PMID- 10736286
OWN - NLM
STAT- MEDLINE
DCOM- 20000426
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 101
IP  - 12
DP  - 2000 Mar 28
TI  - Hypoxia-induced pulmonary blood redistribution in subjects with a history of 
      high-altitude pulmonary edema.
PG  - 1418-22
AB  - BACKGROUND: Pulmonary hypertension has been suggested to play an important role 
      in development of high-altitude pulmonary edema (HAPE), and individual 
      susceptibility has been suggested to be associated with enhanced pulmonary 
      vascular response to hypoxia. We hypothesized that much greater pulmonary 
      vasoconstriction would be induced by acute alveolar hypoxia in HAPE-susceptible 
      (HAPE-s) subjects and that changes in pulmonary blood flow distribution could be 
      demonstrated by radionuclide study. METHODS AND RESULTS: We performed 
      ventilation-perfusion scintigraphy in 8 HAPE-s subjects and 5 control subjects 
      while each was in the supine position and acquired functional images of pulmonary 
      blood flow and ventilation under separate normoxic and hypoxic (arterial oxygen 
      saturation, 70%) conditions. We also measured acceleration time/right ventricular 
      ejection time (AcT/RVET) with Doppler echocardiography under each condition in 
      both groups. Moreover, we assayed human leukocyte antigen (HLA) alleles 
      serologically in the HAPE-s group. Pulmonary blood flow was significantly shifted 
      from the basal lung region to the apical lung region under hypoxia in HAPE-s 
      subjects, although no significant change in regional ventilation was observed. 
      With Doppler echocardiography, HAPE-s subjects showed increased pulmonary 
      arterial pressure during hypoxia compared with control subjects. The magnitude of 
      cephalad redistribution of lung blood flow was significantly higher in the 
      HLA-DR6-positive than in HLA-DR6-negative HAPE-s subjects. CONCLUSIONS: These 
      findings suggest that acute hypoxia induces much greater cephalad redistribution 
      of pulmonary blood flow that results from exaggerated vasoconstriction in the 
      basal lung in HAPE-s subjects. Furthermore, pulmonary vascular hyperreactivity to 
      hypoxia may be associated with HLA-DR6.
FAU - Hanaoka, M
AU  - Hanaoka M
AD  - First Department of Medicine, and Department of Radiology, Shinshu University 
      School of Medicine, Matsumoto, Japan. fountain@matsumoto.ne.jp
FAU - Tanaka, M
AU  - Tanaka M
FAU - Ge, R L
AU  - Ge RL
FAU - Droma, Y
AU  - Droma Y
FAU - Ito, A
AU  - Ito A
FAU - Miyahara, T
AU  - Miyahara T
FAU - Koizumi, T
AU  - Koizumi T
FAU - Fujimoto, K
AU  - Fujimoto K
FAU - Fujii, T
AU  - Fujii T
FAU - Kobayashi, T
AU  - Kobayashi T
FAU - Kubo, K
AU  - Kubo K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-DR6 Antigen)
SB  - IM
MH  - *Altitude Sickness/*complications
MH  - Blood Pressure/physiology
MH  - Echocardiography, Doppler
MH  - HLA Antigens/analysis
MH  - HLA-DR6 Antigen/analysis
MH  - Humans
MH  - Hypoxia/diagnostic imaging/*physiopathology
MH  - Lung/diagnostic imaging
MH  - Pulmonary Circulation/*physiology
MH  - Pulmonary Edema/diagnostic imaging/*etiology
MH  - Radionuclide Imaging
MH  - Stroke Volume
EDAT- 2000/03/29 00:00
MHDA- 2000/04/29 00:00
CRDT- 2000/03/29 00:00
PHST- 2000/03/29 00:00 [pubmed]
PHST- 2000/04/29 00:00 [medline]
PHST- 2000/03/29 00:00 [entrez]
AID - 10.1161/01.cir.101.12.1418 [doi]
PST - ppublish
SO  - Circulation. 2000 Mar 28;101(12):1418-22. doi: 10.1161/01.cir.101.12.1418.