Effects of a leukotriene antagonist on the early hemodynamic manifestations of group B streptococcal sepsis in piglets

R. N. Goldberg, C. Suguihara, M. M. Streitfeld, A. Bancalari, M. R. Clark, Eduardo Bancalari

Research output: Contribution to journalArticle

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Abstract

In order to evaluate the influence of leukotrienes on group B streptococcal (GBS) sepsis we studied the effect of a leukotriene antagonist, FPL 57231, on the early hemodynamic changes occurring secondary to an infusion of live GBS. Paralyzed, mechanically ventilated piglets received a continuous intravenous infusion of bacteria (5 x 108 org/kg/min) while systemic arterial pressure and pulmonary artery pressure were measured continuously. Cardiac output was measured by thermodilution; and plasma samples for determination of thromboxane B2 and 6-keto-PGF(1α) were taken at preset intervals. In addition to GBS, treatment animals received a continuous infusion of FPL 57231 starting 15 min after the bacterial infusion was begun. Study animals as a whole responded to bacteria within 15 min with a marked elevation in pulmonary artery pressure from 13.6 ± 4 to 44.6 ± 6 mm Hg (p<0.001), and a decline in PaO2 (79 ± 9 to 44 ± 5 mm Hg) (p<0.001) and a cardiac output (0.27 ± 0.07 to 0.15 ± 0.06 liter/min/kg) (p<0.0001). In animals treated with FPL 57231 these changes were reversed or significantly attenuated by 60 min. In the control group pH deteriorated significantly to 7.17 ± 0.1 compared to baseline values (p<0.01) by 60 min, while treatment group animals maintained a pH of 7.3 ± 0.23. Thromboxane B2 and 6-keto PGF(1α) were similar in both groups and did not change during the study period. In addition, survival was significantly longer in treatment (191 ± 44 min) compared to control animals (100 ± 32 min) (p<0.01). These data suggest that FPL 57231 may attenuate the early cardiovascular changes accompanying GBS infection and positively influence survival without modifying thromboxane or 6-keto PGF(1α) levels. These results imply that leukotrienes influence the early hemodynamic manifestations of GBS sepsis.

Original languageEnglish
Pages (from-to)1004-1008
Number of pages5
JournalPediatric Research
Volume20
Issue number10
StatePublished - Nov 26 1986

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Leukotriene Antagonists
Sepsis
Hemodynamics
Prostaglandins F
Thromboxane B2
Leukotrienes
Cardiac Output
Pulmonary Artery
Bacteria
Pressure
Thermodilution
Streptococcal Infections
Thromboxanes
Intravenous Infusions
Arterial Pressure
Therapeutics
Control Groups
FPL 57231

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Goldberg, R. N., Suguihara, C., Streitfeld, M. M., Bancalari, A., Clark, M. R., & Bancalari, E. (1986). Effects of a leukotriene antagonist on the early hemodynamic manifestations of group B streptococcal sepsis in piglets. Pediatric Research, 20(10), 1004-1008.

Effects of a leukotriene antagonist on the early hemodynamic manifestations of group B streptococcal sepsis in piglets. / Goldberg, R. N.; Suguihara, C.; Streitfeld, M. M.; Bancalari, A.; Clark, M. R.; Bancalari, Eduardo.

In: Pediatric Research, Vol. 20, No. 10, 26.11.1986, p. 1004-1008.

