Lower Lobe Pulmonary Artery Research Articles

Factors affecting perfusion distribution in canine oleic acid pulmonary edema.

Factors affecting perfusion distribution in oleic acid pulmonary edema were examined in 28 anesthetized open-chest dogs. Sixteen had unilobar oleic acid edema produced by left lower lobe pulmonary artery infusion of 0.03 ml/kg of oleic acid, and 12 had the same amount of edema produced by left lower lobe endobronchial instillation of hypotonic plasma. Lobar perfusion (determined from flow probes) and lobar shunt (determined from mixed venous and lobar venous blood) were measured at base line, 1.5 h after edema, and 10 min after 10 cmH2O positive end-expiratory pressure (PEEP). Fourteen dogs (8 oleic acid, 6 plasma) received sodium nitroprusside (11.72 +/- 7.10 micrograms X kg-1 X min-1). Total and lobar shunts increased to the same extent in all animals. Lobar perfusion decreased by 49.8 +/- 4.8% without nitroprusside and 34.0 +/- 3.6% with nitroprusside in the oleic acid group, corresponding values being 40.3 +/- 0.8% and 26.4 +/- 1.7% in the hypotonic plasma group. PEEP returned perfusion and shunt to base line. In oleic acid edema, most of the decreased perfusion results from mechanical effects of the edema, a smaller fraction results from other vascular effects of the oleic acid, and approximately 30% is reversible by nitroprusside. PEEP normalizes the perfusion distribution.

The acute effects of intralipid on lung function

To determine whether the oleic acid contained in intralipid injures the lung, we measured fractional lobar perfusion, lobar shunt, and edema (wet to dry weight ratios, W/D) in 20 open-chested mechanically ventilated dogs. Five dogs received oleic acid 0.03 g/kg injected into a lower lobe pulmonary artery. Ten received 0.5 cc/kg of 20% intralipid which contains the equivalent amount of oleic acid, five of these animals being heparinized. The same dose of oleic acid was also suspended in intralipid and administered to five heparinized dogs. Shunt and edema were measured in another five heparinized closed-chested dogs receiving 2 g/kg of intralipid IV over 1 hr. Half hour after intralipid or oleic acid, shunts did not change. At 2 1 2 hr, oleic acid alone increased lobar shunt from 4.6 ± 1.4 to 40.8 ± 24.9% while intralipid shunt remained unchanged with and without heparin. Lobar perfusion fell significantly with oleic acid from 29.3 ± 2.3 to 17.8 ± 5.6% while showing no change in the lobes not receiving oleic acid. When oleic acid was suspended in intralipid, shunt and perfusion changed less than with oleic acid alone. Mean W/D of the oleic acid lower lobe exceeded ( P < 0.05) W/D of the other lobes, including the lobe receiving oleic acid suspended in intralipid which had a W/D greater than the lobes receiving intralipid only. We conclude that intralipid has no acute deleterious effects on pulmonary gas exchange, blood flow distribution, or edema. Our data suggest that intralipid may protect the lung from the deleterious effects of fatty acids.

Does increased pulmonary blood flow redistribute towards edematous lung units?

Unilobar pulmonary edema secondary to increased capillary permeability was produced utilizing oleic acid infusion into the left lower lobe pulmonary artery of seven dogs. This model was used to determine whether random changes in cardiac output produced by opening and closing arteriovenous fistulae were associated with changes in fractional perfusion to the edematous lobe (as determined by differentially labeled radiomicrospheres) thus explaining changes in intrapulmonary shunt. With an increase in cardiac output from a mean (+/- SD) of 1.6 +/- 0.5 liters/min to 2.6 +/- 0.8 liters/min (P less than 0.01), mean (+/- SD) injured lobar shunt as measured from O2 contents of lower lobar pulmonary venous blood and mixed venous blood increased from 54.4 +/- 3.0% to 74.4 +/- 22.1% while total intrapulmonary shunt increased from 12.0 +/- 4.0% to 16.0 +/- 3.7% (P less than 0.01). This increase in intrapulmonary shunt was, however, not associated with preferential perfusion of the edematous lobe, the mean (+/- SD) of the perfusion to the edematous lobe expressed as a percentage of the cardiac output being 16.6 +/- 1.6% at the low cardiac output and 16.9 +/- 1.4% at the high cardiac output. It is concluded that redistribution of blood flow towards the edematous lobe does not occur with increases in cardiac output and therefore does not account for the increased intrapulmonary shunt.

Stability in lobar ventilation distribution during change in thoracic configuration.

Stability in lobar ventilation was examined in dogs during bilateral electrophrenic respiration (BEPR) and positive pressure-assisted ventilation (PPAV). Bilateral prior ligation of the lower and middle lobe pulmonary arteries monitoring of upper lobe ventilation as alveolar minute ventilation (VA), middle and lower lobe ventilation as dead space (VD), and VD/VT ratio, both calculated by the Bohr equation. As documented by chest films, transverse and anteroposterior thoracic diameters during BEPR decreased below FRC values whereas thoracic cephalocaudal dimension greatly increased. During PPAV, all thoracic dimensions increased. Despite these dissimilar regional chest movements, VA, VD, and VD/VT ratio were comparable between PPAV and BEPR under conditions of matched tidal volume and respiratory frequency. Stability in upper lobe ventilation during BEPR was maintained by caudal displacement despite the compression of the rib cage, as documented by tantalum bronchography. Lobar-interdependence appears to be the mechanism transmitting negative pleural pressure developed by the diaphragm to the upper lobes via lower and middle lobe inflation.

