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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blood Substitutes / administration & dosage
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Blood Substitutes / pharmacology
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Complement Activation / drug effects*
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Complement Inactivator Proteins / physiology*
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Drug Synergism
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Female
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Hemoglobins / administration & dosage
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Hemoglobins / pharmacology*
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Injections, Intravenous
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Liposomes / administration & dosage
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Liposomes / pharmacology*
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Rats
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Rats, Sprague-Dawley
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Receptors, Complement / physiology*
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Thromboxane B2 / antagonists & inhibitors*
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Thromboxane B2 / blood
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Thromboxane B2 / metabolism*
Substances
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Blood Substitutes
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Complement Inactivator Proteins
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Hemoglobins
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Liposomes
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Receptors, Complement
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Thromboxane B2