The Role of the Pulmonary Afferent Receptors in Producing Hemodynamic Changes during Hyperinflation and Endotracheal Suctioning in an Oleic Acid–Injured Animal Model of Acute Respiratory Failure
Available accessResearch articleFirst published online January, 2000
The Role of the Pulmonary Afferent Receptors in Producing Hemodynamic Changes during Hyperinflation and Endotracheal Suctioning in an Oleic Acid–Injured Animal Model of Acute Respiratory Failure
The purpose of this study was to examine the role of the pulmonary afferent receptors in producing hemodynamic changes during hyperinflation and endotracheal suctioning (ETS) in an oleic acid–injured animal model of acute respiratory failure. Previous investigations of hyperinflation as a method to prevent hypoxia-induced sequelae of ETS have demonstrated unrecognized hemodynamic consequences. In this within-subject, repeated-measures study, instrumented, oleic acid–injured dogs had continuous measurements of heart rate (HR), mean aortic blood pressure (MAP), left ventricular pressure (Plv), pulmonary artery pressure (Ppa), right ventricular afterload (Ppa(tm)), right atrial pressure (Pra), and right ventricular filling pressure (Pra(tm)) during hyperinflation and ETS when the vagi were intact and after the pulmonary branches of the vagus nerves had been severed. After severing the vagi, MAP and Plv were decreased and HR and Ppa were increased. With the vagi severed, there was less variation in MAP and Ppa but increased variation in HR. These findings suggest that vagally mediated reflexes from the lungs produce some, but not all, of the hemodynamic effects associated with hyperinflation and ETS. Continued research is necessary to discover a method of hyperoxygenation and suctioning that does not produce potentially harmful hemodynamic effects.
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