In Reply: — Dicpinigaitis et al. suggest that the results of our body in humans are unexpected in light of recent published studies in humans with cervical spinal cord transections and animal (guinea pig) studies with lidocaine injections directly into the spinal cord. However, we do not think that these findings are contradictory to ours and would like to offer some alternate explanations.

First, in humans with cervical spinal cord transsection, sympathetic neural transmission is interrupted anatomically and not, as in our study, by injection of local anesthetic into the thoracic epidural space that result in substantial local anesthetic plasma concentrations. In fact, our study shows that intravenous administration of a local anesthetic resulted in a significant attenuation to inhaled acetylcholine, which was not significantly different from that observed after epidural administration, despite bronchial sympatholysis. Thus, the effect of the local anesthetic per se seems to play a dominant role and must be considered in the interpretation of the observed effects in our study. Therefore, the findings that, in humans with spinal cord transection, bronchial hyperresponsiveness was present is not unexpected, and we agree that this might be explained on the basis of unopposed parasympathetic airway innervation in this specific patient population.

Second, the extent of direct sympathetic innervation of the bronchial system varies greatly from species to species. In guinea pigs, cats, and dogs, there is a well developed direct sympathetic innervation of the bronchial system, whereas there is only a rare sympathetic innervation of the human airway. [1] Using autoradiographic techniques, an additional sympathetic innervation of the bronchial system in humans has been shown (mainly glands, vessels, and alveolar walls, but not bronchial smooth muscle) and is assumed to have no functional relevance for airway resistance regulation. [1,2] Finally. Peter J. Barnes (1992) writes in his review about modulation of neurotransmission in airways that, in contrast to guinea pigs, cats, and dogs, there is no adrenergic bronchodilator response to direct nerve stimulation in humans. [3] Thus, results obtained from animal models may not represent the regulation of airway resistance in the human bronchial system.

In summary, we do not believe that the arguments raised by Dicpinigaitis et al, are contradictory to our statement that “blockade of pulmonary sympathetic innervation by thoracic epidural anesthesia seems to be of no relevance for airway resistance in humans.”

Harald Groeben, M.D., Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287–279.

Hans-Bernd Hopf, M.D., Zentrum f. Klin. Anaesthesiologie, Heinrich-Heine Univ. Dusseldorf Moorenstrasse 5, D-40001 Dusseldorf, Germany.

(Accepted for publication December 5, 1994).

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