Lactic dehydrogenase activity in lung lymph during hemorrhagic shock, resuscitation and recovery.
Lactic dehydrogenase activity was determined in lung lymph before, during and after hemorrhagic shock to determine if this insult produced pulmonary cellular damage. Lung lymph flow and lymph protein content, reliable indices of fluids filtration rate and microvascular protein permeability were also monitored. The experiment was performed in unanesthetized sheep with a chronic lung lymph fistula. Lymph flow, lymph LDH and protein content did not change during the period of shock. Lymph flow increased significantly during resuscitation but lymph LDH and protein content decreased in relation to plasma values indicating the sieving effect of the microvascular membrane for protein to be intact. The increased flow was most likely caused by an increase in microvascular hydrostatic pressure. Plasma LDH was significantly increased during the 72 hour recovery period with lymph flow, lymph protein and lymph LDH being normal. We therefore found that hemorrhagic shock produced a systemic cellular injury reflected in an increased plasma LDH activity. No pulmonary cellular damage was noted.
D000818:Animals; D001794:Blood Pressure; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D008168:Lung / Q000201:enzymology*; D008196:Lymph / Q000201:enzymology* / Q000502:physiology; D012151:Resuscitation; D012756:Sheep; D012771:Shock, Hemorrhagic / Q000201:enzymology* / Q000503:physiopathology
D007770:L-Lactate Dehydrogenase