Changes of components of the plasma kallikrein-kinin system during experimental lung insufficiency in dogs.

Lung insufficiency was induced in 11 dogs by combined hemorrhagic hypotension (55 mm Hg for two hours) and clamping the portal triad (20 minutes). Four dogs were ventilated spontaneously (group 1). In seven dogs thoracotomy was done giving access to lung biopsies and central hemodynamic measurements (group 2). Five dogs were used as controls without hypotension or clamping. All the dogs in group 1 and 2 developed morphological changes in the lungs characteristic of post-traumatic lung insufficiency. A significant decrease of prekallikrein levels (42% and 34% of initial levels in the two groups, respectively) was found. A significant elevation of the kallikrein activity compared to initial values and the control group was found as well. The antikallikrein levels were reduced to 76% and 67% of initial levels in group 1 and 2, respectively. This reduction was statistically significant. A significant lowering of high molecular weight kininogen was also found, 50% and 28% of initial levels in the two groups. These results demonstrate activation of the kallikrein-kinin system in this experimental model. This can give information on the pathogenesis of post-traumatic lung insufficiency and can explain, for instance, the hypotension and oedema found in this condition. This study also demonstrates that homeostatic functions are altered, this probably being of greater interest than the specific lung alterations described by several authors. Determination of the components of the kallikrein-kinin system can be of diagnostic and prognostic value in post-traumatic lung insufficiency in clinical medicine.