Tracheobronchial blood flow increases with cold air hyperventilation in the dog. The present study was designed to determine whether the cooling or the drying of the airway mucosa was the principal stimulus for this response. Six anesthetized dogs (group 1) were subjected to four periods of eucapnic hyperventilation for 30 min with warm humid air [100% relative humidity (rh)], cold dry air (-12 degrees C, 0% rh), warm humid air, and warm dry air (43 degrees C, 0% rh). Five minutes before the end of each period of hyperventilation, tracheal and central airway blood flow was determined using four differently labeled 15-micron diam radioactive microspheres. We studied another three dogs (group 2) in which 15- and 50-micron microspheres were injected simultaneously to determine whether there were any arteriovenous communications in the bronchovasculature greater than 15 micron diam. After the last measurements had been made, all dogs were killed, and the lungs, including the trachea, were excised and blood flow to the trachea, left lung bronchi, and parenchyma was calculated. Warm dry air hyperventilation produced a consistently greater increase in tracheobronchial blood flow (P less than 0.01) than cold dry air hyperventilation, despite the fact that there was a smaller fall (6 degrees C) in tracheal tissue temperature during warm dry air hyperventilation than during cold dry air hyperventilation (11 degrees C), suggesting that drying may be a more important stimulus than cold for increasing airway blood flow. In group 2, the 15-micron microspheres accurately reflected the distribution of airway blood flow but did not always give reliable measurements of parenchymal blood flow.

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1. We tested the hypothesis that the pattern and the intensity of autonomic mechanisms causing vasoconstriction in the resting bronchial circulation of awake dogs also exists in awake sheep. It was also postulated that sighing behaviour and the associated bronchovascular dilatation induced by non-adrenergic, non-cholinergic (NANC) mechanisms observed in the dog exist in sheep. 2. Bronchial arterial blood flow to lower airways of both lungs of awake sheep was measured continuously using pulsed Doppler flow probes mounted on the bronchial artery at prior thoracotomy. 3. Cumulative and factorial analysis of responses to randomized combinations of autonomic alpha 1-, alpha 2-, beta 1- and beta 2-adrenoceptors and cholinoceptor autonomic blockade suggests that resting vasoconstrictor activity is less in sheep than in dogs. At normal aortic pressure, the autonomic activity of these receptor groups in the sheep lowers bronchial blood flow and conductance by 30%, whereas in the awake dog, the corresponding autonomic effect is 50%. 4. Tonic autonomic control of bronchial conductance can be partitioned in sheep to show significant and separate alpha- and beta-adrenoceptor vasoconstrictor activity at a ratio of 1.8:1, an effect normally offset by a weaker vasodilator alpha-/beta-adrenoceptor interaction. In contrast to the situation in awake dogs, cholinoceptors do not play a role in awake sheep. 5. Nitric oxide (NO) synthase inhibition in sheep using NG-nitro-L-arginine following blockade of alpha- and beta-adrenoceptors and cholinoceptors causes hypertension, but minor changes, if any, in pulmonary pressures or heart rate. Bronchial flow and conductance, however, fall from a higher resting conductance by approximately 50%, suggesting that, normally, resting bronchial flow conductance is dominated by strong tonic NO vasodilator effects that interact with weaker tonic autonomic vasoconstrictor effects. 6. Superimposed (respiratory) behaviours of sighing, sneezing and coughing, which involve negative swings in intrathoracic pressure and the movement of inspired air, evoke large active bronchovascular dilator effects. These appear to be largely NANC in origin and appear to be dependent, in part, on mechanisms associated with NO release. It is postulated that the C-fibre axon reflex using substance P, calcitonin gene-related peptide and neurokinin A may be involved. Vocalization and eructation do not evoke bronchovascular effects.

