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Dibutyryl cyclic AMP attenuates lung responses induced by endotoxin in conscious sheep.
Am Rev Respir Dis. 1992 Jul; 146(1):32-8.AR

Abstract

Dibutyryl cyclic AMP (DBcAMP) could inhibit the production of prostanoids and modulate the pulmonary vascular responses induced by endotoxin. Diffuse lung injury after endotoxemia in sheep is accompanied by the production of prostanoids and an increase in endothelial permeability. To determine whether exogenous DBcAMP could prevent the endotoxin responses, we measured pulmonary hemodynamics, gas exchange, and lung lymph responses to an intravenous infusion of Escherichia coli endotoxin (1.0 micrograms/kg over 30 min) in unanesthetized sheep in the presence and absence of DBcAMP (30 micrograms/kg/min) infused intravenously for 6 h beginning 1 h before endotoxin infusion or for 4.5 h after 30 min of treatment with endotoxin infusion. We also measured circulating leukocytes and lung lymph and plasma concentrations of thromboxane B2 (TXB2) and prostacyclin (6-keto-PGF1 alpha) metabolites by radioimmunoassay. DBcAMP infusion before endotoxin infusion decreased endotoxin-induced pulmonary hypertension and hypoxemia and markedly attenuated the increased lung lymph flow and lymph protein clearance. DBcAMP after endotoxin only attenuated the increased lung lymph flow and lymph protein clearance. DBcAMP treatment both before and after endotoxin infusion blocked endotoxin-induced increases in lung lymph and plasma TXB2 and 6-keto-PGF1 alpha. DBcAMP did not affect the number of circulating leukocytes. Although DBcAMP alone did not affect the pulmonary and systemic hemodynamics and lung lymph balance, the potential that DBcAMP directly modulates the pulmonary vascular responses to endotoxin as a vasodilator could be expected. We conclude that DBcAMP infusion attenuates lung dysfunction caused by endotoxemia, possibly by preventing prostanoid release and modulating the pulmonary vascular responses.

Authors+Show Affiliations

First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

1320821

Citation

Koyama, S, et al. "Dibutyryl Cyclic AMP Attenuates Lung Responses Induced By Endotoxin in Conscious Sheep." The American Review of Respiratory Disease, vol. 146, no. 1, 1992, pp. 32-8.
Koyama S, Toyofuku T, Hirai K, et al. Dibutyryl cyclic AMP attenuates lung responses induced by endotoxin in conscious sheep. Am Rev Respir Dis. 1992;146(1):32-8.
Koyama, S., Toyofuku, T., Hirai, K., Yoshimura, K., Sakai, A., & Kobayashi, T. (1992). Dibutyryl cyclic AMP attenuates lung responses induced by endotoxin in conscious sheep. The American Review of Respiratory Disease, 146(1), 32-8.
Koyama S, et al. Dibutyryl Cyclic AMP Attenuates Lung Responses Induced By Endotoxin in Conscious Sheep. Am Rev Respir Dis. 1992;146(1):32-8. PubMed PMID: 1320821.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dibutyryl cyclic AMP attenuates lung responses induced by endotoxin in conscious sheep. AU - Koyama,S, AU - Toyofuku,T, AU - Hirai,K, AU - Yoshimura,K, AU - Sakai,A, AU - Kobayashi,T, PY - 1992/7/1/pubmed PY - 1992/7/1/medline PY - 1992/7/1/entrez SP - 32 EP - 8 JF - The American review of respiratory disease JO - Am Rev Respir Dis VL - 146 IS - 1 N2 - Dibutyryl cyclic AMP (DBcAMP) could inhibit the production of prostanoids and modulate the pulmonary vascular responses induced by endotoxin. Diffuse lung injury after endotoxemia in sheep is accompanied by the production of prostanoids and an increase in endothelial permeability. To determine whether exogenous DBcAMP could prevent the endotoxin responses, we measured pulmonary hemodynamics, gas exchange, and lung lymph responses to an intravenous infusion of Escherichia coli endotoxin (1.0 micrograms/kg over 30 min) in unanesthetized sheep in the presence and absence of DBcAMP (30 micrograms/kg/min) infused intravenously for 6 h beginning 1 h before endotoxin infusion or for 4.5 h after 30 min of treatment with endotoxin infusion. We also measured circulating leukocytes and lung lymph and plasma concentrations of thromboxane B2 (TXB2) and prostacyclin (6-keto-PGF1 alpha) metabolites by radioimmunoassay. DBcAMP infusion before endotoxin infusion decreased endotoxin-induced pulmonary hypertension and hypoxemia and markedly attenuated the increased lung lymph flow and lymph protein clearance. DBcAMP after endotoxin only attenuated the increased lung lymph flow and lymph protein clearance. DBcAMP treatment both before and after endotoxin infusion blocked endotoxin-induced increases in lung lymph and plasma TXB2 and 6-keto-PGF1 alpha. DBcAMP did not affect the number of circulating leukocytes. Although DBcAMP alone did not affect the pulmonary and systemic hemodynamics and lung lymph balance, the potential that DBcAMP directly modulates the pulmonary vascular responses to endotoxin as a vasodilator could be expected. We conclude that DBcAMP infusion attenuates lung dysfunction caused by endotoxemia, possibly by preventing prostanoid release and modulating the pulmonary vascular responses. SN - 0003-0805 UR - https://www.unboundmedicine.com/medline/citation/1320821/Dibutyryl_cyclic_AMP_attenuates_lung_responses_induced_by_endotoxin_in_conscious_sheep_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm/146.1.32?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -