Comparisons with 14 normal, younger, male native residents of La Paz showed that 20 patients with Monge’s syndrome have significantly higher mean body surface areas, hemoglobin, resting tidal volumes [VT (BTPS)], and resting minute volumes [V_E (BTPS)]. If [V_E (BTPS) is subdivided into its components of alveolar [Va (BTPS)] and dead space ventilations [V_DS (BTPS)], it becomes apparent that the former is significantly smaller and the latter much larger in the Monge patients than in the controls. Alveolar hypoventilation in the Monge group is evidenced by an elevated mean PaCO₂; a lower mean pH of 7.349, contrasted with that of 7.399 in the controls; a PaO₂ of 48.1 mm Hg, compared with 57.7 mm Hg in the normals. Simultaneous surface scanning of the right upper and lower lung zones, using a central venous injection of ¹³¹I-HSA (human iodinated serum albumin), showed a reduction of total isotope activity in the right upper zones of the Monge group.

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The existence of systemic arteries to the lungs has been known for many centuries. Ruysch (1732) claimed to be the first to have described the bronchial arteries, but Galen had already done so in the second century A.D.During the nineteenth century the anatomy of the bronchial arteries was studied in detail and their possible function considered. Reisseisen and von Soemmering (1808) defined the bronchial arteries as " vasa nutritiva " of the lungs, and showed that they accompanied the bronchi. Le Fort (1858) showed that the bronchial arteries continue along the bronchial tree as far as the respiratory bronchioli. Von Luschka (1863) drew attention to the ramification of the bronchial arterioles in the bronchial mucosa and suggested that the capillaries of the bronchial arterioles communicated near the alveolar ducts with those derived from the pulmonary arteries.Virchow (1856) showed that occlusion of a lobar pulmonary artery branch did not result in necrosis of the lobe. He concluded therefore that the viability of the lobe,did not depend on the pulmonary artery, but was maintained by the bronchial arteries. Rindfleisch (1878) considered the bronchial arteries to be end arteries. Kuttner (1878), by dye injections in rabbit lungs, showed that the terminal branches of the pulmonary arteries were nowhere in communication with vessels of a similar calibre, and concluded that communication between the pulmonary artery bed and the bronchial arteries, if it existed, must be capillary only. Zuckerkandl (1881 and 1883) demonstrated that the bronchial arteries supplied the visceral pleura in man, and thought that the capillaries of the pulmonary and bronchial arteries were in communication. Miller (1947), at the beginning of this century, described the course of the bronchial arteries. He showed that they ran from the aorta to the main bronchi and followed these distally to the hila. There they divided and continued in the walls of the bronchi as far as the alveolar ducts. From the fibrous tunic, in which an arterial plexus was formed, small branches penetrated the muscle layer to reach the tunica propria of the bronchus and then continued to run in the long axis of the bronchus.Miller did not think that the problem of anastomosis between the two circulations had been adequately studied by previous workers, and contended that the use of a

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At two altitudes (3,600 and 5,200 m), resident native women (A) showed higher PAco₂ and Paco₂, lower PAO₂ and PaO₂, as well as lower arterial pH, than native males (C) of similar age. Resting minute ventilation (VE/m²), tidal volume (VT) and respiratory frequency (f) were similar. The differences in the alveolar-arterial gas tensions in A stem from larger dead space (VDS), VDS/VT and reduced alveolar ventilation (VA). Newcomer females (B) at both altitudes differed from new- comer males (D) in regard to larger resting VA, f and smaller VT. No differences were demonstrated in size of VDS, VDS/VT or VO₂/BSA; but PAco₂ and PacO₂ were lower, PAO₂ and Pa higher and VE/VO2 and VA/VO₂ (ventilatory equivalents) above those for resting newcomer males. A contrasted with resting B at 3,600 m (12,200 ft), showing higher PAco₂ and Paco₂, lower Pao₂ and arterial pH, reduction in VA and larger VDS/VT. Both C and D at 3,600 and 5,200 m during steady-state 60-W (367 kg/m/min) exercise showed lower PAco₂ and Paco₂, higher arterial pH, smaller VDS and higher VE/VO₂ than exercising A. The latter differed from C exercising at the same work load in that VE/m² and VA were reduced, PAco₂ and Paco₂ were higher, Pa-ao₂ gradients were wider, pH was lower and VDS as well as VDS/VT were larger. Contrasted with B during steady-state 60-W exercise at both altitudes, D showed consistently smaller VDS and larger VA. While both C and A had higher resting f than D, f of newcomer females at La Paz was higher than that of A. Control of ventilation by relating VE to Pao₂ and Paco₂ at rest and exercise at both altitudes showed marked attenuation of hypoxic and hypercapnic drives, particularly in the native resident female, suggesting diminished peripheral chemoreceptor function.

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