Eucapnic hyperventilation, breathing dry air, produces a two- to fivefold increase in airway blood flow in the dog. To determine whether airway blood flow responds similarly in the sheep we studied 16 anesthetized sheep. Seven sheep (1-7) were subjected to two 30-min periods of eucapnic hyperventilation breathing 1) warm humid air [100% relative humidity (rh)] followed by 2) warm dry air [0% rh] at 40 breaths/min. To determine whether there was a dose-response effect on blood flow of increasing levels of hyperventilation of dry air, another nine sheep (8-16) were subjected to four 30-min periods of eucapnic hyperventilation breathing warm humid O2 followed by warm dry O2 at 20 or 40 breaths/min in random sequence. Five minutes before the end of each period of hyperventilation, hemodynamics, blood gases, and tracheal mucosal temperature were measured, and tracheal and bronchial blood flows were determined by injection of 15- or 50-micron-diam radiolabeled microspheres. After the last measurements had been made, all sheep were killed, and the lungs and trachea were removed for determination of blood flow to trachea, bronchi, and parenchyma. In sheep 1-7, warm dry air hyperventilation at 40 breaths/min produced an increase in blood flow to trachea (7.6 +/- 3.5 to 17.0 +/- 6.2 ml/min, P less than 0.05) and bronchi (9.0 +/- 5.4 to 18.2 +/- 8.2 ml/min, P less than 0.05) but not to the parenchyma. When blood flow was compared with the two ventilatory rates (sheep 8-16), tracheal blood flow increased (9.1 +/- 3.3 to 18.2 +/- 6.1 ml/min, P less than 0.05) at a rate of 40 breaths/min but not at 20 breaths/min.(ABSTRACT TRUNCATED AT 250 WORDS)

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We investigated changes in bronchial blood flow (Qbr) associated with capsaicin-induced stimulation of pulmonary C-fibers in seven anesthetized and two unanesthetized sheep. A Doppler flow probe chronically implanted around the common bronchial artery provided a signal (delta F, kHz) linearly related to bronchial arterial blood velocity (Vbr, cm/s), which was proportional to Qbr. An index of bronchial vascular conductance (Cbr, in arbitrary units) was calculated as the ratio of Vbr to systemic arterial pressure (Pa). Right atrial injection of capsaicin evoked a prompt pulmonary chemoreflex (apnea, bradycardia, and hypotension), with immediate increases in Vbr (average +34%) and Cbr (+63%) that reached a maximum approximately 7 s after the injection. A second increase in Vbr, but not in Cbr, occurred approximately 12 s later, coinciding with an increase in Pa. Vagal cooling (0 degrees C) prevented the pulmonary chemoreflex; it also abolished the immediate increases in Vbr and Cbr in four of six sheep and substantially reduced them in two sheep; it did not affect the late increases in Vbr and Pa. Results after atropine indicated that the immediate increases in Vbr and Cbr were mainly cholinergic. In two sheep a small residual vasodilation survived combined cholinergic and adrenergic blockade and may have been due to peripheral release of neurokinins.

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Pulsus paradoxus, a greater than 10 Torr systolic pressure fluctuation during the respiratory cycle, is seen in upper airway obstruction. To test the hypotheses 1) that blood is pooled in the pulmonary circulation with reduced return to the left heart during inspiration and 2) that inspiration increases left ventricular afterload, the following was done. Esophageal pressure (Pes), pericardial pressure (Pp), left atrial transmural pressure (Platm), and left ventricular transmural pressure at end-isovolumic systole (Plvtm) were recorded during partially obstructed inspirations in spontaneously breathing dogs anesthetized with pentobarbital (25 mg/kg). Changes in Pes and Pp were nearly identical (r = 0.9883) confirming that changes in Pes adequately reflect changes in Pp. During inspiration Platm and Plvtm increased 0.5 and 0.4 Torr, respectively, per Torr decrease in Pes suggesting that increased blood return to left atrium and increased left ventricular afterload occur. Similar changes were observed during near constant thoracic volume (total airway block) and cardiac reflex blockade (atropine 0.05 mg/kg and propranolol 0.5 mg/kg). Thus mechanical factors including left ventricular afterload appear of major importance in producing pulsus paradoxus in upper airway obstruction.