RESPIRATORY RESPONSES TO CO2 REBREATHING IN LUNG-TRANSPLANT RECIPIENTS

To evaluate the respiratory responses after lung transplantation, we s tudied the hypercarbic ventilatory response in 20 patients with severe obstructive pulmonary disease and compared it with that of 10 normal subjects. Eleven patients underwent bilateral lung transplantation and 9 patients had single-lung transplantation. All patients had preopera tive hypercapnia (51.3 +/- 9.7 mm Hg) and blunted slopes of CO2 rebrea thing curves for minute ventilation (0.39 +/- 0.20 L . min(-1) . mm Hg -1) and inspiratory occlusion pressure (0.35 +/- 0.30 s(-1)). The hype rcapnia and blunted ventilatory responses persisted at the initial pos toperative test (5.8 +/- 2.0 days) despite improved pulmonary function (preoperative forced expiratory volume in 1 second [FEV(1)], 0.57 +/- 0.16 L; initial postoperative FEV(1), 1.83 +/- 0.65 L; p < 0.001). By the 15th to 30th postoperative day (21.3 +/- 6.0 days), compared with preoperative and initial postoperative values, end-tidal CO2 had norm alized (40.6 +/- 6.9 versus 51.3 +/- 9.7 and 49.6 +/- 10.3 mm Hg; p < 0.005) and was coupled with enhanced ventilatory responses for the reb reathing curve for minute ventilation (1.26 +/- 0.7 versus 0.39 +/- 0. 20 and 0.32 +/- 0.32 L . min(-1) . mm Hg-1; p < 0.005) and the inspira tory occlusion pressure curve (0.98 +/- 7.4 versus 0.35 +/- 0.30 and 0 .41 +/- 0.29 s(-1); p < 0.005). These respiratory responses developed without a change in postoperative pulmonary function (initial postoper ative FEV(1), 1.83 +/- 0.65 L versus last postoperative FEV(1), 1.96 /- 0.66 L; p = not significant). The last postoperative values also we re equivalent to tested normals for end-tidal CO2 (40.6 +/- 6.9 versus 39.9 +/- 4.3 mm Hg), for the minute ventilation curve (1.26 +/- 0.7 v ersus 1.59 +/- 0.48 L . min(-1) . mm Hg-1), and for the inspiratory oc clusion pressure curve (0.98 +/- 0.74 versus 0.86 +/- 0.4 s(-1)). We c onclude that after lung transplantation, patients with severe chronic obstructive pulmonary disease display a restoration of ventilatory res ponsiveness that likely is caused by a readjustment of the CO2 thresho ld at the central chemoreceptor regulatory center.