Kivlen C M, Johnson A, Pittman T, Guile A J, Malik A B
J Appl Physiol Respir Environ Exerc Physiol. 1982 Dec;53(6):1546-50. doi: 10.1152/jappl.1982.53.6.1546.
We examined the effect of converting enzyme inhibition with captopril (SQ 14,225) on pulmonary hemodynamics and on accumulation of extravascular lung water after microembolization in dogs. Pulmonary microembolization, induced with glass beads (200 microns diam), increased the mean pulmonary arterial pressure to approximately 40 Torr in both control and captopril-treated animals. The increase in pulmonary vascular resistance (PVR) in control animals was sustained during the 75 min of study and was associated with an increase in the extravascular lung water content-to-bloodless dry lung weight ratio (W/D) from a normal value of 2.84 +/- 0.22 to 4.53 +/- 0.24 ml/g (P less than 0.01) after embolization. In the captopril-treated group, the PVR increased gradually, such that the value at 75 min postembolization was greater than in controls (P less than 0.05). The W/D in the captopril-treated group of 4.62 +/- 0.19 ml/g was greater than the value of 2.83 +/- 0.10 ml/g in nonembolized captopril-treated animals, but the degrees of edema in the control and captopril-treated animals were not different. A similar degree of embolization induced during infusion of 5 micrograms X kg-1 X h-1 of bradykinin also did not enhance the pulmonary edema, and there was also a greater increase in PVR than in control animals after embolization. These findings suggest that bradykinin does not contribute to the degree of pulmonary edema after microembolization.
我们研究了用卡托普利（SQ 14,225）进行转换酶抑制对犬微栓塞后肺血流动力学及血管外肺水蓄积的影响。用直径200微米的玻璃珠诱导犬发生肺微栓塞，在对照组和卡托普利治疗组动物中，平均肺动脉压均升高至约40托。在75分钟的研究期间，对照组动物肺血管阻力（PVR）持续升高，栓塞后血管外肺水含量与无血干肺重量比（W/D）从正常的2.84±0.22增加到4.53±0.24毫升/克（P<0.01）。在卡托普利治疗组中，PVR逐渐升高，栓塞后75分钟时的值高于对照组（P<0.05）。卡托普利治疗组的W/D为4.62±0.19毫升/克，高于未栓塞的卡托普利治疗动物的2.83±0.10毫升/克，但对照组和卡托普利治疗组动物的水肿程度无差异。在输注5微克·千克-1·小时-1缓激肽期间诱导的类似程度的栓塞也未加重肺水肿，且栓塞后PVR的升高也高于对照组动物。这些发现提示缓激肽对微栓塞后肺水肿的程度无影响。
