ABSTRACT
Hypoxic pulmonary pressor response (HPPR) was observed witb a preparation of perfused lungs in situ in rats, and the effects of deoxy-2-glucose (2DG), verapamil, and dipyridamole on HPPR were studied.During bypoxia (inhalation of 3% oxygen for 10 minutes) , there was a 50% increase on average in pulmonary arterial pressure in the perfused lungs in situ in rats. 2DG inhibited the first and second but enhanced the seventh and eighth HPPR. Both verapamil and dipyridamole depressed HPPR.On the basis of the results, the author suggests that the mechanism of HPPR might originate from the lungs themselves. There might be a close relation between the glucose-energy metabolism and the occurrence of HPPR, the trans-membranous influx of calcium might play a certain role in the development of HPPR, and adenosine would probably participate in the regulation of HPPR.