Reduction In Spinal Cord Blood Flow Research Articles

Real-time monitoring of spinal cord blood flow with a novel sensor mounted on a cerebrospinal fluid drainage catheter in an animal model

The aim of our study was to develop a novel monitoring system for spinal cord blood flow (SCBF) to test the efficacy of the SCBF sensor in an animal model. The sensor system consisted of 2 optical fibers, a pedestal for fiber fixation, and a mirror for the laser reflection and was incorporated into a cerebrospinal fluid drainage catheter. In vivo studies were performed in a swine model (n=10) to measure SCBF during spinal cord ischemia induced by clamping the descending thoracic aorta and supra-aortic neck vessels, when necessary. A temporary low cardiac output model was also created by inflow clamping of the inferior vena cava to analyze the quantitative changes in SCBF during this maneuver. The developed SCBF monitoring catheter placed intrathecally could detect SCBF in all the swine. The SCBF after aortic crossclamping at the fourth intercostal level exhibited diverse changes reproducibly among the swine, with a >25% reduction in SCBF in 5 pigs, an increase in 3, and no significant changes in 2. Consistent reductions were recorded during inferior vena cava occlusion. The mean SCBF decreased by 32% after inferior vena cava occlusion when the cardiac output had decreased by 27%. We have developed a novel SCBF sensor that could detect real-time changes in spinal cord perfusion in a swine model. The device holds promise to detect imminent ischemia or ensure acceptable blood perfusion in the spinal cord and could further enhance our understanding of spinal cord circulation.

MK 801, an OBS N-methyl-D-aspartate channel blocker, does not improve the functional recovery nor spinal cord blood flow after spinal cord compression in rats

Damage to the central nervous system is followed by local release of excitatory amino acids, e.g. glutamate. These have been claimed to increase the metabolic need of already hypoxic neurons, and thereby to promote cell death. To investigate whether N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms are involved in the damage consequent to spinal cord injury, 20 rats were exposed to 5-min compression of the thoracic spinal cord produced with a load of 35 g on a 2.2 x 5 mm sized plate. One group of animals was given a noncompetitive NMDA channel blocker, MK-801, in a dose of 10 mg/kg b.w and one group saline alone. The neurologic function was evaluated on the inclined plane for 4 days when spinal cord blood flow (SCBF) was measured with the 14C-iodoantipyrine autoradiographic technique. One day after trauma the animals in both groups were paraparetic and exhibited a significantly decreased capacity angle at the inclined plane test (about 35 degrees compared with about 63 degrees before compression). Thereafter, the motor function improved slightly, but to a similar extent in the two groups. On Day 4, gray and white matter SCBF was similar in the two groups. The results indicate that MK 801 in the dose used does not prevent the development of neurologic dysfunction or the reduction in SCBF after spinal cord compression.

The relationships among the severity of spinal cord injury, motor and somatosensory evoked potentials and spinal cord blood flow

To characterize the changes in axonal function in the motor and somatosensory tracts of the cord after spinal cord injury (SCI) and to correlate these changes with spinal cord blood flow (SCBF), the relationships among the severity of SCI, motor and somatosensory evoked potentials (MEPs and SSEPs) and SCBF were examined. Fifteen rats received a 1.5 g (n = 5), 20 g (n = 5) or 56 g (n = 5) clip compression injury of the cord at C8. SCBF at the injury site was measured by the hydrogen clearance technique 35 min before and 30 min after SCI. Concomitantly MEPs from the cord at T10 (MEP-C) and from the sciatic nerve (MEP-N) and SSEPs were recorded. A linear relationship ( r = −0.89, P < 0.002) was found between the severity of SCI and the reduction in SCBF at the injury site. Linear discriminant analysis revealed that both the MEP ( P < 0.0001) and SSEP ( P < 0.003) were significantly related to the severity of SCI. Furthermore, the amplitude of the MEP ( r = 0.65, P < 0.0001) and SSEP ( r = 0.58, P < 0.0011) was significantly correlated with the posttraumatic SCBF. Multiple regression revealed that both the severity of cord injury and the degree of posttraumatic ischemia were significantly related to axonal dysfunction after SCI. While the MEP was more sensitive to injury than the SSEP, the SSEP more accurately distinguished between mild and moderate severities of cord injury. Axonal conduction in the motor and somatosensory tracts of the cord was significantly correlated with the reduction in posttraumatic SCBF and, therefore, these data provide quantitative evidence linking posttraumatic ischemia to axonal dysfunction following acute cord injury. Furthermore, this study validates the hypothesis that the combined recording of MEPs and SSEPs is an accurate technique to assess the physiological integrity of the cord after injury.

