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Biomedical subjects

M C Wallace

Publications and source records attributed to M C Wallace.

88 records · Page 5Linked to original sources
PubMed1987

Chronic regenerative changes in the spinal cord after cord compression injury in rats.

Long-term regenerative changes and pathological effects after acute compression injury of the spinal cord were studied in rats. Twenty adult female Wistar rats underwent cord injury by the extradural clip compression technique at T6-7. Following injury, extradural electrodes attached to receiver-stimulators that were implanted subcutaneously were placed proximal and distal to the injury site. The animals were maintained in cages with electromagnetic fields created by encircling antennae. The control animals were in a field adjusted to a frequency below the sensitive frequency range of the receiver-stimulators so that they received no spinal cord stimulation. After 15-20 weeks of continuous spinal cord stimulation, histological sections of the cords were assessed and scored blindly for pathological changes including magnitude and extent of cord injury, and cystic cavitation, and for regenerative changes including proliferation of axons, Schwann cells and ependymal cells, and formation of myelin. In all 20 animals, there was a complete absence of normal cord tissue at the injury site, and cystic cavitation was frequently present at the injury site and beyond. Extensive regenerative changes were seen in all animals including regeneration of axons, Schwann cells and ependymal cells, and formation of myelin. Statistical analysis did not show a significant difference between treatment and control groups.

Animals↗
PubMed1987

Effect of alternating current stimulation of the spinal cord on recovery from acute spinal cord injury in rats.

The therapeutic value of electrical stimulation of the spinal cord was studied in rats injured by acute compression of the spinal cord. Twenty adult Wistar rats underwent cord compression at T6-7 by the extradural clip compression technique at a force of 125 g for 1 minute. After injury and group randomization, stimulating electrodes were placed extradurally, proximal and distal to the injury site, and attached to a small, implantable receiver-stimulator. The receiver was secured to the paraspinal muscles and implanted subcutaneously, overlying the thoracic spine. The animals were maintained in specially designed cages with encircling antennae attached to radio frequency transmitters. The 10 treatment animals were subjected to a 460-kHz electromagnetic field, pulsed at a frequency of 10 Hz. The receivers converted the pulsed radio frequency into square-wave pulses at the cord electrodes (width 1 ms, frequency 10 Hz). The 10 control animals were exposed to a similar field but with a frequency below the range of the tuned receiver, and therefore they did not receive the square-wave pulse. Clinical recovery was assessed by the inclined plane technique which measures the maximum angle of inclination attained without falling. After 15 weeks of continuous spinal cord stimulation, the inclined plane performance was not significantly different between the two groups (treatment group mean, 44.4 +/- 5.4; control group mean, 41.7 +/- 7.9). This is the first experimental study of the effect of long-term continuous electrical stimulation on spinal cord recovery in mammals. The methods required and the technical aspects involved in achieving continuous stimulation, and the guidelines for future study of this modality are discussed.

Acute Disease↗
PubMed1987

Successful improvement of blood pressure, cardiac output, and spinal cord blood flow after experimental spinal cord injury.

Thirty-seven rats were anesthetized and ventilated and had continuous monitoring of mean systemic arterial pressure (MSAP) and central venous pressure (CVP). The animals underwent a 60-g clip compression injury at T-1 for 1 minute. Fifteen minutes after injury, microspheres were used to measure cardiac output (CO) and spinal cord blood flow (SCBF). Each animal was then randomized into one of five groups. Four groups received intravenous infusions for 1 hour each of 5% albumin, autologous packed cells, low molecular weight dextran, or autologous whole blood to maintain the MSAP. The fifth group served as a control group and received an infusion of normal saline. Seventy-five minutes after injury, CO and SCBF were measured. The posttraumatic reduction in CO was significantly improved by all four treatment infusions. However, only autologous whole blood and dextran successfully reversed the posttraumatic hypotension. Dextran significantly elevated the CVP (P less than 0.01) and reduced the hematocrit (P less than 0.01). Whole blood improved SCBF in all segments of the spinal cord by nearly 100% (P less than 0.05), and dextran increased SCBF by 200% (P less than 0.01). Thus, the most marked improvements in MSAP, CO, and SCBF were produced by hypervolemia and hemodilution associated with dextran infusion. The therapeutic implications of this reversal of local and systemic changes in acute spinal cord injury are discussed.

