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Canadian Journal of Anesthesia, Vol 24, 661-677, Copyright © 1977 by Canadian Anesthesiologists' Society

Pulmonary Vascular Effects of Acetylsalicylic Acid, Chloroquine, Dextran and Methylprednisolone Given after Haemorrhagic Shock in Dogs

WILLIAM H. NOBLE B.A., M.D., D.A., F.R.C.P.(C)1, CHRISTOPHER E. FAMEWO M.B., B.S., D.A., F.R.C.P.(C)1, and M. BERNADETTE GARVEY B.Sc., M.D., F.R.C.P.(C)2

1 Department of Anaesthesia, St. Michael's Hospital and University of Toronto, Toronto, Ontario, Canada
2 Division of Haematology, Department of Medicine, St. Michael's Hospital and University of Toronto, Toronto, Ontario, Canada

We have described increases in lung water and pulmonary vascular resistance and reduced myocardial performance in both pigs and dogs after two hours of haemorrhagic shock followed by re-infusion of blood. In this experiment haemorrhagic shock was induced by removing blood to ACD blood packs in five groups of dogs. After two hours of shock, blood was re-infused and NaHCO3 was given to correct the metabolic acidosis of shock. One group of dogs remained as control and received no drugs. Experiments were carried out on three other groups of dogs with one of aspirin, dextran and methylprednisolone given intravenously at the end of the shock period and before blood was re-infused. To allow absorption, chloroquine was given intramuscularly before the period of shock in the fifth group of dogs. In the group with no drugs pulmonary vascular resistance (PVR) increased 95 per cent (significant) from the control period to the end of the experiment. PVR in the control period was not significantly different from PVR at the end of the experiment in any drug group. However, chloroquin was associated with the greatest increase in PVR between these times (77 per cent N.S.). PVR actually fell from control levels to the end of the experiment in both the aspirin (-3.4 per cent N.S.) and dextran (-2.9 per cent N.S.) groups. PVR rose (14 per cent N.S.) from the control period to the end of the experiment in the methylprednisolone group. The aspirin, dextran and methylprednisolone PVR results are all significantly different from the "no drug" group. In both the aspirin and dextran groups platelet aggregation was inhibited. Only the methylprednisolone group had a significant increase in lung water (21 per cent) and the smallest increase in lung water occurred in the aspirin group (9.8 per cent N.S.). We could not relate lung water changes to PVR changes. The lung water changes were compatible with interstitial pulmonary oedema and did not lead to serious gas exchange problems. Myocardial performance appeared improved with dextran and methylprednisolone after shock.

We conclude that while dextran and methylprednisolone confer some benefit in preventing increases in PVR and lung water after haemorrhage shock, aspirin is the best drug of those studied in preventing these changes.






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Copyright © 1977 by the Canadian Anesthesiologists' Society.