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Hypoxia and the Pulmonary Circulation Thorax: First Published As 10.1136/Thx.49.Suppl.S19 on 1 September 1994

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Hypoxia and the Pulmonary Circulation Thorax: First Published As 10.1136/Thx.49.Suppl.S19 on 1 September 1994 Thorax 1994;49 Supplement:S19-S24 S19 Hypoxia and the pulmonary circulation Thorax: first published as 10.1136/thx.49.Suppl.S19 on 1 September 1994. Downloaded from Inder S Anand The first description of the effects of hypoxia arterial segments upstream from arterioles on the pulmonary circulation was made by 30-50 ,um in diameter.'7 Laser technology later Bradford and Dean in the UK exactly 100 confirmed hypoxic vasoconstriction in small years ago.' However, scientific interest in this (30-200 ,um diameter) arterioles.'8 How re- field only began with the discovery of hypoxic duced oxygen tension triggers pulmonary pulmonary vasoconstriction in the cat by von vasoconstriction is still being investigated, but Euler and Liljestrand2 in 1946, and in man a we do know that a reduction in oxygen tension year later in Andre Coumand's laboratory.3 in the lung depolarises resting membrane po- Despite extensive research in this field for tential of pulmonary vascular smooth muscle, nearly half a century, we still do not fully resulting in Ca2" influx through the voltage understand the mechanism of hypoxic vaso- dependent Ca2" channels.'9 The mechanism constriction or why the response of the pul- by which hypoxia is sensed by the pulmonary monary vasculature to hypoxia is diametrically vascular smooth muscle remains unclear. For opposite to that of the systemic circulation. a long time a vasoconstrictive mediator has Teleologically, hypoxic pulmonary vaso- been thought to be involved. A number of constriction serves a useful purpose. It acts as a potential mediators such as histamine,20 sero- local homeostatic mechanism and, by diverting tonin, noradrenaline,22 angiotensin II,23 vaso- blood away from the unventilated or poorly constrictive prostaglandins,24 leukotrienes,25 ventilated lung, helps to maintain ventilation- reduced ATP,26 and cytochrome P-45027 have perfusion homogeneity and thus arterial oxy- been investigated and excluded. The en- genation. It is not surprising, therefore, to find thusiasm for a possible mediator of hypoxic that a similar response exists in most animal pulmonary vasoconstriction has therefore species." waned, and there is increasing interest in the hypothesis that oxygen tension is sensed dir- ectly by the vascular smooth muscle. The pos- Mechanism of acute hypoxic pulmonary sible role of K+ channels in hypoxic pulmonary vasoconstriction vasoconstriction has been suggested for some The mechanism by which a fall in oxygen time,2829 but the most exciting development in http://thorax.bmj.com/ tension is sensed and translated into vaso- this field has been the finding by Weir and constriction in the pulmonary circulation is colleagues that hypoxia inhibits an outward K+ still not fully understood. We know that pul- current in isolated pulmonary arterial smooth monary vasoconstriction is initiated within sec- muscle cells causing depolarisation of the rest- onds of the onset of alveolar hypoxia,9 and that ing membrane potential.30 This could then lead the pulmonary artery pressure gradually rises to an influx of extracellular Ca2+ through the over the next few minutes. It is a remarkable voltage-dependent Ca2+ channels and con- coincidence that the sequently to vasoconstriction. It is stimulus-response curve interesting on September 28, 2021 by guest. Protected copyright. of the pulmonary vasculature to hypoxia in that the type I cells in the carotid body also humans resembles that of the carotid body sense hypoxia by a similar mechanism.3132 Fur- chemoreceptors to acute hypoxia and of the ther studies are needed to define these K+ bone marrow to chronic hypoxia.'0'3 In each channels more fully, and to determine how they case the threshold of Po2 is approximately are modulated by hypoxia. 70-80 mmHg. Below this value the response becomes increasingly strong. The inflection point of each ofthese curves is almost identical Effects of chronic hypoxia to that of the haemoglobin oxygen dissociation The clinical effects ofhypoxia are most evident curve, suggesting that similar mechanisms may in chronic hypoxic states. In addition to vaso- be involved in the sensing of oxygen in these constriction, structural changes in the terminal diverse systems in the body. portions of the pulmonary arterial tree33 and polycythaemia34 contribute to the maintenance of chronic hypoxic pulmonary hypertension. Site of hypoxic pulmonary This occurs when the alveolar oxygen tension vasoconstriction remains below the threshold for pulmonary The small muscular pulmonary arteries are the vasoconstriction of approximately 75 mm Hg. major site of hypoxic pulmonary vaso- Such a degree of chronic