Mink S N, Becker A, Unruh H, Kepron W
Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3E OZ3.
J Appl Physiol (1985). 1998 Mar;84(3):782-90. doi: 10.1152/jappl.1998.84.3.782.
We examined the effect of anaphylactic shock on the longitudinal distribution of pulmonary vascular resistance (PVR) in ragweed-sensitized dogs in which PVR was partitioned into an upstream arterial component (Rus) and a downstream venous and capillary component (Rds). We also assessed whether Rus and Rds would be reduced by pretreatment with histamine H1- and H2-receptor blocking agents and with cyclooxygenase and lipoxygenase pathway inhibitors. Anesthetized animals were examined on separate occasions 3 wk apart in which one of the treatments was randomly given. The pulmonary arterial occlusion technique was used to determine segmental pressure drops. During ragweed challenge, PVR increased approximately 4 times compared with the preshock value (3.04 vs. 12. 07 mmHg . l-1 . min; P < 0.05). Although both Rus and Rds increased postshock, the greatest relative increase occurred in Rds. None of the treatments reduced partitioned resistances compared with no treatment. Our results show that, under conditions of anaphylactic shock, increases in Rus and Rds could not be ascribed to release of histamine or products of the cyclooxygenase and lipoxygenase pathways.
我们研究了过敏性休克对豚草致敏犬肺血管阻力（PVR）纵向分布的影响，其中PVR被分为上游动脉成分（Rus）和下游静脉及毛细血管成分（Rds）。我们还评估了组胺H1和H2受体阻断剂以及环氧化酶和脂氧合酶途径抑制剂预处理是否会降低Rus和Rds。对麻醉动物在间隔3周的不同时间进行检查，每次随机给予一种处理。采用肺动脉闭塞技术测定节段性压力降。在豚草激发期间，PVR与休克前值相比增加了约4倍（3.04对12.07 mmHg·l-1·min；P<0.05）。虽然休克后Rus和Rds均增加，但Rds的相对增加最大。与未治疗相比，没有一种处理能降低分割后的阻力。我们的结果表明，在过敏性休克条件下，Rus和Rds的增加不能归因于组胺或环氧化酶和脂氧合酶途径产物的释放。
