Abstract：
OBJECTIVES:The urinary bladder wall can be separated into two major compartments: the urothelium (mucosa) and the detrusor smooth muscle. Specific dysfunctions of both layers have been linked to ischemia, which may induce significant cellular and subcellular membrane damage via the activation of selective calcium dependent and independent hydrolytic enzymes. Preliminary to investigating changes in cell membrane composition induced by ischemia, we measured the free fatty acid (FFA) and phospholipid (PL) content of normal rabbit bladder muscle and mucosal cellular and subcellular membranes, and characterized the endogenous lipase activity. METHODS:Rabbit bladders were excised and the muscle and mucosal layers separated; each layer was homogenized, then fractionated by differential centrifugation. Endogenous lipase activity of the homogenates, and FFA and PL concentrations of the homogenates and subcellular fractions were measured. RESULTS:(1) The basal FFA concentration of the mucosal homogenates was 5 times that of the muscle homogenates. (2) The basal PL concentrations of the two tissues were similar. (3) Subcellular studies: FFA concentration was greatest in the mitochondrial fraction of both compartments. In the mucosa, PL concentration was significantly greater in the mitochondria and microsomes than in the other fractions; in the smooth muscle, the PL concentration was highest in the mitochondria. (4) The maximal endogenous lipase activity was 10 times higher in the mucosal homogenates than in the muscle homogenates. CONCLUSIONS:These results are consistent with those of previous studies which indicate that the mucosa is metabolically more active than the resting smooth muscle, which may cause the mucosa to be significantly more sensitive than the muscle to hypoxic/ischemic damage.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
O'Connor LJ,Nicholas T,Levin RMdoi
10.1007/978-1-4615-4737-2_20subject
Has Abstractpub_date
1999-01-01 00:00:00pages
265-73eissn
0065-2598issn
2214-8019journal_volume
462pub_type
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