Animals↗
PubMed1987

Recovery of spinal cord function induced by direct current stimulation of the injured rat spinal cord.

Direct current stimulation has been shown by others to enhance the regeneration of several types of tissues, including nervous tissue in some species. The purpose of the present experiment was to assess the value of direct current stimulation for enhancing the recovery of spinal cord function after clip compression injury of the rat spinal cord. Twenty Wistar rats underwent a 1-minute, 50-g clip compression injury at T-1, after which electrodes were placed epidurally with the anode proximal and the cathode distal to the injury site. These electrodes were attached to a stimulator implanted subcutaneously. Ten animals received stimulators that produced a constant current of 14 microA, and the remainder received stimulators with no electrical output and served as controls. Assignment of stimulators was random, and the treatment group was not identified until sacrifice. Neurological function was tested weekly for 15 weeks by the inclined plane technique, after which the animals were killed and the injured cords were examined for histological evidence of regeneration. The mean inclined plane result for the treatment group (39 +/- 5 degrees) was significantly better than that for the control group (31 +/- 6 degrees) (P less than 0.02), although there was no significant difference in histological findings between the two groups. Thus, direct current stimulation of the injured mammalian spinal cord produced improvement in neurological function and warrants further investigation.

Animals↗
PubMed1986

Spinal cord blood flow measured with microspheres following spinal cord injury in the rat.

A decrease in spinal cord blood flow (SCBF) is a known sequela of spinal cord injury. The radioactive microsphere technique permits repeated measurement of spinal cord blood flow (SCBF) and cardiac output (CO) in the same experimental animal. The purpose of this study was to adapt the radioactive microsphere technique for use in the rat extradural clip compression injury model used in our laboratory. Thirteen adult Wistar rats were anaesthetized and ventilated. Mean systemic arterial pressure (MSAP) was recorded continuously. Control animals (n = 8) did not have a surgical procedure whereas the injured animals (n = 5) underwent a C7-T1 laminectomy followed by a one minute, 50 gram extradural clip compression injury at T1. Radioactive microspheres were used for two blood flow and CO determinations in both groups. MSAP fell 59% in the injured animals (p less than 0.01), but this was not accompanied by significant changes in heart rate or CO. There was a 50% reduction in SCBF in the injured cord (p less than 0.02), and there were significant reductions in cerebral blood flow (p less than 0.05) and cerebellar blood flow (p less than 0.02) following spinal cord injury.

Animals↗
PubMed1986

Failure of naloxone to improve spinal cord blood flow and cardiac output after spinal cord injury.

It has been reported that the narcotic antagonist, naloxone, can improve spinal cord blood flow (SCBF) and clinical recovery after experimental spinal cord injury produced by the weight-dropping technique. The purpose of the present study was to determine the effect of naloxone on SCBF, cardiac output (CO) and blood flow to other organs following clip compression injury. Rats were anesthetized, paralyzed and ventilated, with mean systemic arterial pressure (MSAP) recorded continuously. After a C-7-T-1 laminectomy and a 1-minute acute compression injury with a 50-g clip at T-1, rats were given injections of radioactive microspheres for measurement of SCBF, CO, and blood flow to other organs. The first determination was made 15 minutes after injury and a second was made after a 1-hour treatment with naloxone. Treated animals each received an intravenous bolus injection of naloxone (10 mg/kg) followed by a 1-hour intravenous infusion (2 mg/kg/hour). Naloxone failed to improve posttraumatic SCBF in the injured spinal cord. In addition, naloxone did not prevent posttraumatic hypotension or the progressive decline in CO seen between 15 and 75 minutes after injury. Thus, this study does not support the previous claims of a beneficial effect of naloxone on posttraumatic SCBF and MSAP.

Animals↗
PubMed1986

Relationship between posttraumatic ischemia and hemorrhage in the injured rat spinal cord as shown by colloidal carbon angiography.

