Complement activation and thromboxane secretion by liposome-encapsulated hemoglobin in rats in vivo: inhibition by soluble complement receptor type 1.

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.

Histopathologic study following administration of liposome-encapsulated hemoglobin in the normovolemic rat.

Liposome encapsulated hemoglobin is being developed as an artificial resuscitative fluid for in vivo oxygen delivery. In the present report, we examine the effect of accumulation of liposome encapsulated hemoglobin on the structure of reticuloendothelial organs following administration of liposome encapsulated bovine hemoglobin in the normovolemic rat. We have also examined the administration of the liposome vehicle, tetrameric bovine hemoglobin, and liposome encapsulated bovine hemoglobin that had been lyophilized with 300 mM trehalose and rehydrated just before injection.

Complement activation in rats by liposomes and liposome-encapsulated hemoglobin: evidence for anti-lipid antibodies and alternative pathway activation.

Intravenous injection of hemoglobin-containing liposomes (LEH) caused a significant reduction in plasma hemolytic complement activity in rats on a time scale of minutes. Liposomes without hemoglobin also caused complement consumption, but less than LEH, while free hemoglobin was without effect. Consistent with complement activation, the LEH-induced drop in plasma hemolytic complement activity was closely paralleled by an increase in plasma thromboxane B2 level.

Transient changes in the mononuclear phagocyte system following administration of the blood substitute liposome-encapsulated haemoglobin.

We have examined the effects of administration of the blood substitute, liposome-encapsulated haemoglobin (LEH), in the normovolaemic rat. Test groups included LEH, lyophilized EH, the liposome vehicle, unencapsulated haemoglobin and normal saline, which were injected into the tail vein (n = 6; n = 3 for sham and saline groups). Administration of LEH (2.

Liposome encapsulated hemoglobin: long-term storage stability and in vivo characterization.

Liposome Encapsulated Hemoglobin (LEH) has been the focus of research and development at the Naval Research Laboratory in an effort to find a viable oxygen-carrying resuscitative fluid. Previous reports from our laboratory have shown that LEH binds and releases oxygen in a manner similar to red blood cells, and that it can sustain life when red cell hematocrits are decreased to critical levels. We have also reported on LEH with regards to preparative methods, scale-up feasibility, toxicity, hemodynamics, hemoglobin P50 modification by coencapsulation of organic phosphates, liposomal surface modification, and storage strategies.

UV irradiation of lymphocytes triggers an increase in intracellular Ca2+ and prevents lectin-stimulated Ca2+ mobilization: evidence for UV- and nifedipine-sensitive Ca2+ channels.

UV irradiation induces in vitro and in vivo immunosuppression. Because mobilization of intracellular calcium ([Ca2+]i) represents a central step in cell activation and immune response, we investigated the effect of UV irradiation on Ca2+ homeostasis. Using indo-1 and cytofluorometry, [Ca2+]i kinetics in UVC- or UVB-exposed human peripheral blood leukocytes (PBL) and Jurkat cells were determined in parallel with functional assays.