BRONCHIAL ARTERY LIGATION MODIFIES PULMONARY-EDEMA AFTER EXPOSURE TO SMOKE WITH ACROLEIN

BRONCHIAL ARTERY LIGATION MODIFIES PULMONARY-EDEMA AFTER EXPOSURE TO SMOKE WITH ACROLEIN
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DOI:
10.1152/jappl.1989.67.3.1001
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发表时间:
1989-09-01
影响因子:
3.3
通讯作者:
BURKE, J
BURKE, J
中科院分区:
医学2区
文献类型:
--
作者:
HALES, CA;BARKIN, P;BURKE, J

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Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 .+-. 2 (SE) min from 148 .+-. 16 to 376 .+-. 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was wide-spread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (.ltoreq. 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 .+-. 3 min, P < 0.05) and lessened the magnitude (232 .+-. 30 ml, P < 0.05) at 166 .+-. 3 min after acrolein-smoke exposure. In five animals with one pulmonary artery tied, pulmonary edema after acrolein-smoke occurred in the lung with the pulmonary artery tied (EVLW/dry lung wt = 5.64 .+-. 0.54), as well as in the lung without the artery tied (EVLW/dry lung wt = 6.3 .+-. 0.5) and thus showed the bronchial artery can be a major source of EVLW in acrolein-smoke-induced pulmonary edema.