Abstract
Objective: There have been several studies that have already explored the potential beneficial role of cyclo-oxygenase (CO) inhibitors on oleic acid (OA)-induced lung injury in different species. These studies report no significant effect of CO inhibition, though thromboxane B2 (TxB2) was effectively blocked. However, recent studies indicate that pre-treatment with aspirin (ASA) preserve gas exchange in OA lung injury in dogs. Aim of our study has been to evaluate the potential beneficial effects of the pre-treatment with low doses of ASA on gas exchange, hemodynamics, respiratory mechanics, prostanoids and lung histology in OA-induced lung injury in sheep. Design: 0.09 ml/kg of OA was administered into the right atrium of 14 anaesthetized sheep. Six received a bolus of ASA (10 mg/kg i. v.) 30 min before OA, the others saline as placebo. Measurements and results: Pulmonary and tissue gas exchange, pulmonary and systemic hemodynamics, respiratory system mechanics, TxB2 and 6-keto-PGF1α, leukocytes and platelets concentrations were measured throughout the subsequent 3 h and lung histology was effected at end-experiment. The principal findings of our study are: 1) ASA reduces OA-induced early pulmonary vasoconstriction and bronchoconstriction, parallelled by a suppression of TxB2 generation; 2) the late increase in pulmonary artery pressure and airway resistance due to OA is not inhibited by ASA; 3) the early disturbance in pulmonary gas exchange is reduced by ASA, whereas the late severe deterioration is exaggerated by ASA; 4) the stability of tissue exchange ratio (R) at ≈1 in ASA-group compared to its fall to ≈0.7 in controls. Conclusion: Our findings suggest that ASA: 1) is only effective to treat the very transient TxB2-induced pulmonary vasoconstriction resulting in hydrostatic edema, and it is ineffective, even accentuates, the subsequent major pulmonary endothelial cell injury leading to alveolar flooding that is unrelated to TxB2; 2) has a transient protective effect on the TxB2-induced early bronchospasm; 3) has a biphasic behaviour on gas exchange, with a benefit which lasts only one hour and then results in a worse gas exchange; 4) has an immediate, stabilizing, persisting effect on R, contrasting with its transient effect on pulmonary hemodynamics and PaO2.
| Original language | English |
|---|---|
| Pages (from-to) | 13-21 |
| Number of pages | 9 |
| Journal | Intensive Care Medicine |
| Volume | 19 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 1993 |
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Keywords
- Acute lung injury
- Adult respiratory distress syndrome
- Aspirin
- Pulmonary and tissue gas exchange
- Pulmonary hypertension
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
Cite this
Aspirin effect on early and late changes in acute lung injury in sheep. / Chelucci, G. L.; Boncinelli, S.; Marsili, M.; Lorenzi, P.; Allegra, A.; Linden, M.; Chelucci, A.; Merciai, V.; Cresci, F.; Rostagno, C.; Gensini, G. F.; Lockhart, A.; Milic-Emili, J.
In: Intensive Care Medicine, Vol. 19, No. 1, 01.1993, p. 13-21.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Aspirin effect on early and late changes in acute lung injury in sheep
AU - Chelucci, G. L.
AU - Boncinelli, S.
AU - Marsili, M.
AU - Lorenzi, P.
AU - Allegra, A.
AU - Linden, M.
AU - Chelucci, A.
AU - Merciai, V.
AU - Cresci, F.
AU - Rostagno, C.
AU - Gensini, G. F.
AU - Lockhart, A.
AU - Milic-Emili, J.
