelets and the lining of blood vessels (endothelium) has been studied extensively. Platelets are blood cells involved in blood clotting. There are molecules on the surface of platelets and endothelium that allow the cells to attach to the endothelium. Platelets also secrete substances that can cause blood vessels to dilate. Endothelium in turn can secrete substances such as endothelium-derived relaxing factor (EDRF) that inhibit platelets. In some diseases such as atherosclerosis, diabetes and hypertension, endothelium does not relax in the presence of EDRF. Platelets may not function properly in patients with vascular diseases. Several treatments can restore proper platelet and endothelial function, including drugs, hormones and diet.

Blood vessels, Blood platelets

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