Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Abstract

Free fatty acid (FFA), diacyiglycerol (acyl2-Gro), icosanoid, phospholipid, and cholesterol levels were measured in samples of cat spinal cord (L2) that were frozen in situ (i) with vertebrae intact, (ii) at various times after laminectomy, and (iu) at various times after laminectomy with compression trauma to the spinal cord. Tissue samples either were grossly dissected into gray and white portions prior to FFA and acyl2Gro analysis or were used whole for the other lipid types. Gray matter total FFA and acyl2Gro values were abnormally high in samples frozen with vertebrae intact and in those frozen 10 min after laminectomy. This indicates that the surgical procedures resulted in some perturbation of spinal cord lipid metabolism. If the experimental animals were allowed to recover for 90 min after laminectomy, the gray matter FFA and acyl2Gro levels were greatly reduced. Compression of the spinal cord with a 170-g weight for 1, 3, or 5mm (following 90 min of recovery after laminectomy) caused significant elevations of total FFA, acyl2Gro, icosanoids, and phosphatidic acid and significant decreases in ethalamine plasmalogens and cholesterol. Among the total FFA, arachidonic acid was found to have the largest relative increase. Comparisons of gray and white matter demonstrate that, in general, changes in white matter FFA and acyl2Gro were similar to those seen in gray matter. However, the increases in white matter levels of FFA and acyl2Gro were delayed, occurring after the elevations in gray matter. For some FFA (e.g., arachidonate), the rise in white matter occurred as gray matter levels were decreasing. This suggests that the initial alteration in spinal cord lipid metabolism after trauma was in gray matter but, with time, spread radially into white matter.

Effect of indomethacin on motor activity and spinal cord free fatty acid content after experimental spinal cord injury in rabbits

“…The data correlate well with earlier published reports. [7][8][9]12,[28][29][30] Loss or decrease of motor activity is the most prominent and the most functionally relevant result of the spinal cord injury. 31 Motor disturbances observed in the rabbits that experienced trauma in response to the force of 150 g cm were not the result of the laminectomy procedure.…”

“…7,8,32 A significant loss of motor function occurs in severe cases as a result of haemorrhagic necrosis of central grey matter that begins within minutes of the injury. The degeneration of long tracts of the white matter is evident within 24-36 h. A very likely site of post-traumatic molecular damage is the cell membrane that undergoes marked alterations of integrity and function.…”

“…Severe impact spinal cord injury results in decreased total phospholipid content for up to 3 days following injury, 9 but no major class of phospholipids is selectively hydrolysed. [7][8][9]11 Impact injury to the spinal cord is associated with a biphasic increase in FFA level in spinal cord tissue. 9 The first increase, observed within 5 min of spinal cord trauma, is followed by a decline 30 min after the injury.…”

“…[7][8][9][10] FFAs are the components of membrane phospholipids, having an important role in maintaining the structure and functions of the cell membranes. Severe impact spinal cord injury results in decreased total phospholipid content for up to 3 days following injury, 9 but no major class of phospholipids is selectively hydrolysed.…”

Effects of trapidil on intestinal mucosal barrier function and bacterial translocation after intestinal ischemia and reperfusion in an experimental rat model

“…14 The release of free arachidonic acid, which is the precursor of prostaglandins and thromboxane A 2 (TXA 2 ), activates phospholipase, leading to increased prostanoid production, free radical release, and lipid peroxidation. 15 Moreover, in a previous study, 16 light and electron microscopy were used to show that trapidil significantly reduced cellular damage and edema at the injury zone. This finding 16 was explained by the membrane-stabilizing effect of trapidil, which results from inhibition of TXA 2 synthesis.…”