Time-dependent changes in pulmonary vascular responses to acute hypoxia during and after cold exposure in rats

• Published in: European journal of applied physiology Vol. 100; no. 3; pp. 341 - 344
• Main Authors: Koizumi, Tomonobu, Ruan, Zonghai, Asano, Kouji, Sakai, Akio
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01-06-2007
• Subjects: Acclimatization - physiology; Angiotensin; Angiotensin II; Angiotensin II - physiology; Animals; Chronic exposure; Cold Temperature; Hypoxia; Hypoxia - physiopathology; Male; Pulmonary arteries; Pulmonary Artery - physiopathology; Random Allocation; Rats; Rats, Sprague-Dawley; Rodents; Time Factors; Vasoconstriction; Vasoconstriction - physiology
• ISSN: 1439-6319; 1439-6327
• DOI: 10.1007/s00421-007-0436-5

This study evaluated time-dependent alterations in pulmonary vascular reactivity to acute hypoxia and to the administration of angiotensin II (AT-II) during and after chronic exposure to cold using isolated perfused lung specimens from rats. Animals were exposed to a cold environment (3.5 (mean) +/- 1.0 (SD) degrees C) or to a normal temperature (24.0 +/- 1.0 degrees C) for 7 days. The isolated lungs were taken serially and pulmonary vascular responses to acute hypoxia and AT-II were examined. Both the pulmonary vascular responses to acute hypoxia and to AT-II were significantly reduced 9 h after the exposure to cold. The diminished vascular response to AT-II was restored to the pre-exposure level after 5 days of cold exposure and then sustained. On the other hand, the reduced response to acute hypoxia was sustained for the first 7 days during exposure to cold and then returned to the pre-exposure level during sustained exposure to cold. After removal from the 7 days of cold exposure, the pulmonary vascular response to acute hypoxia was immediately restored. Thus, during exposure to cold, pulmonary vascular response to acute hypoxia was more sustained than the AT-II-induced vasoconstriction. We concluded that cold exposure alters pulmonary vascular responses to acute hypoxia and AT-II in rats, but that the response to acute hypoxia is more sustained than that of AT-II.