Ischemic Nerve Injury Research Articles

The effect of ulinastatin on reduced nerve conduction velocity and blood pressure.

Application of a pneumatic tourniquet in orthopedic surgery is sometimes followed by hypotension and paralysis. Seventy-five patients scheduled for knee joint surgery were examined to evaluate the effects of ulinastatin on changes in blood pressure, venous pH and motor nerve conduction by pneumatic tourniquet application above the knee joint. In fifty-five of the patients, the femoral vein of the operating side was cannulated with a catheter to obtain venous blood samples before and after tourniquet application. 300,000 Unit of ulinastatin (UST) was administered intravenously before inflation of the tourniquet in 10 patients. In the other sixteen patients, the motor nerve conduction velocity (MNCV) of the peroneal nerve was measured before inflation and after release of the tourniquet. In the UST-free group, the reduced blood pressure and pH persisted for more than 15 min, while in the UST-treated group, the reduced blood pressure returned to the normal leven in 15 min. In the control group, femoral venous P(O)(2) continued to increase after 10 min, but that in the UST-treated group returned to the normal range. Tourniquet application significantly reduced peroneal MNCV. Pre-and post-treatment with UST significantly lessened the reduction of MNCV induced by the tourniquet. It is concluded that UST may have protective and therapeutic effects on ischemic nerve injury, induced by the application of a turniquet.

Neovascularization after ischemic nerve injury

Because angioneogenesis is associated with wound repair, neovascularization may play an important role in regeneration after nerve injury. This hypothesis was tested in the present study in which the number and distribution of endoneurial capillaries were determined 6 weeks after ischemic nerve injury. The density of capillaries was increased in the central fascicular regions of the distal sciatic and proximal tibial nerves at sites of ischemic injury. This was accompanied by a decrease in intercapillary distance. Neovascularization may be a response to ischemia or a consequence of nerve degeneration or regeneration, the mechanisms of which are poorly understood.

Spatial distribution of capillaries in rat nerves: Correlation to ischemic damage

Computerized imaging was used to assess the spatial distribution of capillaries (number, density, and intercapillary distance) in normal rat sciatic nerve and its branches, to be able to make inferences about their distribution to central fascicular degeneration typical of ischemic nerve injury. Capillary density was significantly less in the central regions of fascicles than in outer contour areas in sciatic and proximal tibial nerves, the difference being greater in large fascicles. The mean of the minimum intercapillary distance was significantly greater in the central fascicular region of fascicles of the sciatic but not of the tibial and peroneal nerves. These anatomic characteristics may be a factor in ischemic-induced central fascicular degeneration. A decrease in the number of capillaries in a region might lead to impaired oxygen diffusion when blood flow to the region is compromised.

Conduction velocity and conduction block after experimental ischaemic nerve injury

The effect of ischaemic nerve injury on conduction in the tibial branch of the sciatic nerve has been studied in rabbits. Ischaemic nerve damage was produced in 40 animals by ligation of the common and external or the internal and external iliac arteries. Conduction in the motor fibres to the small foot muscles was examined at intervals after operation, with nerve stimulation in the thigh and at the ankle. Ascending nerve action potentials in the tibial nerve were also studied. In 8 animals there was evidence of widespread degeneration of myelinated fibres; muscle action potentials could not be activated by nerve stimulation and nerve action potentials were absent. In contrast there were 14 animals in which arterial ligation appeared to produce little, if any, nerve degeneration; in this group there was no significant change in motor or afferent velocity. The remaining 18 animals showed changes of intermediate severity. While nerve degeneration was extensive, it was never complete, and in 9 nerves examined 5–11 days after surgery, conduction block between the thigh and ankle could be demonstrated in surviving fibres. In the other 9 nerves there was no block in surviving fibres but maximal motor velocity was significantly reduced. In no case did the conduction block affect more than a minority of the motor fibres, the remainder undergoing complete degeneration. This was in keeping with the histological appearances which showed a relatively small amount of paranodal and segmental demyelination compared with the amount of Wallerian degeneration.