W. Kirk

Increased surface tension favors pulmonary edema formation in anesthetized dogs' lungs.

The possibility that surface tension may affect the hydrostatic transmural pressure of pulmonary vessels and the development of pulmonary edema was studied in anesthetized, open-chested dogs. Isogravimetric pressure (the static intravascular pressure at which transmural osmotic and hydrostatic pressures are balanced such that net fluid flux is zero and lung weight is constant) was measured in nine animals under three conditions: (a) control, normal surface tension, at an alveolar pressure of 30 cm H2O with the apenic lung at room temperature; (b) after increasing surface tension by cooling and ventilating at a low functional residual capacity, at an alveolar pressure sufficient to produce the same lung volume present during control measurements; and (c) after restoring surface tension by rewarming while holding the lung at a high inflation volume, again at the control lung volume. Lung volumes were established from external dimensions and confirmed +/- 10% by deflation spirometry. The isogravimetric pressure (relative to alveolar pressure) was significantly less with increased surface tension than during either the initial control condition (P less than 0.01), or when the surface tension has been restored (P less than 0.01). Similar changes occurred in each of three additional studies performed with control alveolar pressures of 10 cm H2O. Thus, increased surface tension favors fluid leakage presumably because it increases the microvascular transmural pressure.

The drainage routes of the bronchial blood flow in anesthetized dogs

It is generally accepted that the bronchial blood flow from extrapulmonary airways drains to the systemic veins through the bronchial veins, while that from the intrapulmonary airways drains into the pulmonary vasculature and eventually the left heart. This concept has not been confirmed by physiologic studies in live animals. We measured the routes taken by radionuclide-labeled Diethylenetriamine pentaacetate (DTPA) deposited in the extrapulmonary and the intrapulmonary airways in dogs. In living, anesthetized open chest animals, the pulmonary circulation of the left lower lobe was isolated and perfused with autologous heparinized blood. 99mTc DTPA was deposited on the mucosa of the extrapulmonary left mainstem bronchus just beyond the main carina (extrapulmonary deposition) and 111In DTPA on that of an intrapulmonary left lower lobe segmental bronchus (intrapulmonary deposition). Sequential blood samples from the right heart and from the isolated left lower lobe pulmonary circuit were counted for radioactivity, corrected for the volume in which they were distributed and for the bronchial blood that flowed into the isolated left lower lobe circuit, and expressed as the ratio of systemic to pulmonary drainage from each deposition site. The extrapulmonary tracer drained mostly to the systemic veins (84% of total) but also into the pulmonary circulation (16% of total). The intrapulmonary tracer drained mostly into the pulmonary circulation (70% of total) but also into the right heart (30% of total). Since tracers from both deposition sites drained to both circulations, the bronchial vasculature is continuous between the systemic (right heart) and the pulmonary circulation. Thus, it may provide a pathway for blood flow between the right and left heart.

Temperature dependence of intraparenchymal bronchial blood flow.

Previous studies suggested that bronchial vascular resistance, like that of the skin, changes with the temperature of the surrounding tissue. To investigate this phenomenon, we recorded anastomotic (systemic to pulmonary) (Qbrs-p) and total (Qbr) bronchial blood flow over a temperature range centered on normal. In 7 open-chested dogs the in situ left lower lobe (LLL) was separately ventilated (30 degrees C, 5% CO2 in humidified air) and was suspended in a fabric net from a strain gauge for continuous recording of weight. The pulmonary circulation of the LLL was pump-perfused at 255 +/- 69 ml/min in a closed circuit with temperature set at 30, 33, 36, 39 and 42 degrees C. Qbrs-p was measured as overflow from the LLL vascular circuit corrected for LLL weight changes. Qbr, tracheal, mid-esophageal and coronary flow were measured with 15 mu radiolabelled microspheres injected in the left atrium. The animals core temperature and that of the humidified air around the LLL were held constant. Qbr and Qbrs-p were equal and reached a peak at 36 degrees C with lower levels of flow at higher and lower temperatures. Esophageal, tracheal and coronary flow and cardiac output did not change nor did pressures in the systemic and LLL pulmonary artery and in the LLL airways. An intralobar change in temperature above or below 36 degrees C decreases only the lobar bronchial blood flow and does not influence blood flow to other nearby tissues including those vascularized by the bronchial circulation.

