PREVENTION BY ULINASTATIN OF DECREASED CARBONIC-ANHYDRASE ACTIVITY-INDUCED BY PMN ELASTASE IN-VITRO

Disturbed carbon dioxide (CO2) elimination in adult respiratory distre ss syndrome (ARDS) has been considered to result from the dead space c reated by microthrombosis and vasoconstriction. However, another distu rbance factor in CO2 elimination has been reported; the chemical dead space resulting from the inhibition of carbonic anhydrase (CA). This e xperiment was conducted to quantify the inhibition of CA activity by p olymorphonucleocyte (PMN) elastase, which increases in ARDS. Different flasks containing solutions of CA, buffer, elastase, ulinastatin (an elastase antagonist), CA with PMN elastase, and CA with both PMN elast ase and ulinastatin were prepared. Each flask was injected with sodium bicarbonate labeled with radioactive carbon (C-14) and was shaken for 20 minutes; CA activity in each flask was measured by calculating the decrease in the coefficient (K) of C-14. It was observed that CA acti vity was inhibited dose-dependently by PMN elastase and that the inhib ited activity was recovered by ulinastatin, which can inhibit PMN elas tase. These findings indicate that CA activity in vitro could be inhib ited by PMN elastase, which increases in ARDS, and suggests that distu rbance of CO2 elimination could be reduced by using ulinastatin. It wa s concluded that ulinastatin could prevent the CA activity induced by PMN elastase in vitro.