Reflex cardiovascular responses to lung inflation: A review
Introduction
Even the first authors studying the effects of lung inflation on heart rate in anesthetizised (morphine) dogs reached different conclusions. Einbrodt (1860)found that positive pressure lung inflation within the range of 7–40 mmHg produced mainly bradycardia, whereas Hering (1871)with the same degrees of inflation observed above all tachycardia. However, when Hering raised the intrapulmonary pressure in his preparations to a considerable level (over 40–50 mmHg), bradycardia often appeared. Therefore, he attributed Einbrodt's results to the use of too high lung inflation pressures.
However, not all the subsequent investigators confirmed the findings of Hering. Some of them observed a bradycardia independent of the degree of the inflations, others found only a brief transient tachycardia followed by a persistent bradycardia. Probably these controversies made Aviado and Schmidt (1955)conclude that the reflex effects of normal lung inflation were predominantly respiratory and the circulatory effects were insignificant.
Nevertheless, nowadays, as before, the most popular standpoint is Hering's conception. Daly (1986), generalizing the data of various authors, arrived at a conclusion that lung inflations with small pressures (<14 mmHg) lead to reflex tachycardia from the pulmonary stretch receptors, whereas inflations with higher pressures caused bradycardia from pulmonary J receptors. Daly and co-workers (Daly, 1986) found that stimulation of pulmonary stretch receptors by lung inflation evokes not only tachycardia but a reflex peripheral vasodilation with arterial hypotension as well.
However, Daly's concept does not allow complete explanation of some well established facts. Several authors have detected reflex inflation tachycardia with a intrapulmonary pressure considerably higher than 14 mmHg (up to 40–50 mmHg), the concomitant arterial hypotension being caused by mechanical and not by reflex mechanisms (Looga, 1956, Earnest et al., 1968, Hayashi, 1969). In other studies, the inflation bradycardia was obtained with intrapulmonary pressures considerably lower than 14 mmHg (Looga, 1964, Stinnett, 1981, Nail et al., 1994). Other studies established that concomitantly with inflation tachycardia the arterial pressure and systemic vascular resistance did not always fall but often rose (Saalfeldt, 1933, Looga, 1965, Hainsworth, 1974, Angell-James et al., 1981, Wood et al., 1985).
My own work in this field1 suggested that lung inflation caused simultaneous changes in the activity of a number of different receptors with a potential capability to evoke reflex cardiovascular responses. Depending on the concrete experimental circumstances one of these reflexes would prevail. In the following, an attempt will be made to specify the main receptors involved and the interrelationships between the various reflexes.
Section snippets
Arterial baroreceptors
Fig. 1 demostrates the pattern of typical cardiovascular responses in anesthetized dogs (morphine+urethane) with a graded bilateral increase in intrapulmonary pressure (Looga, 1956). In general, tachycardia and arterial hypotension occurred during the lung inflation and bradycardia and hypertension after return to control conditions. This effect increased with increasing inflation pressure. The results are in accord with the data of Hering (1871)and numerous other authors.
The described response
Slowly adapting pulmonary stretch receptors
Adequate stimulation of pulmonary stretch receptors is feasible if (1) lung inflation does not substantially disturb the blood flow in the pulmonary vessels and aorta and (2) if the surgical trauma is brought to a minimum.
I achieved such an experimental situation by inflating not both lungs simultaneously, but only one of their lobes (the diaphragmatic lobe) in intact anesthetized (morphine+urethane) dogs (Looga, 1964). The result was invariably a fall in the systemic arterial pressure and
Unidentified pulmonary mechanoreceptors
A brief cardioacceleration and arterial hypertension with concomitant peripheral vasoconstriction can be observed on a single moderate positive or negative pressure lung inflation, on a single deep inspiration and in the inspiratory phases of the natural slow breathing and positive pressure artificial ventilation. Usually, this response has been believed to originate reflexly from lungs.
The pulmonary origination of the reflex pressor response to single moderate positive pressure lung inflation
Interactions between cardiovascular reflexes on lung inflation
When the lungs are inflated, only one cardiovascular reflex from all the previously described ones may appear, while the others will support or inhibit it (competition for the final common path). Which of these reflexes will predominate will depend on the concrete experimental conditions and upon the species.
In the case of bilateral positive pressure lung inflation, it is the pressor reflex from sino-aortic baroreceptors that usually predominates. Although the fall in arterial pressure is
General summary and conclusions
(1) It is concluded that in all likelihood the reflex tachycardia observed by Hering (1871)in bilateral positive pressure lung inflation did not originate from pulmonary receptors as he thought, but from sino-aortic baroreceptors.
(2) The present discussion has shown that adequate stimulation of slowly adapting pulmonary stretch receptors causes bradycardia, peripheral vasodilation and arterial hypotension but not tachycardia with vasodilation or vasoconstriction as has been widely accepted.
(3)
Acknowledgements
I am grateful to Prof. Johannes Piiper and Prof. Enn Seppet for many helpful discussions.
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