Factors Influencing Collateral Blood Flow to the Dog's Lung

Abstract

The collateral circulation of the lung, i.e., that part of the bronchial flow which drains into the pulmonary veins, was studied by a heart-lung arrangement in which the lesser and systemic circuits of dogs could be perfused separately. In this preparation the collateral supply amounted to 0.5 to 1 per cent of the total arterial flow under approximately normal conditions. The changes in this collateral flow under a variety of experimental conditions were studied. These included variable systemic, venous and pulmonary pressures, lung collapse, air embolism, and actions of CO2 and serotonin.

Acute alveolar hypoxia increases bronchopulmonary shunt flow in the dog.

“…The major hemodynamic and neural determinants of bronchopulmonary flow have been studied by several groups over the past four decades. The majority of investigators (3)(4)(5)(6)(7)(8)(9) have found that systemic arterial pressure, independent of cardiac output, is one of the principal factors determining bronchopulmonary shunt flow. Although the exact anatomic location of the connections between the bronchial and pulmonary circulations is a subject of some controversy (10, 1 1), all agree that the pulmonary arterial and venous pressures, reflecting the "outflow pressure" ofthe bronchopulmonary anastomoses, are also principal determinants.…”

“…Although the exact anatomic location of the connections between the bronchial and pulmonary circulations is a subject of some controversy (10, 1 1), all agree that the pulmonary arterial and venous pressures, reflecting the "outflow pressure" ofthe bronchopulmonary anastomoses, are also principal determinants. Systemic venous pressure, as a determinant of the outflow pressure of the bronchial veins, can modify the fraction of bronchial arterial blood that flows into the broncho-pulmonary anastomoses (5,6). Increasing intrapulmonary pressure and positive end-expiratory pressure can decrease bronchopulmonary flow independent of primary changes in intravascular pressures (7,9,(12)(13)(14)(15).…”

Hemodynamic reactions in the acute phase of massive pulmonary embolism

“…The higher left ventricle output was always associated with collateral blood flows in the lungs, i.e., with the entry of blood from systemic into pulmonary vessels via anastomoses between these vessels. Extensive research of collateral circulation in the lungs [8][9][10][11][13][14][15][16]18,19] revealed the existence of intervessel communications of the following types. First, anastomoses between bronchial and pulmonary vessels at precapiltary, capillary, and postcapillary levels have been described in mammals of various species.…”

“…Normally, the collateral blood flow in the lungs amounts to 0.3-3.5% of the left ventricle output, although individual variations can be considerable [8][9][10][11]18]. The possibility of augmenting collateral blood flow in cases of pulmonary artery occlusion (PAO) has been under discussion for a long time.…”

“…On the one hand, blood inflow to bronchial arteries and the magnitude of collateral flow in the pulmonary vascular bed are directly related to changes in pressure and blood flow in the aorta and inversely related to changes in these variables in the pulmonary arteries [7,8,18], precapillary anastomoses between systemic and pulmonary vessels are poorly developed in initially healthy individuals and cannot ensure substantial blood flow in PAO [10,14,16,19], blood inflow to the lungs via systemic arteries decreases within an hour of experimental pulmonary embolism [15], and bronchial blood flow is not enhanced nor bronchopulmonary arterial collateral developed in patients during the first 30 days of pulmonary embolism [161. On the other hand, it has been shown that the outflow of collateral blood to the left atrium is directly related to changes in pressure in the fight atrium [8,18], welldeveloped anastomoses normally exist between systemic and pulmonary veins [7], and the outflow of collateral blood to the left atrium is markedly increased in experimental animals with acute PAO [13,18]. In the present study M P E was accompanied by the rise in the systolic and end-diastolic pressures in the right ventricle, a rise of the mean pressure in the right atrium, and moderate falls in the aortic pressure and blood flow (Fig, 1, b, and Table 1).…”