Changes in collateral ventilation with increased vascular pressure and edema formation.
To test the hypothesis that development of hemodynamic edema results in decreased collateral ventilation, we rapidly volume-expanded anesthetized dogs with volumes equivalent to 10 (n = 5) and 15% (n = 5) of body weight. We measured collateral resistance (Rcoll), pulmonary arterial pressure, and left ventricular end-diastolic pressure before, during, and for 1-2 h after the infusion. Lungs were subsequently processed for microscopic examination and measurement of extravascular lung water content. During the infusion, Rcoll increased modestly independent of the fluid-infusion rate or the rate of increase in vascular pressures. After the infusion, Rcoll continued to increase to maximum levels 2-33 times base line even though pressures decreased dramatically. At the end of the experiment, Rcoll returned to base line in one dog and was 3-15 times base line in the other dogs. These changes bore no relationship to the severity of edema formation. Until alveolar flooding occurs, accumulation of lung interstitial fluid and changes in collateral ventilation appear to be coincident events rather than causally related variables.
D000403:Airway Resistance; D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure; D001834:Body Water / Q000032:analysis; D004285:Dogs; D008168:Lung / Q000032:analysis; D008170:Lung Compliance; D011312:Pressure; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000503:physiopathology*; D012119:Respiration