Respiratory response to pulmonary vascular congestion in intact conscious dogs.
Clinical disorders associated with pulmonary venous hypertension frequently result in tachypnea and hyperpnea. The response to pulmonary vascular congestion (PVC) in anesthetized or decerebrate animals has consisted of modest and bidirectional changes in respiratory rate with no hyperpnea. We hypothesized that anesthesia or decerebration in previous animal experiments may have attenuated the hyperpneic response that would otherwise have been evident. A conscious dog model was developed in which the left lower lobe (LLL) pulmonary circulation could be reversibly isolated and pressurized. Occluders were placed outside the LLL pulmonary artery (PA) and vein. Two fine catheters were introduced through the wall of the LLLPA distal to the arterial occluder. A pleural catheter was used to monitor pleural pressure swings. After recovery from surgery PVC was initiated by inflation of the occluders and injection of warm saline or fresh warm blood through one of the catheters. PVC resulted in decreased breathing frequency and hypopnea in six of seven intact unanesthetized dogs. The remaining dog exhibited a transient rapid shallow breathing pattern. In four dogs tested using the same preparation under anesthesia, the response to PVC was an increase instead of a decrease in breathing frequency. We conclude that the presence of higher brain function does not promote tachypnea or hyperpnea in response to PVC. Mechanisms other than PVC, per se, likely account for the tachypnea and hyperpnea observed in clinical disorders associated with pulmonary venous hypertension.
Giesbrecht
G G
GG
Respiratory Investigation Unit, University of Manitoba, Winnipeg, Canada.
Younes
M
M
D000399:Air Pressure; D000758:Anesthesia; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002404:Catheterization; D004285:Dogs; D011652:Pulmonary Circulation / Q000502:physiology; D011668:Pulmonary Veno-Occlusive Disease / Q000503:physiopathology*; D012119:Respiration / Q000502:physiology*; D012121:Respiration, Artificial