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 (≥ 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.