Abstract
The existence of a highly surface-active lining at the air-tissue interface in the lungs of a wide variety of species is well established, even though the exact chemical nature of the substance in situ is the subject of controversy (3). Tooley et al. (5) and Bolande and Klaus (1) reported that extracts obtained from the lungs of guinea pigs 2-4 hr after bilateral cervical vagotomy exhibited higher minimum surface tensions than similar extracts obtained from control animals, although the latter investigators felt that the altered surface properties of lung extracts obtained postvagotomy were secondary to the development of pulmonary edema.
Pulmonary edema is the inevitable consequence of bilateral cervical vagotomy, and edemagenesis could easily mask any effect which interruption of the parasympathetic nerve supply to the lungs might have on the production and/or release of pulmonary surfactant. It was therefore felt that postganglionic parasympathetic blockade with atropine would aid in revealing whether alterations in pulmonary surfactant following vagotomy were the result of the interruption of parasympathetic nerves, or whether the alterations were secondary to pulmonary edemagenesis.
Materials and Methods. Eighty Duncan-Hartley guinea pigs (320-380g) were randomly assigned to either a treatment or control group; each group was composed of equal numbers of each sex. The treatment group received atropine, 10 mg/kg, sc (as the SO4), while the control animals received normal saline (1 ml/kg) by the same route. Injections were given at 6-hr intervals. One half of the animals of each group were sacrificed 12 hr after the first atropine dose, and the remaining animals were sacrificed at 24 hr, i.e., 12 hr after the second dose of atropine. A similar study was carried out on male albino Sprague-Dawley rats, 170-200g.
Two additional studies were carried out on rats, as follows:
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