Adult female Wistar rats underwent extradural clip compression injury of the spinal cord at T-1. A force of 40 g was applied for 1 minute; this moderately severe injury renders animals paraparetic. We performed colloidal carbon angiography with Aquablak on four animals at 15 minutes, 2 hours, and 24 hours after injury. The entire spinal cord was then removed, frozen, and sectioned serially at 250 micron. The sections were examined microscopically for patterns of ischemia and hemorrhage at the site of compression injury and at adjacent and remote sites in the spinal cord. There was a marked lack of filling of the arterioles, capillaries, and venules at the injury site. In addition, there was a specific anatomical distribution of the ischemic areas in that ischemia of the white matter occurred in areas supplied by arteries that traversed adjacent hemorrhagic gray matter. For example, ischemia of the ventral funiculus was consistently seen adjacent to hemorrhage in the ventral gray matter. Similarly, ischemia of the dorsal white columns was related to hemorrhagic lesions surrounding the feeding vessels in the dorsal gray matter. This study also demonstrates the usefulness of a new colloidal carbon suspension (Aquablak) for documenting the pathophysiology of posttraumatic ischemia of the spinal cord. The results suggest that ischemic lesions in the white matter are anatomically related to hemorrhagic lesions in the gray matter. The pathophysiology of this relationship is unknown, but may include thrombosis, vasospasm, or direct injury of the feeding vessels.

Angiography↗
PubMed1986

Failure of blood transfusion or naloxone to improve clinical recovery after experimental spinal cord injury.

Thirty adult Wistar rats underwent an extradural clip compression injury of 50 g of force for 1 minute at T-1. After injury, the animals were randomly separated into three groups: the control group received a saline infusion for the 2-hour treatment period; the second group was given a blood transfusion over 2 hours titrated to maintain mean systemic arterial pressure (MSAP) at preinjury levels; and the third group received an intravenous bolus dose of naloxone (10 mg/kg), followed by a 2-hour infusion of intravenous naloxone (2 mg/kg/minute). The rats were observed postoperatively for 15 weeks, during which their clinical recovery was measured weekly by the inclined plane technique. At 15 weeks, the spinal cords were removed and prepared for histological assessment. The blood pressure before, during, and immediately after injury did not differ statistically among the three groups. During the initial 2 hours after injury, blood transfusion produced a significant increase in MSAP (P less than 0.02) and hematocrit (P less than 0.001), but naloxone infusion did not result in a significant change in MSAP. Performance on the inclined plane at 15 weeks was 35.6 +/- 6 degrees, 32.7 +/- 4 degrees, and 36.1 +/- 6 degrees for the control, transfusion, and naloxone groups, respectively, and no significant differences were found (P greater than 0.05). Histological examination confirmed a consistent injury of moderate severity in all three groups with no major differences among groups. Thus, this study demonstrates no significant clinical benefit either from a blood transfusion to maintain MSAP or from naloxone given by bolus and infusion after an extradural clip compression injury of the rat spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Posttreatment MR findings in spinal dural arteriovenous malformations.

PURPOSE: To review the MR findings in 17 patients with spinal dural arteriovenous malformations and compare posttreatment MR with clinical outcome in 10 patients. METHODS: Extramedullary flow voids, cord swelling, and intramedullary signal changes were recorded in 17 patients. Enhancement and vessel cospicuity were assessed in 10 patients given gadopentetate dimeglumine. In 10 patients, follow-up MR was correlated with clinical outcome. RESULTS: Of the 17 patients, 14 (82%) had abnormal subarachnoid vessels, 11 (65%) had cord enlargement, and 16 (94%) had hyperintensity on T2-weighted images. In 3 patients, the vessels were better seen with contrast, and 6 had cord enhancement. On posttreatment MR, the vessels were no longer evident in 7 of 10 patients, cord swelling resolved in 9 of 9 patients, the the T2 hyperintensity resolved or was less evident in 9 of 9 patients. Eight patients had clinical improvement, and 2 stabilized. CONCLUSIONS: Follow-up MR showed resolution of most of the findings in spinal dural arteriovenous malformation. There was some correlation between MR and clinical outcome, but MR evaluation could not distinguish those who had improved from those who stabilized.

Adult↗