Abstract
The lesser circulation is affected by a considerable variety of diseases that involve the heart or lungs. Blood flow in the pulmonary vessels may be compromised by destruction of lung parenchyma and excessive positive alveolar pressure as in chronic obstructive lung disease, by frank obstruction of vessels, large or small, as in pulmonary thrombo-embolic disease, by obstruction to the outflow of blood as in diseases of the pulmonary veins, mitral valve or left ventricle, or by changes in the arteries due to chronic overloading as in several congenital heart conditions with left-to-right shunts. The response of the pulmonary circulation is conditioned by the necessity of maintaining sufficient perfusion of the lungs for effective gas exchange to take place, without allowing hydrostatic pressures in the capillaries to exceed plasma oncotic pressure so much as to result in frank edema. Ignoring for the moment the role of the lymphatics in draining away interstitial transudate to dispel such edema, it seems reasonable that one of the responses of the pulmonary arteries will be to protect the capillary bed by developing increased resistance to perfusion.
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Friedman, P.J., Harley, R.A., Liebow, A.A. (1972). Comparative Pathophysiology of Pulmonary Hypertension: Development of a Model. In: Bloor, C.M. (eds) Comparative Pathophysiology of Circulatory Disturbances. Advances in Experimental Medicine and Biology, vol 22. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-3213-8_13
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