Species with collateral ventilation have an auxiliary respiratory mechanism that could protect them, under certain circumstances, from regional alveolar hypoxia. Species without collateral ventilation may have a greater potential for routinely experiencing regional hypoxia; to maintain ventilation-perfusion balance they would have to rely on pulmonary vasoconstriction. We tested these ideas by ventilating a sublobar region of pig lung (no collateral ventilation) with 13% O2 while the rest of the lung was ventilated with 30% O2. Blood flow, as measured by radioactive microsphere distribution to the sublobar region, was reduced 50% during hypoxia. The hypoxia-induced vasoconstriction effectively defended arterial PO2. When a vasodilator was infused, regional blood flow increased to control levels; shunt fraction rose, and arterial PO2 fell. In dogs (collateral ventilation present) the same experimental maneuvers had no significant effect on regional end-tidal gases or on microsphere distribution, indicating that collateral ventilation was able to maintain ventilation-perfusion balance. When regional hypoxia was created in dogs by overcoming collateral ventilation with slightly positive airway pressure in the sublobar region, the dog acted like the pig and used hypoxic vasoconstriction to shift approximately 30% of the blood flow away from the hypoxic alveoli.

Abstract. The plasma concentration of atrial natriuretic polypeptide was measured in eight healthy men during two grades of exercise performed in the supine position on a bicycle ergometer. The plasma concentration of atrial natriuretic polypeptide slightly increased during the first exercise test with 20% of the maximal oxygen uptake and it approximately doubled during the second exercise with 40% of the maximal oxygen uptake (from 15.5 ± 5.5 (mean ± sd) pmol/l to 31.8 ± 10.7 pmol/l). The increase in the plasma level of atrial natriuretic polypeptide in the second exercise was significantly greater than that in the first one. The plasma norepinephrine level and plasma renin activity showed significant increases during the second exercise test. Heart rate and systolic blood pressure also increased in response to the graded exercise. The increase in the plasma concentration of atrial natriuretic polypeptide during exercise was significantly correlated with the increase in heart rate, systolic blood pressure, and the plasma norepinephrine concentration (r = 0.75, r = 0.71 and r = 0.51, respectively). These results indicate that the plasma concentration of atrial natriuretic polypeptide increases in response to the intensity of a workload, and suggest that exercise is a useful test to evaluate the releasing function of atrial natriuretic polypeptide in the heart.

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We assessed 12 patients with hyperventilation syndrome (HVS) who had experienced hypoxaemia (PaO2 < 60 Torr or SaO2 < 90%) despite the lack of any other organic disease and variability in their blood gas data. Hypoxic and hypercapnic ventilatory responses were measured in nine. Eight of the 12 patients had been referred from other hospitals to our institution for hypoxaemia of unknown origin. Mean PaO2 (n = 12) at rest (non-attack stage) was 87.3 +/- 7.5 Torr (mean +/- SD). Their (n = 9) hypoxic (-0.53 +/- 0.32 l/min/%; range 0.12-0.99) and hypercapnic (2.01 +/- 0.76 l/min/Torr; range 0.69-3.17) ventilatory responses were both within the normal range in our laboratory. The patients with HVS had variable blood gas data, and some of them also exhibited hypercapnia (PaCO2 > 45 Torr). Clinicians who treat patients with HVS should be aware of the possibility of hypoxaemia, even when ventilatory responses are normal. Physicians should also consider HVS as a diagnosis when treating patients with hypoxaemia of unknown origin.