The mechanism of liposome accumulation in infarction.
This paper explores the mechanism(s) whereby liposomes accumulate in chronically ischaemic myocardium and intestine. Plasma prepared from venous blood obtained at sites of myocardial and intestinal infarction does not promote the lysis of positively and negatively charged liposomes in vitro. Albumin-bound lysophosphatidylcholine (greater than or equal to 2 mM) lyses positively and negatively charged liposomes in vitro at similar rates. [99mTc]Diethylenetriamine pentaacetic acid (DTPA) entrapped in positively charged liposomes was accumulated in ischaemic rat caecum/colon 6 and 24 h after mesenteric ligation. Presumably allied to the accumulation of liposomal components, necrotic caecum/colon showed marked Ca2+ accumulation and phospholipid depletion. It is postulated that Ca2+ and Ca2+-activated membrane phospholipases may be implicated in the mechanism of liposome accumulation in chronic ischaemia.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004285:Dogs; D007238:Infarction / Q000378:metabolism*; D007422:Intestines / Q000098:blood supply*; D008081:Liposomes / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism*; D004369:Pentetic Acid; D010740:Phospholipases / Q000378:metabolism; D051381:Rats; D013667:Technetium; D016284:Technetium Tc 99m Pentetate
D008081:Liposomes; D013667:Technetium; D004369:Pentetic Acid; D010740:Phospholipases; D002118:Calcium; D016284:Technetium Tc 99m Pentetate