Cooling the pulmonary blood in dogs alters activity of pulmonary vagal afferents.

In open-chest anesthetized dogs with left and right lungs ventilated separately, we recorded changes in firing of right lung vagal receptors when 1.25 ml/kg cold (5 degrees C, 20 degrees C) blood were injected into the nonperfused right pulmonary artery. With the right lung inflated at constant pressure, effects of cold blood on individual pulmonary stretch receptors (PSRs) were frequency dependent, with discharge increasing or remaining unchanged if control frequency was low and decreasing if it was high. Consequently average PSR discharge was unchanged by cold blood when airway pressure was maintained at 5 cmH2O, but it decreased at pressures of 10 and 15 cmH2O. Cold blood stimulated rapidly adapting receptors (RARs) at all three pressures. Injection of blood at 37 degrees C had no effect. We conclude that changes in PSR activity account for the tachypnea induced by pulmonary arterial injection of cold blood (G. G. Giesbrecht and M. Younes. J. Appl. Physiol. 69: 1435–1441, 1990). With the right lung phasically ventilated, cold blood decreased PSR discharge in inflation, caused high-threshold PSRs to fire in deflation, and stimulated RARs. Pulmonary C-fibers were unaffected by cold blood. We suggest that PSRs and RARs initiate respiratory changes during hypothermia or exercise-induced asthma.