Regional CO2 tension quantitatively mediates homeostatic redistribution of ventilation following acute pulmonary thromboembolism in pigs

quantitatively mediates homeostatic redistribution of ventilation following acute pulmonary thromboembolism in pigs. J Appl Physiol 107: 755–762, 2009. First published July 16, 2009; doi:10.1152/japplphysiol.00245.2009.—Previous studies reported that regional CO2 tension might affect regional ventilation (V ˙ ) fol-lowing acute pulmonary thromboembolism (APTE). We investigated the pathophysiology and magnitude of these changes. Eight anesthe-tized and ventilated piglets received autologous clots at time 0 min until mean pulmonary artery pressure was 2.5 times baseline. The distribution of V ˙ and perfusion (Q ˙ ) at four different times (5, 30, 60, 120 min) was mapped by fluorescent microspheres. Regional V ˙ and Q˙ were examined postmortem by sectioning the air-dried lung into 900–1,000 samples of 2 cm3 each. After the redistribution of regional Q ˙ by APTE, but in the scenario assuming that no V ˙ shift had yet occurred, CO2 tension in different lung regions at 30 min post-APTE (PXCO2) was estimated from the V ˙ /Q ˙ data and divided int