Effects of aortic occlusion on regional spinal cord blood flow and somatosensory evoked potentials in sheep: Kaplan BJ, Friedman WA, Gravenstein N, et al. Neurosurgery 1987;21:668-75

The precise mechanism underlying spinal cord injury resulting from aortic occlusion is not well understood; such injury remains a devastating complication associated with thoracoabdominal aortic repair. This elegant study documents the changes in somatosensory evoked potentials (SEPs) resulting from aortic clamping and correlates these changes with alterations in regional spinal cord blood flow (SCBF). Eleven sheep had left thoracotomy with elaborately monitored general anesthesia. The aorta was cross-clamped for 30 minutes just distal to the subclavian artery in nine animals; two additional animals served as nonclamped controls. After tibial nerve stimulation, SEPs were continuously recorded from nerve action potential at the hip, lumbar, cervical, and cortical montages. SCBF was determined at five specific points during the experiment: control before clamping, immediately after clamping, on initial change in SEP, 30 minutes after clamping, and 30 minutes after reperfusion. At each point, radioactive microspheres labeled with one of five different isotopes corresponding to the appropriate interval were injected into the left atrium. The two control animals received the five injections, each 15 minutes apart, without aortic clamping. After the final injection, animals were killed; the spinal cord was removed and divided into lumbar, thoracic, and cervical sections and the dorsal columns, lateral columns, and cortical gray matter separated. Regional SCBF was then calculated from the ratio of the radioactivity in the specimen relative to that of a reference organ and expressed as milliliters per 100 gm tissue per minute. SCBF was not affected by repetitive microsphere injections as demonstrated in the two control animals. In contrast, the nine experimental animals exhibited two distinct patterns of alterations with aortic clamping. Most animals (seven of nine) demonstrated total loss of SEPs within 15 minutes of aortic occlusion. Thirty minutes after reperfusion, evoked responses of diminished amplitude returned in only three animals and not at all in the remaining four. These seven animals also demonstrated profound reduction in thoracolumbar SCBF to both white and gray matter and subsequent reactive hyperemia after reperfusion. In two experimental animals SEPs were preserved, and the initial reduction in amplitude observed within 5 minutes of clamping resolved during the 30-minute period of ischemia. These two animals also developed a marked reduction in SCBF, which returned to 50% of baseline levels 30 minutes after clamping, corresponding to the recovery of SEP. Therefore spinal cord ischemia is associated with profound alternations in SEPs and the magnitude and duration of diminished evoked responses seem to correlate with similar reductions in SCBF. The derived data suggest that preservation of SEP is associated with maintenance of SCBF above 20 ml/100 gm tissue/min; SCBF less than 10 ml/100 gm tissue/min results in obliteration of SEP. The more peripheral the nerve tissue, the more resistance to ischemia. The data support the validity of SEPs in reflecting alterations in SCBF and underscore the value of this measure in further investigations of ischemic spinal cord injury.

The effect of trimethaphan-induced hypotension on canine spinal cord blood flow. Measurement at different cord levels using radiolabelled microspheres.

Controlled hypotension which is used during scoliosis surgery to improve operating conditions and minimize transfusion requirements may decrease spinal cord blood flow (SCBF). Previous studies using hydrogen washout, an invasive technique, have shown that trimethaphan-induced hypotension is associated with a decrease in SCBF, whereas hypotension induced with sodium nitroprusside or nitroglycerin is not. To determine whether the decrease seen with trimethaphan represented a generalized rather than regional spinal cord phenomenon, SCBF was measured at three separate cord levels (T2-3, 7-8, L2-3) using a noninvasive radionuclide-labelled microsphere technique. When the mean arterial pressure was reduced by 50%, SCBF decreased 35 to 45% at all levels of the cord examined, and remained at this reduced level during the period of hypotension. The results confirm that trimethaphan-induced hypotension is associated with a significant reduction in SCBF and that this occurs throughout the spinal cord during the period of hypotension.