hypoxia is seen in constriction. Oxygen tension of both the al- conditions like chronic bronchitis and em- veolar air and the pulmonary artery perfusate physema, hypoventilatory states, and in its pure can directly influence these vessels, although form at high altitude. It is therefore interesting alveolar hypoxia is much more effective.'4-6 that an almost identical "remodelling" of the VA Medical Center, Minneapolis, Staub and colleagues used the micropuncture pulmonary vasculature occurs in response to Minnesota 55417, USA technique to show that hypoxia increased pul- alveolar hypoxia in these diverse states. In 1968 I S Anand monary vascular resistance predominantly in Donald Heath and his colleagues coined the S20 Anand term "hypoxic hypertensive pulmonary vas- Andes who have lived at high altitude far longer culature disease" to describe this form of pul- than their American counterparts appear to Thorax: first published as 10.1136/thx.49.Suppl.S19 on 1 September 1994. Downloaded from monary vascular disease.35 The most striking develop a lesser degree of pulmonary hyper- effect of alveolar hypoxia is muscularisation of tension despite being at higher altitude. Pul- pulmonary arterioles <70 ,um in diameter which monary artery pressures are normal in these normally contain only a single elastic lamina subjects at 2240 m (15 (2) mm Hg)43 and without any smooth muscle. This distal ex- 2640 m (13 (3) mm Hg),44 mildly increased at tension of smooth muscle causes the small altitudes between 3700 and 4370 m (20 (3) to pulmonary arterioles to develop a distinct 23 (4) mm Hg),45-4 and moderately increased media with smooth muscle sandwiched be- at an altitude of 4540 m (28 (10) mm Hg).49 tween an inner and an outer elastic lamina. The curve relating pulmonary artery pressure This was first described in Quechua Indians of and ambient oxygen tension is less steep in the Cerro de Pasco (4330 m) in the Peruvian Andes Andean people than in their North American by Arias-Stella and Saldafia.36 Later Heath and counterparts, which suggests a blunted hypoxic coworkers37-39 made a number of studies on vasoconstrictive response. This may be a Quechuas, Aymaras, mestizos, and white res- manifestation ofadaptation to chronic hypoxia. idents of La Paz, Bolivia (3800 m) and, while Unfortunately few data are available from confirming muscularisation of pulmonary ar- the Himalayas where large populations also live terioles, found that remodelling was much more at high altitude. Roy catheterised seven men at complex than had originally been envisaged by Leh, Ladakh (3600 m) who were presumably Arias-Stella and Saldafia.36 Moreover, con- ofLadakhi origin.50 The pulmonary artery pres- siderable individual and ethnic variations in the sure at rest was 20 (4 5) mm Hg and rose to response to high altitude hypoxia were seen. 26 (5) mm Hg with modest exercise. The rest- Remodelling was more common in the Aymara ing pressures are, therefore, almost identical to and Quechua Indians than the mixed mestizos those quoted for the Andean people at similar or long term white residents of La Paz. Heath altitude. The Andean highlanders, however, et al also found longitudinal smooth muscle in showed a greater increase in pulmonary artery the intima of small pulmonary arteries and pressure with similar exercise (32 (8) mm Hg). development of inner muscular tubes of cir- Does this mean that the Himalayan people are cularly orientated smooth muscle cells, internal less reactive to hypobaric hypoxia than the to the fascicles oflongitudinal muscle, lining the Andean highlanders? Groves and coworkers pulmonary arteries and arterioles.3839 Similar have recently reported the pulmonary artery histological changes are seen in patients with pressures in the native Tibetan highlanders of chronic obstructive lung disease at sea level,40 Lhasa, Tibet (3600 M).5' They found normal but the development of longitudinal muscle pressures at rest (15 (1) mg, PIo2 = 97 mm Hg) and inner muscular tubes in the intima is much which did not increase significantly with further more prominent and occurs more frequently. hypoxia (19 (3) mm Hg, PIo2 = 62 mm Hg). http://thorax.bmj.com/ The similarity of the remodelling in cor pul- Higher pulmonary artery pressures have been monale and in the natives of high altitude reported in two Chinese studies from Quinghai suggests that it is caused by sustained alveolar province in Tibet (3950 m) but it is un- hypoxia. It remains unclear, however, how pul- clear whether they studied Tibetan or Han monary arterioles come to be muscularised. It subjects.5253 is unlikely to be the result of work hypertrophy We have examined the lungs of seven La- since these vessels have no muscle in normal dakhi highlanders who had never been to low subjects and hypoxic vasoconstriction occurs altitude and who suffered accidental deaths. on September 28, 2021 by guest. Protected copyright. in
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