Mechanism of pulmonary vascular injury in high altitude pulmonary edema.
| Project/Area Number |
60480216
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Shinshu University School of Medicine |
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Principal Investigator |
KUSAMA Shozo Shinshu University School of Medicine Professor, 医学部, 教授 (70020708)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Akio Shinshu University School of Medicine Assistant, 医学部, 助手 (70020758)
UEDA Gou Shinshu University School of Medicine Professor, 医学部, 教授 (10020702)
KUBO Keishi Shinshu University School of Medicine Assistant, 医学部, 助手 (80143965)
KOBAYASHI Toshio Shinshu University School of Medicine Assistant Professor, 医学部, 講師 (80020775)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥9,500,000 (Direct Cost: ¥9,500,000)
Fiscal Year 1986: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 1985: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | High altitude / Pulmonary edema / Artificil climatic chanber / Thromboxane <A_2> / Decompression / Denitrogenation / 肺空気塞栓 |
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| Research Abstract |
To examine the hypothesis that high altitude pulmonary edema might be caused by intravascular air bubble formation during decompression, two experiments were performed by using awake sheep with chronic lung lymph fistula.
1) Effects of thromboxane synthase inhibition on air emboli lung injury in sheep. We tested the effects of OKY-046, a thromboxane synthase inhibitor, on lung injury induced by 2 hour of pulmonary air infusion in the pulmonary artery. Air infusion caused sustained pulmonary hypertension and an increase in pulmonary vascular permeability. The levels of <TxB_2> and 6-keto- <PGF_(1(alpha))> in both plasma and lung lymph were significantly elevated during the air infusion. <TxB_2> concentration in plasma obtained from the left atrium was higher than that from the pulmonary artery at 15 min of air infusion. When sheep were pretreated with OKY-046(10mg/kg, iv) prior to the air infusion, increases in <TxB_2> were prevented. The pulmonary arterial pressure, however, increased s
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imilarly to that of untreated sheep. The increase in lung lymph flow was significantly supressed during the air infusion. These data suggest that the pulmonary hypertension observed during air embolism is not caused by <TxA_2> . We also tested the effects of dibutyryl cyclic AMP on air emboli lung injury in awake sheep.
2) Effects of hypobaria on lung fluid balance in awake sheep during rapid exposure to 6600m-simulated high altitude. We observed that under both 6600m-simulated hypoxic hypobaria (barometric pressure 326mmHg, <FIO_2> 0.21) and 6600m-simulated normoxic hypobaria (barometric pressure 326mmHg, <FIO_2> 0.65), lung lymph flow significantly increased. But exposure to 6600m-simulated normoxic hypobaria (barometric pressure 326mmHg, <FIO_2> 0.65) after pretreatment with a 2 hour-pure oxygen inhalation caused no changes in lung lymph flow. These results suggest that rapid exposure to hypobaria causes an increase in pulmonary vascular permeability and that intravascular air bubble formation might account for this permeability change. Less
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(1 results)
Research Products
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