Spinal Cord Blood Flow during Spinal Anesthesia in Dogs

To examine the effects of subarachnoid tetracaine and epinephrine on spinal cord blood flow (SCBF), lumbar SCBF and cerebral blood flow (CBF) were measured simultaneously by the hydrogen clearance technique in dogs (n = 45) anesthetized with halothane. The lumbar subarachnoid administration of tetracaine, 5 mg dissolved in 1 ml of a 7.5% dextrose solution had no significant effect on either SCBF or CBF for 4 hr even though arterial blood pressure and heart rate decreased significantly. After subarachnoid epinephrine alone (100, 300, and 500 micrograms), SCBF varied widely but did not change significantly with any of the injections, nor did CBF. Responses of SCBF to hypercapnia and to acute blood loss during spinal anesthesia with tetracaine were also examined. Increased PaCO2 (from 35 to 57 mm Hg) increased both SCBF and CBF similarly before and after subarachnoid tetracaine; SCBF increased from 26.8 +/- 9.0 ml X 100 g-1 X min-1 (mean +/- SD) before to 34.2 +/- 13.6 ml X 100 g-1 X min-1 during hypercapnia during spinal anesthesia, which was almost identical to the increase (from 31.5 +/- 8.1 ml X 100 g-1 X min-1 to 39.9 +/- 6.0 ml X 100 g-1 X min-1) before spinal anesthesia. Whereas acute blood loss (approximately 20% of estimated blood volume) during spinal anesthesia with tetracaine caused a 23% reduction of SCBF (P less than 0.05), in the absence of tetracaine SCBF remained unchanged during hemorrhagic hypovolemia.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

The response of spinal cord blood flow to high-dose barbiturates.

The response of spinal cord blood flow (SCBF) to high-dose barbiturate therapy is documented. In nine mongrel dogs with an arterial pCO2 (PaCO2) of 40 mm Hg, sodium thiopental was administered to produce 30, 60, 120, and 240 seconds of electroencephalographic (EEG) burst suppression. At 30-second intervals of EEG suppression, cervical and thoracic cord segments demonstrated a decrease in SCBF of 47% and 39%, respectively, from control values. Isoelectric EEG intervals longer than 30 seconds were not associated with any further significant decrease in SCBF. In 13 other dogs and in the absence of barbiturates, hypocapnia to 20 mm Hg from PaCO2 of 60 mm Hg produced reductions in SCBF of 89% for the cervical and 82% for the thoracic segments. In the presence of thiopental-induced 30- to 60-second intervals of EEG silence, the decrement in SCBF in response to the same degree of hypocapnia was 83% and 75%, respectively, although the absolute value of this reduction was half that without barbiturates. These findings of a significant reduction in SCBF in response to high-dose barbiturate therapy are suggestive of a protective effect of barbiturates upon spinal cord injury as occurs in the brain. Further studies of the influence of barbiturates upon spinal cord compressive syndromes are indicated.

Spinal cord blood flow after acute experimental cord injury in dogs

Spinal cord blood flow (SCBF) was measured in dogs before and following acute injury with 300 or 500 g-cm force (GCF). In addition, the responses to high and low PaCO 2 and low PaO 2 levels were studied. The hydrogen clearance technique was used and 0.3 mm platinum electrodes were placed in grey matter, central white matter or peripheral white matter of the L2 segment. The pre-trauma flows were: grey matter 12.5 ± 2.7; central white matter 14.4 ± 3.6 and peripheral white matter 15.1 ± 4.2 ml/100 g/min. Following a 300 GCF injury, a marked and progressive reduction in SCBF occurred in the grey and central white matter. This was present for the subsequent 4 hr of the study. The flow was lower than pre-trauma values during the second hour in the grey matter (9.0 ± 1.4) and the third hour in the central white matter (10.8 ± 1.8). By the fifth hour after trauma the flow in the grey matter was 5.0 ± 3.5 and in the central white matter 9.7 ± 1.5. In the peripheral white matter the SCBF was 10 ± 3.7 during the third hour but subsequently the flow increased to 11.5 ± 3.9. Paired t-tests showed that this was still significantly lower than pre-trauma levels. Two dogs showed a hyperaemic response which was persistent in one case but only temporary in the other dog. The vasodilatatory effect of CO 2 was lost after trauma and in some cases a steal phenomenon was present. The sensitivity to an increase in CO 2 was 0.48 ± 0.23 ml/100 g/min Hg before injury and this decreased to 0.0075 ± 0.137 during the second hour after injury. The vasodilatation to hypoxia (30–40 mm Hg) was also absent but the vasoconstrictor effect to low PaCO 2 appeared better preserved. These findings also applied to the peripheral white matter where the SCBF was not significantly reduced. The results were similar but more pronounced after 500 GCF injury. The results show that following injury the central areas of the cord become rapidly and progressively ischaemic. The peripheral white matter does retain a reasonably normal flow depending on the magnitude of the impact force. However, the vessels in all these areas lose their ability to respond to normal physiological stimuli.