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Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung.

Publication ,  Journal Article
Huang, YC; Kennedy, TP; Su, YF; Watkins, WD; Whorton, AR; Piantadosi, CA
Published in: J Appl Physiol (1985)
January 1993

Platelet-activating factor (PAF) and the interferons (IFN) are released during sepsis and the adult respiratory distress syndrome. The proinflammatory nature of PAF and anti-inflammatory property of IFN led us to investigate interactions between these two mediators in an isolated perfused lung (IPL) preparation. In the IPL, mean pulmonary arterial pressure (Ppa), lung weight gain, and peak airway pressure (Paw) were monitored continuously for 1 h in six groups of rabbits: 1) control, 2) the IFN-alpha/beta inducer polyinosinic:cytidylic acid (polyI:C) alone, 3) PAF alone, 4) polyI:C + PAF, 5) indomethacin + PAF, and 6) AA861 (a 5-lipoxygenase inhibitor) + PAF. At the end of 1 h, microvascular pressure was determined by double-occlusion technique and partition of total pulmonary vascular resistance (RT) was calculated. Serial eicosanoid concentrations in the perfusate also were measured. PAF increased Ppa, Paw, lung weight gain, and RT. These changes were associated with increased thromboxane B2 and decreased leukotriene production. PolyI:C, which induced high levels of serum IFN in rabbits, blocked the PAF-induced increase in Ppa, Paw, lung weight gain, and RT, similar to indomethacin and AA861. PolyI:C suppressed PAF-stimulated release of thromboxane B2 and increased leukotriene levels in the perfusate. The PAF-induced lung responses also were attenuated by pretreatment with human recombinant IFN. These data indicate that polyI:C protects against PAF-induced responses in the rabbit IPL, most likely via its induction of IFN. This effect is related in part to inhibition of thromboxane A2 production stimulated by PAF and leukotrienes.

Duke Scholars

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

January 1993

Volume

74

Issue

1

Start / End Page

251 / 258

Location

United States

Related Subject Headings

  • Vascular Resistance
  • Recombinant Proteins
  • Rabbits
  • Pulmonary Edema
  • Poly I-C
  • Platelet Activating Factor
  • Physiology
  • Microcirculation
  • Male
  • Lung Diseases
 

Citation

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ICMJE
MLA
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Huang, Y. C., Kennedy, T. P., Su, Y. F., Watkins, W. D., Whorton, A. R., & Piantadosi, C. A. (1993). Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung. J Appl Physiol (1985), 74(1), 251–258. https://doi.org/10.1152/jappl.1993.74.1.251
Huang, Y. C., T. P. Kennedy, Y. F. Su, W. D. Watkins, A. R. Whorton, and C. A. Piantadosi. “Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung.J Appl Physiol (1985) 74, no. 1 (January 1993): 251–58. https://doi.org/10.1152/jappl.1993.74.1.251.
Huang YC, Kennedy TP, Su YF, Watkins WD, Whorton AR, Piantadosi CA. Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung. J Appl Physiol (1985). 1993 Jan;74(1):251–8.
Huang, Y. C., et al. “Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung.J Appl Physiol (1985), vol. 74, no. 1, Jan. 1993, pp. 251–58. Pubmed, doi:10.1152/jappl.1993.74.1.251.
Huang YC, Kennedy TP, Su YF, Watkins WD, Whorton AR, Piantadosi CA. Protection against platelet-activating factor-induced injury by interferon inducer in perfused rabbit lung. J Appl Physiol (1985). 1993 Jan;74(1):251–258.

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

January 1993

Volume

74

Issue

1

Start / End Page

251 / 258

Location

United States

Related Subject Headings

  • Vascular Resistance
  • Recombinant Proteins
  • Rabbits
  • Pulmonary Edema
  • Poly I-C
  • Platelet Activating Factor
  • Physiology
  • Microcirculation
  • Male
  • Lung Diseases