Complement activation and thromboxane secretion by liposome-encapsulated hemoglobin in rats in vivo

Inhibition by soluble complement receptor type 1

J. Szebeni, Helmut Spielberg, Richard O. Cliff, Nabila M. Wassef, Alan S. Rudolph, Carl R. Alving

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Intravenous administration of liposome-encapsulated hemoglobin (LEH) in rats led to an early (within 15 min) decline of hemolytic complement (C) activity in the plasma along with a significant, parallel rise in thromboxane B2 (TXB2) levels. The TXB2 response was inhibited by co-administration of soluble C receptor type 1 (sCR1) with LEH, as well as by C depletion with cobra venom factor. These observations provide evidence for a causal relationship between LEH-induced C activation and TXB2 release, and suggest that sCR1 could be useful in attenuating the acute respiratory, hematological and hemodynamic side effects of LEH described earlier in the rat.

Original languageEnglish
Pages (from-to)347-355
Number of pages9
JournalArtificial Cells, Blood Substitutes, and Immobilization Biotechnology
Volume25
Issue number4
Publication statusPublished - Jul 1997

Fingerprint

Complement Receptors
Liposomes
Complement Activation
Thromboxanes
Hemoglobin
Thromboxane B2
Rats
Hemoglobins
Chemical activation
Hemoglobin C
Hemodynamics
Intravenous Administration
Complement System Proteins
Plasmas

ASJC Scopus subject areas

  • Biomedical Engineering
  • Hematology
  • Biotechnology
  • Biomaterials

Cite this

Complement activation and thromboxane secretion by liposome-encapsulated hemoglobin in rats in vivo : Inhibition by soluble complement receptor type 1. / Szebeni, J.; Spielberg, Helmut; Cliff, Richard O.; Wassef, Nabila M.; Rudolph, Alan S.; Alving, Carl R.

In: Artificial Cells, Blood Substitutes, and Immobilization Biotechnology, Vol. 25, No. 4, 07.1997, p. 347-355.

Research output: Contribution to journalArticle

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