Lysosomal enzyme pattern in lung lymph and blood during E. coli sepsis in sheep

Abstract

Systemic release of lysosomal enzymes and local release in the pulmonary microcirculation from sequestrated and activated leucocytes could be an important factor in the development of the lung microvascular injury seen after septicaemia. The maximal activities of 11 lysosomal acid hydrolases (acid phosphatase, α- and β-glucosidase, α- and β-galactosidase, α-mannosidase, β-acetylglucosaminidase, β-glucuronidase, arylamidase and cathepsins B and C) were measured in serum and lung lymph from seven sheep before and after infusion of live E. coli bacteria. In the early phase of septicaemia (the first hour) the activities of eight enzymes were increased in serum and/or lung lymph (1.1 to 2× pre-infusion values). In the late phase, 3–4 h after sepsis, there were significantly elevated serum activities of β-glucosidase (5.4×), α- and β-galactosidases (2.7×, 1.5×), β-acetylglucosaminidase (2.0×) arylamidase (1.2×) and cathepsin B (1.7×). In lymph acid phosphatase (1.7×), α- and β-glucosidases (1.6×, 6.4×), α- and β-galactosidases (2.1×, 1.7×). β-acetylglucosaminidase (2.6×), and β-glucuronidase (4.0× pre-infusion) were elevated. The findings of a heterogenicity of changes in serum and lymph activities, as well as the large molecular sizes of some of the enzymes with changed activities indicated to us that permeability changes were not major causes of increased lymph enzyme activities. The results could indicate a local release of enzymes either from sequestrated leucocytes or lung tissue due to local reactions in the lung or lung microvessels. The heterogenous changes in activities for the various lysosomal enzymes as found in the present study indicated that measurement of only one enzyme could be misleading. Furthermore, in order to obtain an over all view of lysosomal enzyme involvement in septicaemia, both local and systemic enzyme activities ought to be studied.

Key words:

• acid hydrolases
• lung injury
• microvascular permeability
• pulmonary pathophysiology