Research output: Contribution to journalArticle

Goldberg, RN, Suguihara, C, Streitfeld, MM, Bancalari, A, Clark, MR & Bancalari, E 1986, 'Effects of a leukotriene antagonist on the early hemodynamic manifestations of group B streptococcal sepsis in piglets', Pediatric Research, vol. 20, no. 10, pp. 1004-1008.
Goldberg, R. N. ; Suguihara, C. ; Streitfeld, M. M. ; Bancalari, A. ; Clark, M. R. ; Bancalari, Eduardo. / Effects of a leukotriene antagonist on the early hemodynamic manifestations of group B streptococcal sepsis in piglets. In: Pediatric Research. 1986 ; Vol. 20, No. 10. pp. 1004-1008.
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abstract = "In order to evaluate the influence of leukotrienes on group B streptococcal (GBS) sepsis we studied the effect of a leukotriene antagonist, FPL 57231, on the early hemodynamic changes occurring secondary to an infusion of live GBS. Paralyzed, mechanically ventilated piglets received a continuous intravenous infusion of bacteria (5 x 108 org/kg/min) while systemic arterial pressure and pulmonary artery pressure were measured continuously. Cardiac output was measured by thermodilution; and plasma samples for determination of thromboxane B2 and 6-keto-PGF(1α) were taken at preset intervals. In addition to GBS, treatment animals received a continuous infusion of FPL 57231 starting 15 min after the bacterial infusion was begun. Study animals as a whole responded to bacteria within 15 min with a marked elevation in pulmonary artery pressure from 13.6 ± 4 to 44.6 ± 6 mm Hg (p<0.001), and a decline in PaO2 (79 ± 9 to 44 ± 5 mm Hg) (p<0.001) and a cardiac output (0.27 ± 0.07 to 0.15 ± 0.06 liter/min/kg) (p<0.0001). In animals treated with FPL 57231 these changes were reversed or significantly attenuated by 60 min. In the control group pH deteriorated significantly to 7.17 ± 0.1 compared to baseline values (p<0.01) by 60 min, while treatment group animals maintained a pH of 7.3 ± 0.23. Thromboxane B2 and 6-keto PGF(1α) were similar in both groups and did not change during the study period. In addition, survival was significantly longer in treatment (191 ± 44 min) compared to control animals (100 ± 32 min) (p<0.01). These data suggest that FPL 57231 may attenuate the early cardiovascular changes accompanying GBS infection and positively influence survival without modifying thromboxane or 6-keto PGF(1α) levels. These results imply that leukotrienes influence the early hemodynamic manifestations of GBS sepsis.",
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AB - In order to evaluate the influence of leukotrienes on group B streptococcal (GBS) sepsis we studied the effect of a leukotriene antagonist, FPL 57231, on the early hemodynamic changes occurring secondary to an infusion of live GBS. Paralyzed, mechanically ventilated piglets received a continuous intravenous infusion of bacteria (5 x 108 org/kg/min) while systemic arterial pressure and pulmonary artery pressure were measured continuously. Cardiac output was measured by thermodilution; and plasma samples for determination of thromboxane B2 and 6-keto-PGF(1α) were taken at preset intervals. In addition to GBS, treatment animals received a continuous infusion of FPL 57231 starting 15 min after the bacterial infusion was begun. Study animals as a whole responded to bacteria within 15 min with a marked elevation in pulmonary artery pressure from 13.6 ± 4 to 44.6 ± 6 mm Hg (p<0.001), and a decline in PaO2 (79 ± 9 to 44 ± 5 mm Hg) (p<0.001) and a cardiac output (0.27 ± 0.07 to 0.15 ± 0.06 liter/min/kg) (p<0.0001). In animals treated with FPL 57231 these changes were reversed or significantly attenuated by 60 min. In the control group pH deteriorated significantly to 7.17 ± 0.1 compared to baseline values (p<0.01) by 60 min, while treatment group animals maintained a pH of 7.3 ± 0.23. Thromboxane B2 and 6-keto PGF(1α) were similar in both groups and did not change during the study period. In addition, survival was significantly longer in treatment (191 ± 44 min) compared to control animals (100 ± 32 min) (p<0.01). These data suggest that FPL 57231 may attenuate the early cardiovascular changes accompanying GBS infection and positively influence survival without modifying thromboxane or 6-keto PGF(1α) levels. These results imply that leukotrienes influence the early hemodynamic manifestations of GBS sepsis.

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