PY - 1993/1
Y1 - 1993/1
N2 - Objective: There have been several studies that have already explored the potential beneficial role of cyclo-oxygenase (CO) inhibitors on oleic acid (OA)-induced lung injury in different species. These studies report no significant effect of CO inhibition, though thromboxane B2 (TxB2) was effectively blocked. However, recent studies indicate that pre-treatment with aspirin (ASA) preserve gas exchange in OA lung injury in dogs. Aim of our study has been to evaluate the potential beneficial effects of the pre-treatment with low doses of ASA on gas exchange, hemodynamics, respiratory mechanics, prostanoids and lung histology in OA-induced lung injury in sheep. Design: 0.09 ml/kg of OA was administered into the right atrium of 14 anaesthetized sheep. Six received a bolus of ASA (10 mg/kg i. v.) 30 min before OA, the others saline as placebo. Measurements and results: Pulmonary and tissue gas exchange, pulmonary and systemic hemodynamics, respiratory system mechanics, TxB2 and 6-keto-PGF1α, leukocytes and platelets concentrations were measured throughout the subsequent 3 h and lung histology was effected at end-experiment. The principal findings of our study are: 1) ASA reduces OA-induced early pulmonary vasoconstriction and bronchoconstriction, parallelled by a suppression of TxB2 generation; 2) the late increase in pulmonary artery pressure and airway resistance due to OA is not inhibited by ASA; 3) the early disturbance in pulmonary gas exchange is reduced by ASA, whereas the late severe deterioration is exaggerated by ASA; 4) the stability of tissue exchange ratio (R) at ≈1 in ASA-group compared to its fall to ≈0.7 in controls. Conclusion: Our findings suggest that ASA: 1) is only effective to treat the very transient TxB2-induced pulmonary vasoconstriction resulting in hydrostatic edema, and it is ineffective, even accentuates, the subsequent major pulmonary endothelial cell injury leading to alveolar flooding that is unrelated to TxB2; 2) has a transient protective effect on the TxB2-induced early bronchospasm; 3) has a biphasic behaviour on gas exchange, with a benefit which lasts only one hour and then results in a worse gas exchange; 4) has an immediate, stabilizing, persisting effect on R, contrasting with its transient effect on pulmonary hemodynamics and PaO2.
AB - Objective: There have been several studies that have already explored the potential beneficial role of cyclo-oxygenase (CO) inhibitors on oleic acid (OA)-induced lung injury in different species. These studies report no significant effect of CO inhibition, though thromboxane B2 (TxB2) was effectively blocked. However, recent studies indicate that pre-treatment with aspirin (ASA) preserve gas exchange in OA lung injury in dogs. Aim of our study has been to evaluate the potential beneficial effects of the pre-treatment with low doses of ASA on gas exchange, hemodynamics, respiratory mechanics, prostanoids and lung histology in OA-induced lung injury in sheep. Design: 0.09 ml/kg of OA was administered into the right atrium of 14 anaesthetized sheep. Six received a bolus of ASA (10 mg/kg i. v.) 30 min before OA, the others saline as placebo. Measurements and results: Pulmonary and tissue gas exchange, pulmonary and systemic hemodynamics, respiratory system mechanics, TxB2 and 6-keto-PGF1α, leukocytes and platelets concentrations were measured throughout the subsequent 3 h and lung histology was effected at end-experiment. The principal findings of our study are: 1) ASA reduces OA-induced early pulmonary vasoconstriction and bronchoconstriction, parallelled by a suppression of TxB2 generation; 2) the late increase in pulmonary artery pressure and airway resistance due to OA is not inhibited by ASA; 3) the early disturbance in pulmonary gas exchange is reduced by ASA, whereas the late severe deterioration is exaggerated by ASA; 4) the stability of tissue exchange ratio (R) at ≈1 in ASA-group compared to its fall to ≈0.7 in controls. Conclusion: Our findings suggest that ASA: 1) is only effective to treat the very transient TxB2-induced pulmonary vasoconstriction resulting in hydrostatic edema, and it is ineffective, even accentuates, the subsequent major pulmonary endothelial cell injury leading to alveolar flooding that is unrelated to TxB2; 2) has a transient protective effect on the TxB2-induced early bronchospasm; 3) has a biphasic behaviour on gas exchange, with a benefit which lasts only one hour and then results in a worse gas exchange; 4) has an immediate, stabilizing, persisting effect on R, contrasting with its transient effect on pulmonary hemodynamics and PaO2.
KW - Acute lung injury
KW - Adult respiratory distress syndrome
KW - Aspirin
KW - Pulmonary and tissue gas exchange
KW - Pulmonary hypertension
UR - http://www.scopus.com/inward/record.url?scp=0027412440&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027412440&partnerID=8YFLogxK
U2 - 10.1007/BF01709272
DO - 10.1007/BF01709272
M3 - Article
C2 - 8440792
AN - SCOPUS:0027412440
VL - 19
SP - 13
EP - 21
JO - Intensive Care Medicine
JF - Intensive Care Medicine
SN - 0342-4642
IS - 1
ER -