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With a routine body plethysmograph with computerized calculation of airway resistance (Rt) and intrathoracic gas volume (IGV) on 11 healthy volunteers the correlations between Rt, IGV, breathing frequency (15-120) and flow (1.4-4.2 l/s) were examined. Rt increases significantly with increasing flow. In the range of clinical examinations with increasing frequency in the range between 15 and 30/min the flow increases only for a small amount. The increase of airway resistance in this range is very small. At an increase of the flow from 1 to 2 l/s an increase of Rt of 20% can be expected. An increase of the flow for 300% (1.25-5.0 l/s) is followed by an increase of Rt for 60%. IGV values are not influenced by these different frequencies and flows.

The bronchomotoric reaction following ACH-aerosol in low concentrations is dependend on the position of the body on dogs. Up till one maximal reaction the increase of the airway resistance is always stronger in the lateral position. Nevertheless the breathing minute volume is constant. Concentration reaction curves will be shown. Arterial blood gases, heart rate, and pressure in the arteria femoralis were also measured. The different strongness of the reaction following ACH-inhalation will be caused by the predominantely unilateral ventilation of the animals in the lateral position.

On 18 dogs the effects of hypoxia (12, 10, 7.5% O2) and hypoxia and hypercapnia (10% O2 + 5, 7.5, 11% CO2) on breathing, pulmonary vascular resistance, cardiac output and on the arterial and venous oxygen pressure were investigated. The relationship between arterial oxygen pressure to Pap as to vascular resistance is not in the mean linear. There are good, bad and nearly nonresponders in respect to the vascular resistance on the dogs. Therefore, calculation and evaluation of mean values are less helpful. A similar variation on men could help to understand also better the large scatter which is always shown on correlations between PO2a : Pap or PO2a : vascular resistance. Also the different pattern of the V/Q relationship may be influenced by the amount of the vascular response to local alveolar hypoxia. An increase of PCO/a potentiates the local vasoconstrictor effect of hypoxia. Mainly this was seen in the range between hypocapnia and moderate rates of hypercapnia. Hypoxia shows an increase of breathing frequency, hypercapnia shows and increase in tidal volume. Also under hypercapnia there are nonresponders and better responders in response to the vascular resistance in the lung circulation. Mechanical airway obstruction is followed by an increase of tidal volume; obstruction caused by acetylcholine is followed by a decrease of tidal volume and an increase of breathing frequency. Changes in the arterial blood gases are caused by changes in the ventilation perfusion relationship only under acetylcholine obstruction. Influences on the lung circulation by the airway obstruction under these experimental conditions as direct effects are small or not existent.

The study was carried out in anesthetized, intubated and spontaneously breathing dogs. The aim of this study was to examine the responsiveness of the tracheo-bronchial system to inhalative ACh. It was considered that any change in ACh-sensitivity signifies the involvement of receptors in the lung itself. Increased pressure in the right heart and main pulmonary artery did not affect the ACh-sensitivity. Whereas, the sustained pulmonary vascular congestion produced by blocking the ascending aorta or by glass bead embolism provoked greater ACh-sensitivity. Increased ACh-sensitivity was also observed in unilateral pulmonary artery occlusion. ACh-sensitivity was greater in the later part of occlusion or vascular congestion and persisted even after the occlusion or block was withdrawn. It is concluded that the increased ACh-sensitivities in pulmonary vascular congestion and in unilateral pulmonary artery occlusion are due to the formation of edema and atelectasis respectively. Anyway, the disturbance of the metabolism of the receptor cells around the small vessels of the lung circulation seems to be essential.

Respiratory hypersensitivity and systemic effects after local application of Ascaris suum extract on the segmental bronchus and after its intravenous infusion are studied on four boxer dogs. Influence of ipsilateral vagus blockade on the respiratory hyperreactivity after intrabronchial application of ascaris was also investigated on the same dogs. Ascaris extract was applied in liquid form directly through a catheter into the right segmental bronchus. Egg albumin was applied in the same way for control. Local application of ascaris was repeated after ipsilateral central vagus blockade and once more after recovering vagus effect by lavage. At the end of the experiments ascaris extract was infused intravenously. The parameters studied were: deltaP(oes) mm Hg/100 ml TV (as a measurement of flow resistance in the airways), respiratory rates, arterial blood gases and pH, heart frequency, systemic blood pressure and histamine concentration per milliliter of plasma. All the animals presented a remarkable respiratory distress with local ascaris application, which could be clearly avoided with ipsilateral central vagus blockade. This respiratory hyperreactivity was not observed after intravenous infusion of ascaris extract, but a significant systemic effect, which was not the case after local application, could be observed.

Respiratory hypersensitivity and the effect of unilateral vagus blockade on the same, after the use of Ascaris extract aerosol, are studied in three boxer dogs with spontaneous reactivity to this aerosol. The dogs were exposed initially to Ascaris extract aerosol, and this exposure was repeated after unilateral vagus blockade and after its lavage. The principal parameters, deltaPoes (mm Hg)/100 ml TV, are given as a measurement of airway flow resistance and respiratory rates. The spontaneous respiratory distress observed in all the animals after exposure to the mentioned aerosol was avoided with unilateral blockade of the nervus vagus.

The role of the vagus nerves on resting respiratory resistance (R1) and dynamic lung elastance (Edyn) and the mechanism of action of inhaled aerosol of histamine (Hist) and acetylcholine (ACH) were studied in anesthetized spontaneously breathing and artificially ventilated dogs. Observations were also extended to study the effect of electrical stimuli to cut ends of both vagi alone and during inhalation of aerosols. Bilateral cervical vagal blockade by local application of novocaine solution (2.5%) or bilateral vagotomy reduced resting R1 and Edyn and prevented increase of these parameters following inhalation of aerosols of Hist or ACH in spontaneously breathing dogs. However, the similar vagal blockade or vagotomy in artificially ventilated animals showed neither an influence on resting R1 and Edyn nor could it prevent their increase following the exposure to aerosol of Hist or ACH. Electrical stimuli to the peripheral cut ends of vagi induced slight increase in R1 and Edyn, but the effect on heart rate and systemic blood pressure was very strong. The combined effects of aerosol of Hist or ACH and electrical stimuli were additive. It is concluded that inhalation of aerosol of Hist or ACH produced two kinds of effects on respiration: (1) Increased respiratory rates with reduced tidal volume and with bronchoconstriction which were vagus-dependent (spontaneous breathing model), and (2) bronchoconstriction which was a direct response of smooth muscle without involving a reflex (artificial ventilation model).