Mechanism of increased tracheo-bronchial response to inhalative acetylcholine aerosol in pulmonary vascular congestion and unilateral pulmonary artery occlusion.
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was greater in the later part of occlusion or vascular congestion and persisted even after the occlusion or block was withdrawn.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.
D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology*; D000336:Aerosols; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D001794:Blood Pressure; D001980:Bronchi / Q000187:drug effects / Q000503:physiopathology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005260:Female; D008297:Male; D011651:Pulmonary Artery; D011655:Pulmonary Embolism / Q000503:physiopathology*; D012123:Pulmonary Ventilation / Q000187:drug effects; D012119:Respiration / Q000187:drug effects*; D013990:Tidal Volume; D014132:Trachea / Q000187:drug effects / Q000503:physiopathology
D000336:Aerosols; D000109:Acetylcholine