The electron microscopic alterations of the alveolar septum in advanced hemodynamin and alloxan-induced pulmonary edema were compared. Pulmonary edema was produced in anesthetized dogs by means of increased lefy atrial pressure and hemodilution and by allocan administration. Sections of pulmonary tissue from these dogs and similarly anesthetized controls were processed for and examined by light and electron microscopy. In the hemodynamic form of edema the interstitial fluid collects only in the collagen-containing portions of the septum. The endothelium, epithelium, their respective basement membranes and large portions of the air-blood barrier are unaffected. Alloxaninduced edema, in contrast, is characterized by degeneration of both endothelium and epithelium and by the appearance of fibrin within the alveoli. The hemodynamic type of pulmonary edema appears to result from an accentuation of the normal process of fluid exchange within the lung. Allocan-induced edema, on the other hand, is a pathologic process. The functional implications of these results are discussed.

Four infants with Down syndrome developed cor pulmonale and heart failure in association with chronic upper airway obstruction. Features of the sleep apnea syndrome were conspicuous; namely, noisy breathing with retraction, cyanosis and frequent apnea during sleep, and daytime lethargy and somnolence. The clinical picture masqueraded as cyanotic congenital heart disease. Arterial blood gas analyses revealed alveolar hypoventilation, especially during sleep. The nature of the obstructive element was variable. Adenoidectomy provided partial relief in one patient, and tonsillectomy and adenoidectomy resulted in temporary improvement in two others. Three patients were markedly benefitted by tracheostomy. Functional inspiratory pharyngeal closure was demonstrated fluorographically in one patient. Infants with Down syndrome may be predisposed to upper airway obstruction by virtue of hypoplasia of facial and oropharyngeal structures and generalized hypotonia. Additional obstructive elements may be contributed by hypertrophied lymphoid tissue, excessive secretions, and glossoptosis. Removal of the obstructive element is helpful, but functional obstruction may only be relieved by tracheostomy.

Summary. The forces governing the movement of water across the pulmonary capillaries were studied in 39 intact, spontaneously breathing dogs. A situation favoring the net movement of water out of the pulmonary capillaries was created by means of partial pulmonary venous obstruction (left atrial balloon catheter) followed by rapid saline hemodilution. A predetermined difference between pulmonary capillary and plasma colloid osmotic pressures was maintained for periods of 1 to 2 hours. Left atrial (PLA) and plasma colloid osmotic pressures (7rp1) were measured directly. The water content of the lungs was measured serially by an indicator-dilution technique, and at autopsy by drying the lungs. The rate of accumulation of lung water was measured in four groups of animals: in three of the groups, the capillary hydrostatic and colloid osmotic pressures were varied; in the fourth group, the right lymphatic duct was obstructed in addition.The average rate of water accumulation in the lungs varied in a nonlinear way with the level of the capillary hydrostatic-plasma colloid osmotic pressure difference and was unaffected by the level of the capillary hydrostatic pressure. At low levels of PLA -7rpl, water accumulated in the lung at an average rate of 0.09 g per g dry lung per hour per mm Hg pressure difference.At higher levels of PLA -7rpl the average rate of accumulation was 0.22 g per g per hour per mm Hg AP; in most of the experiments in this group water accumulated in the lungs slowly during the first 30 minutes of the test period and more rapidly as the period was extended. Obstruction of right lymphatic duct outflow did not alter the rate of water accumulation. Based on the control data of the present experiments, the pericapillary pressure in normal lungs is estimated to be of the order of -9 mm Hg in the normal dog lung. The filtration coefficient for the pulmonary capillaries is estimated to be of the order of one-tenth to one-twentieth of that for canine muscle capillaries. The data of the present study indicate that edema formation in lung tissue cannot be defined solely in terms of intravascular forces, but may be governed to a significant degree by changes in pericapillary forces in the pulmonary interstitium.

FIGURE 1X-ray of the chest showing the positions of the different catheters in the aorta (Ao), the right atrium (RA), the left atrium (LA), the pulmonary artery (PA), the inferior vena cava (1VC), and the esophagus (Es). TIME OF INFUSION m i n FIGURE 2Hemodynamic events during the experimental production of pulmonary engorgement and edema (dog no. 41). Inflation of the balloon in the left atrium, followed promptly by the rapid infusion of saline, produced abrupt increase in left atrial and pulmonary arterial mean pressures (top panel); at the same time, there was a decrease of colloid osmotic pressure, hematocrit, and total proteins. High pressure in the left atrium was maintained for one hour by adjusting rate of infusion.

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