Reflex depression of cardiovascular function during lung inflation.

These experiments were intended 1) to determine the cardiovascular reflex response initiated by lung inflation and 2) to determine the autonomic neural mechanisms that mediate the reflex responses. To test only the reflex effects of lung inflation and eliminate the associated mechanical effects thereof, we isolated the left airway and left pulmonary artery of dogs and performed static inflations of the left lung. Left lung inflation (LLI) to 30 cmH2O caused left ventricular systolic pressure, heart rate, and hindlimb vascular resistance to fall 20, 31, and 15%, respectively. When the hearts were paced to eliminate Bowditch effects, LLI caused left ventricular contractility, which was measured as dP/dt at 30 mmHg developed pressure and as the maximal rate of shortening of the contractile element, to fall 23 and 20%, respectively, and cardiac output (stroke volume) to fall 31%. Transection of the left cervical vagus nerve, interrupting most afferent and some efferent pathways from the left lung, virtually eliminated subsequent cardiovascular responses to LLI. Hindlimb vasodilation was mediated by alpha-adrenergic activity, and the fall in left ventricular contractile state was caused by a reduction in beta-adrenergic activity. The reflex bradycardia was mediated by increased cholinergic and decreased beta-adrenergic activity. These data establish that reflex mechanisms exist whereby expansion of the lung can reflexly modulate heart rate, ventricular contractility, systemic vasomotor tone, cardiac output, and stroke volume independent of the direct mechanical influence of lung expansion on these circulatory phenomena.