Shock lung--experimental studies on a haemorrhagic hypovolaemic rabbit model.
An experimental model of haemorrhagic hypotension was standardized using rabbits to investigate the shock lung syndrome over a period of 120 minutes. Acute hypovolaemia was induced by withdrawal of blood under anaesthesia to a mean arterial pressure of 30 +/- 5 mmHg within 10 minutes. The mean leucocyte counts and the release of lysosomal enzymes (acid phosphatase and beta-glucuronidase) in the blood and in lung tissue, as well as the metabolic capacities of lung tissue in terms of protein and lipid biosynthesis, were investigated at set intervals after 30, 60, 90 and 120 minutes. The results indicate a progressive decline in leucocyte numbers over 120 minutes to about 40% of the original. An immediate granulocytopenia was observed with a relative lymphocytosis within 30 minutes. The beta-glucuronidase and acid phosphatase contents of the plasma increased with time; beta-glucuronidase activity increased progressively as leucocytes disappeared from the circulation. Concomitantly, the capacity of the lung tissue to synthesize protein and lipids was retarded with time, becoming significantly lower than baseline values after 60 minutes of hypovolaemia. The decline in leucocyte numbers in the circulation correlated well with the increase in beta-glucuronidase activity and the retarded metabolic capacity of the lung tissue.
D000135:Acid Phosphatase / Q000097:blood; D000818:Animals; D005966:Glucuronidase / Q000097:blood; D006400:Hematocrit; D007958:Leukocyte Count; D008055:Lipids / Q000032:analysis; D008168:Lung / Q000032:analysis; D011506:Proteins / Q000032:analysis; D011817:Rabbits; D012128:Respiratory Distress Syndrome / Q000378:metabolism*; D012769:Shock / Q000378:metabolism*; D013997:Time Factors
D008055:Lipids; D011506:Proteins; D000135:Acid Phosphatase; D005966:Glucuronidase