THE EFFECT OF BRONCHIAL VENOUS PRESSURE ON PULMONARY EDEMA IN THE DOG

We examined the effect of elevating systemic venous pressure on the rate of edema formation in the left lower lobes (LLL) of anesthetized, open-chested dogs. The pulmonary circulation of the LLL was isolated using cannulae in the artery and vein which were attached to blood-filled reservoirs. The LLL was distended to an alveolar pressure of 25 cm H2O with 5% CO2 and air, and suspended from a strain gauge which allowed continuous weight recording. The pulmonary vascular pressures were raised so all of the LLL was in zone III. The rate of weight change occurring over the last 4 minutes of a 6 minute period of this pulmonary vascular pressure rise was taken to represent the control transvascular fluid flux. The rate of weight gain of the LLL was then determined with the same pulmonary vascular pressure elevation only when downstream bronchial venous pressure alone, downstream lymphatic pressure alone, or when both downstream lymphatic and bronchial venous pressures were elevated. The transvascular fluid flux was increased when downstream bronchial venous pressure was elevated. When only downstream lymphatic pressure was elevated there was no augmentation of transvascular fluid flux. These findings suggest that when a lung is already subjected to raised pulmonary vascular pressure sufficient to cause edema, acute elevation of bronchial systemic venous pressure augments the net rate of outward fluid flux, while downstream lymphatic pressure elevation does not.

Pulmonary artery infusion of prostacyclin increases labor bronchial blood flow

Intrapulmonary systemic to pulmonary bronchial blood flow [Qbr (s-p)] decreases with administration of cyclooxygenase inhibitors. This effect may be due to a decrease in the production of vasodilating prostaglandins and reflect either a decrease in the total intrapulmonary bronchial blood flow (Qbr), or a redistribution of the intrapulmonary systemic venous return. In nine open chested dogs the left lower lobe (LLL) was isolated and perfused in situ. Blood flow to the extrapulmonary airways (Qep), and Qbr were measured by the reference flow technique. Qbr (s-p) was measured as the overflow from the closed LLL perfusion circuit. After ibuprofen, PG-I2 was infused into the LLL PA and the Qbr (s-p) was continuously monitored. Qbr, and Qep were measured before and after ibuprofen, and during and after the PG-I2 infusion. The upstream pressure for Qbr (s-p) was estimated with and without PG-I2 infusion. After ibuprofen the Qep, Qbr, and Qbr (s-p) fell to 45, 22, and 17%, respectively, of the pre-ibuprofen values (P less than 0.05). PG-I2 increased the Qbr (s-p) and Qbr (P less than 0.05), while Qep was unchanged. During all experimental conditions the simultaneous measurements of Qbr and Qbr (s-p) were not different from each other (P less than 0.001). The upstream pressure for Qbr (s-p) increased from 30 to 50 cm H2O (P less than 0.05). Intralobar bronchial blood flow is drained almost entirely through the pulmonary circulation, and PG-I2 in the LLL pulmonary circulation increases systemic blood flow to the LLL, probably acting at the level of a systemic arteriole.

Positive End-Expiratory Pressure Decreases Bronchial Blood Flow in the Dog

Positive end-expiratory pressure (PEEP) increases pulmonary vascular resistance, but its effect on the bronchial circulation is unknown. We have compared two techniques for measuring bronchial blood flow in anesthetized, open-chest, ventilated dogs at varying levels of PEEP. Bronchial blood flow ( Qbr ) to the left lower lobe (LLL) and trachea was measured with radiolabeled microspheres. Total Qbr was partitioned into tracheal, bronchial, and parenchymal fractions. We also measured the bronchopulmonary anastomotic flow ( Qbra ) by attaching cannulas from the lobar pulmonary artery and vein to reservoirs, interrupting the LLL pulmonary blood flow and collecting the flow going into the reservoirs. We measured Qbr and Qbra in 10 animals ventilated with varying levels of PEEP (3, 10, and 15 cmH2O) applied randomly. Pulmonary venous pressure was kept at 0 cmH2O. There was no difference observed between Qbr and Qbra at PEEP 3 and 10 cmH2O, but at PEEP 15 cmH2O, Qbr was greater than Qbra , suggesting that at low left atrial pressures bronchial blood flow drains mainly to the left atrium, whereas at elevated alveolar pressures a larger fraction empties into the right side of the heart. PEEP decreased LLL Qbr and Qbra (P less than 0.01). That fraction of Qbr going to the trachea did not change with PEEP. However, the bronchial and parenchymal fractions decreased.