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Effect of leukotriene inhibitor LY-171883 on the pulmonary response to Escherichia coli endotoxemia.
Crit Care Med. 1990 Feb; 18(2):190-7.CC

Abstract

The effect of the leukotriene D4 (LTD4) receptor antagonist, LY-171883, on the respiratory and cardiovascular changes in endotoxemia was studied in 20 unanesthetized sheep. In group 1 (n = 2), 4 mg/kg LY-171883 was injected iv. In group 2 (n = 12), Escherichia coli endotoxin (1 micrograms/kg) was infused iv, and in group 3 (n = 6), 4 mg/kg LY-171883 was administered 15 min before and 30 min after the same dose of endotoxin. Infusion of LY-171883 in group 1 did not alter baseline ventilatory and cardiovascular measurements. A two-phase pulmonary response was observed in group 2: an early pulmonary hypertension phase in which pulmonary artery pressure (PAP) increased from 18.7 to 51.2 mm Hg (p less than .001), with a fall in cardiac index (CI) from 171 to 114 ml/min.kg (p less than .01). The ratio of peak inspiratory/expiratory flow rate (PIF/PEF) increased from 1.08 to 1.35 (p less than .01) and the respiratory rate from 50 to 70 breath/min (p less than .005) 30 min postendotoxin. The flow rate measured at midexpiration time (V50) decreased from 81% to 25% of its peak expiration (p less than .001) and the airway resistance increased from 3.8 to 32.7 cm H2O/L.sec (p less than .001). The second permeability phase was characterized by an increase in pulmonary lymph flow (QL) from 8.5 to 35.2 ml/h (p less than .01), a decrease in PaO2 from 76 to 61 torr (p less than .01), and an increase in pulmonary shunt ratio (Qsp/Qt) from 16% to 31% (p less than .005).(

ABSTRACT

TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Department of Surgery B, Hadassah University Hospital, Jerusalem, Israel.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1967569

Citation

Gross, D, et al. "Effect of Leukotriene Inhibitor LY-171883 On the Pulmonary Response to Escherichia Coli Endotoxemia." Critical Care Medicine, vol. 18, no. 2, 1990, pp. 190-7.
Gross D, Ben Dahan J, Landau EH, et al. Effect of leukotriene inhibitor LY-171883 on the pulmonary response to Escherichia coli endotoxemia. Crit Care Med. 1990;18(2):190-7.
Gross, D., Ben Dahan, J., Landau, E. H., & Krausz, M. M. (1990). Effect of leukotriene inhibitor LY-171883 on the pulmonary response to Escherichia coli endotoxemia. Critical Care Medicine, 18(2), 190-7.
Gross D, et al. Effect of Leukotriene Inhibitor LY-171883 On the Pulmonary Response to Escherichia Coli Endotoxemia. Crit Care Med. 1990;18(2):190-7. PubMed PMID: 1967569.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of leukotriene inhibitor LY-171883 on the pulmonary response to Escherichia coli endotoxemia. AU - Gross,D, AU - Ben Dahan,J, AU - Landau,E H, AU - Krausz,M M, PY - 1990/2/1/pubmed PY - 1990/2/1/medline PY - 1990/2/1/entrez SP - 190 EP - 7 JF - Critical care medicine JO - Crit Care Med VL - 18 IS - 2 N2 - The effect of the leukotriene D4 (LTD4) receptor antagonist, LY-171883, on the respiratory and cardiovascular changes in endotoxemia was studied in 20 unanesthetized sheep. In group 1 (n = 2), 4 mg/kg LY-171883 was injected iv. In group 2 (n = 12), Escherichia coli endotoxin (1 micrograms/kg) was infused iv, and in group 3 (n = 6), 4 mg/kg LY-171883 was administered 15 min before and 30 min after the same dose of endotoxin. Infusion of LY-171883 in group 1 did not alter baseline ventilatory and cardiovascular measurements. A two-phase pulmonary response was observed in group 2: an early pulmonary hypertension phase in which pulmonary artery pressure (PAP) increased from 18.7 to 51.2 mm Hg (p less than .001), with a fall in cardiac index (CI) from 171 to 114 ml/min.kg (p less than .01). The ratio of peak inspiratory/expiratory flow rate (PIF/PEF) increased from 1.08 to 1.35 (p less than .01) and the respiratory rate from 50 to 70 breath/min (p less than .005) 30 min postendotoxin. The flow rate measured at midexpiration time (V50) decreased from 81% to 25% of its peak expiration (p less than .001) and the airway resistance increased from 3.8 to 32.7 cm H2O/L.sec (p less than .001). The second permeability phase was characterized by an increase in pulmonary lymph flow (QL) from 8.5 to 35.2 ml/h (p less than .01), a decrease in PaO2 from 76 to 61 torr (p less than .01), and an increase in pulmonary shunt ratio (Qsp/Qt) from 16% to 31% (p less than .005).(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0090-3493 UR - https://www.unboundmedicine.com/medline/citation/1967569/Effect_of_leukotriene_inhibitor_LY_171883_on_the_pulmonary_response_to_Escherichia_coli_endotoxemia_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=1967569.ui DB - PRIME DP - Unbound Medicine ER -