Patterns of normal pulmonary venous flow in man.

Although pressures in the left atrium and pulmonary veins in normal hearts and in diseased states have been extensively measured in man by cardiac catheterization techniques, knowledge of the patterns of flow in the pulmonary veins is almost entirely lacking. I have utilized a radiological method, the technique of wedged pulmonary angiography, to study the patterns of flow velocity in the pulmonary veins of man in the normal pulmonary circulation. The method used, wedged pulmonary angiography, has previously been described in detail (Raphael and Steiner, 1967). Water-soluble contrast medium is forced through the pulmonary capillary bed from a cardiac catheter which has been passed through the systemic venous system and right heart into a wedge position in a right lower lobe pulmonary artery. The vascular arrangement of the lung consists of discrete “vascular lobules” (Jacobson, 1963). Therefore, the contrast medium is channelled into the draining vein of the injected vascular lobule in high concentration ...

Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular response to hypoxia.

The highly reactive pulmonary vascular bed of the neonatal calf was utilized to determine whether the hypoxic pulmonary pressor response is modified by alpha-adrenergic blockade with phenoxybenzamine (Group A) or by tissue catecholamine depletion with reserpine (Group B). In addition, in Group A, the effects of hypoxia on the pulmonary circulation were compared and contrasted with those of l-norepinephrine (alpha-receptor stimulator) and isoproterenol (beta-receptor stimulator). In Group A, changes in pulmonary vascular resistance were calculated from measurements of appropriate pressures and of pulmonary blood flow (electromagnetic flowmeter). The increase in pulmonary vascular resistance produced by hypoxia was not diminished by alpha-adrenergic blockade. However, blockade abolished the pulmonary vasoconstrictor effect of norepinephrine. During hypoxic pulmonary vasoconstriction, the administration of either norepinephrine or isoproterenol lowered the pulmonary vascular resistance both before and after alpha-blockade. While this may be a true vasodepressor effect of these drugs it may also reflect passive changes in the pulmonary vessels secondary to an increased pulmonary blood flow.THE PULMONARY VASCULAR RESPONSE TO HYPOXIA IN THE RESERPINIZED CALVES (GROUP B) WAS TESTED UNDER THREE CIRCUMSTANCES: (1) in the awake animal, (2) in the anesthetized animal prepared in the same way as those in Group A, and (3) during constant flow perfusion of the left lower lobe pulmonary artery. From these studies it was concluded that tissue catecholamine depletion did not diminish the pulmonary vascular response to hypoxia.Thus, neither alpha-adrenergic blockade nor tissue catecholamine depletion prevents the hypoxic pulmonary pressor response. Furthermore, alpha-blockade prevents the pulmonary vasoconstrictor response to norepinephrine but not to hypoxia. Therefore it is concluded that hypoxic pulmonary vasoconstriction is not mediated through adrenergic receptor stimulation or release of endogenous catecholamines.

Angiopulmonary Tomography: A Preliminary Report

The angiographic dissection of blood vessels in a specific body plane is a relatively new radiological concept and would appear to have marked diagnostic potential. Nephrotomography, as described by Evans (2) and Lowman and DeLuca (5), gave the first indication that the combination of contrast material injections and laminagraphy could be used to enhance the vascular and parenchymal visualization of an organ. In 1960, Liese (4) showed that intravenous aortography synchronized with multisection laminagraphy would better define the origins and proximal segments of the renal arteries. Rocca (6) as well as du Boulay (1) have also used this approach to better define the normal and abnormal vascular architecture of the brain. In the last several years, pulmonary angiography has come to play an increasingly important role in the diagnosis of pulmonary thrombosis. It has been used also, to a lesser extent, in the definition of carcinomatous invasion of pulmonary vessels. The principal limitation of conventional pulmonary angiography has been the lack of precise definition of the extent of vessel involvement by thrombus or tumor. In some instances, there may be uncertainty about vessel abnormalities due to overlapping vessel, heart, or lung shadows. In order to evaluate the improved resolution of vascular detail which could be obtained by coupling angiography with tomography, a series of canine experiments were carried out. Figure 1, A, is a film at three seconds in an angiographic series made in an animal in which a mock thrombus (collar button in lumen sewn to vessel wall) had been created in the left lower lobe pulmonary artery. The luminal defect is barely discernible, and the shadow seen could be confused with overlying lung, rib, or heart. The single-plane angiopulmonary tomogram (Fig. 1, B) shows to good advantage the button as well as the wire ligature used. In a second animal, wire sutures were placed about the left lower lobe artery as shown in Figure 2, A. The degree of constriction produced by the ligatures and the detail of the involved and adjacent vessels are well defined in the angiopulmonary tomogram (Fig. 2, B). Figure 3, A, is a LogEtronic copy of a pulmonary angiogram of a patient with a bronchogenic carcinoma growing in the right hilus. Marked narrowing and invasion of the right upper lobe artery are shown well in both the conventional angiogram and the angiotomogram (Fig. 3, B). Tumor obliteration of a major branch of the right lower pulmonary artery was suspected in the conventional angiogram and could be confirmed in the angiotomogram. Comment An initial consideration in the development of the described technic was the difficulty in obtaining the exact level of interest during the angiopulmonary tomogram as well as proper timing of the tomographic exposure. Satisfactory timing can be achieved through reference to the conventional pulmonary angiogram which is carried out as the first step in the study.