Minnear F L, Kivlen C M, Malik A B
J Appl Physiol Respir Environ Exerc Physiol. 1983 Oct;55(4):1079-84. doi: 10.1152/jappl.1983.55.4.1079.
Bradykinin (BK, 0.03-3.11 micrograms X kg-1 X min-1) was infused intravenously for 4-5.5 h to assess its effects on pulmonary transvascular fluid and protein exchange in three groups of artificially ventilated sheep prepared with lung lymph fistulas. In group I, BK was infused alone for 5.5 h. In group II, BK and captopril (SQ 14,225), an inhibitor of angiotensin-converting enzyme (ACE), were infused together because the effects of BK may be attenuated by its rapid degradation in the lung by ACE. In group III, BK was infused in the presence of propranolol, a beta-adrenergic antagonist, to prevent any permeability-decreasing effects of beta-adrenergic activation. The dosages of BK used, which decreased systemic arterial blood pressure by 10-20 mmHg, did not alter either pulmonary transvascular fluid and protein exchange or pulmonary hemodynamics at any time during infusion of BK alone or in combination with captopril or propranolol. Raising pulmonary microvascular pressure (Pmv) by inflating a left atrial balloon during the last 2 h of infusion in all three groups slightly increased pulmonary lymph flow and markedly decreased the lymph-to-plasma protein concentration ratio. These results are comparable with those obtained after increasing Pmv in normal anesthetized sheep and indicate that BK did not alter the pulmonary vascular permeability to proteins.
在三组制备了肺淋巴瘘的人工通气绵羊中，静脉输注缓激肽（BK，0.03 - 3.11微克×千克⁻¹×分钟⁻¹）4 - 5.5小时，以评估其对肺跨血管液体和蛋白质交换的影响。在第一组中，单独输注BK 5.5小时。在第二组中，同时输注BK和卡托普利（SQ 14,225），一种血管紧张素转换酶（ACE）抑制剂，因为BK的作用可能会因其在肺中被ACE快速降解而减弱。在第三组中，在普萘洛尔（一种β肾上腺素能拮抗剂）存在的情况下输注BK，以防止β肾上腺素能激活产生的任何降低通透性的作用。所使用的BK剂量使体循环动脉血压降低了10 - 20 mmHg，在单独输注BK或与卡托普利或普萘洛尔联合输注期间的任何时候，均未改变肺跨血管液体和蛋白质交换或肺血流动力学。在所有三组输注的最后2小时内，通过充盈左心房球囊提高肺微血管压力（Pmv），可使肺淋巴流量略有增加，并显著降低淋巴与血浆蛋白浓度比。这些结果与在正常麻醉绵羊中提高Pmv后获得的结果相当，表明BK不会改变肺血管对蛋白质的通透性。
