(Stroke. 1996;27:1859-1864.)
© 1996 American Heart Association, Inc.
Articles |
Somatosensory Evoked Potentials Correlate With Neurological Outcome in Rabbits Undergoing Cerebral Air Embolism
the Cardiovascular Anesthesia Research Laboratory (D.K.R.) and the Department of Anesthesia (D.K.R., F.D., B.J.H., A.S., M.M.T.), University of Iowa, College of Medicine, Iowa City.
Correspondence to Bradley J. Hindman, MD, Department of Anesthesia, University of Iowa, College of Medicine, Iowa City, IA 52242. E-mail Brad-Hindman@uiowa.edu.
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Abstract |
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Background and Purpose Somatosensory evoked potentials (SSEPs) have been used as an outcome measure in models of cerebral air embolism despite the lack of studies correlating SSEPs with other measures of neurological injury. We examined the relationship between SSEPs and neurological impairment in the setting of cerebral air embolism.
Methods Anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 µL/kg of air into the internal carotid artery. SSEPs were recorded at intervals for the subsequent 2 hours. After the final recording the anesthetic was discontinued, and the animals recovered. Animals were neurologically evaluated at 3 and 24 hours after cerebral air embolism on a scale of zero (normal) to 97 (coma) points.
Results There was a clear relationship between the dose of air and 2-hour SSEP amplitude (P=.00003). SSEP amplitudes at 2 hours were inversely correlated with neurological impairment scores at 3 hours (
=-0.71, P<.0001). SSEP amplitudes at 2 hours were less in animals that died (11±16%; n=9) than in those that survived to 24 hours (53±20%; n=9) (P=.0008).
Conclusions These results support SSEPs as an index of neurological impairment in this model of cerebral air embolism.
Key Words: air embolism • outcome • somatosensory evoked potentials • rabbits
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Introduction |
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Somatosensory evoked potentials (SSEPs) are widely used as an index of neurological injury in experimental models of cerebral air embolism. With this index, pathophysiological mechanisms have been proposed, interventions have been tested, and therapeutic recommendations have been made.1 2 3 4 5 6 7 8 9 10 11 Despite its common use, alteration of SSEP amplitude has not been correlated with other indices of neurological outcome in the setting of cerebral air embolism. Specifically, it is unknown whether the amplitude of the cortical component of the SSEP has any relation to more standard measures of injury, such as infarct volume, number of dead cells, or neurological examination. Cerebral air embolism produces a diffuse multifocal injury.2 12 13 Therefore, it is uncertain whether SSEPs, which test neurons in a specific pathway, would correlate with the degree of neurological injury.
Using a modification of the cerebral arterial air embolism model in rabbits of Helps et al,14 we previously established a dose-response relationship between the amount of cerebral arterial air injected and both early (3 to 4 hours) and late (24 hours) neurological outcome.15 Using a further modification of that model, we investigated the relationship between SSEP amplitude and neurological outcome.
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Materials and Methods |
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Experimental protocols were approved by the Animal Care and Use Committee of the University of Iowa in accordance with the Guide for the Care and Use of Laboratory Animals, National Institutes of Health publication No. 85-23, revised 1985.
New Zealand White rabbits of either sex (weight, 2.5 to 3.4 kg) were randomly preassigned to receive either saline or one of three doses of intra-arterial air: 50, 100, or 150 µL/kg (n=3 in saline group; n=5 in each air embolism group). Anesthesia was induced in nonfasted animals by inhalation of 5% isoflurane in oxygen. After cannulation of an ear vein and orotracheal intubation with a 3.0-mm-ID cuffed tube (Mallinckrodt), animals were paralyzed with a single dose of succinylcholine (1 mg/kg IV). Animals were ventilated with 2.0% isoflurane in 30% oxygen/balance nitrogen to achieve normocarbia and monitored with a calibrated anesthetic agent analyzer (Datex, Puritan-Bennett). Throughout the surgery, normal saline was infused intravenously at 4 mL·kg-1·h-1. Rectal temperature was maintained at 37°C to 38°C with a servo-controlled heating pad.
Animals were placed prone in a stereotaxic frame (Kopf Instruments), and the scalp was shaved. The skin was washed with povidone-iodine solution (Purdue Fredrick Co), and all subsequent procedures were performed in aseptic fashion. After skin incision, a 2-mm burr hole was drilled over the left frontoparietal cortex to expose dura. A 1-mm thermocouple (K-type, L-08419-02, Cole Parmer) was placed between the cranium and dura to monitor epidural temperature. The bone defect was filled with bone wax. Stainless steel screws for recording evoked potentials were placed into the skull with the active electrode located over the parietal region, 4-mm lateral to the midline and 2-mm anterior to the coronal suture. The reference electrode was placed in midline into maxillary bone. Animals were then turned supine and, through the left femoral artery, a saline-filled polyethylene catheter (PE-90, Intramedic) was advanced into the abdominal aorta for arterial pressure monitoring and intermittent blood sampling. At this point, isoflurane was discontinued (45 minutes before air injection) and methohexital was administered as a bolus of 10 mg/kg IV, followed by a continuous infusion to give 10 mg·kg-1·h-1. Methohexital was continued throughout the remainder of the experiment to avoid isoflurane inhibition of the evoked potential and yet still allow for the rapid anesthetic recovery required for neurological assessment.
Through a midline neck incision, the left external, internal, and common carotid arteries were isolated, and a branch of the external carotid (usually the facial) was selected for cannulation. Other branches of the external carotid were ligated with 4-0 silk, and all bleeding points were carefully cauterized. At this point, the following baseline physiological measurements were obtained: mean arterial pressure, epidural temperature, expired isoflurane concentration, arterial pH, PO2, PCO2 (IL1304, Instrumentation Laboratory), hemoglobin concentration (OSM3 [rabbit absorption coefficients], Radiometer), and plasma glucose concentration (YSI model 27, Yellow Springs Instrument Co). Baseline SSEPs were then obtained by stimulation of the median nerve by needle electrodes inserted into the right forepaw (see below). After isolation of the carotid arterial system, a temporary aneurysm clip was placed across the left common carotid just proximal to its bifurcation. A saline-filled PE-50 catheter was introduced retrograde through the facial branch of the external carotid and directed into the proximal 1 to 2 mm of the internal carotid. Care was take to avoid entrapment of air in either the facial or internal carotid arteries.
After physiological data collection, air (or saline) was injected into the internal carotid by infusion pump (model 11, Harvard Apparatus) at 10 µL/s, followed by 0.5 mL of normal saline. Thereafter, the aneurysm clip was removed from the common carotid and the injection catheter was withdrawn, reestablishing continuity between the internal and common carotid arteries. The air injection catheter was subsequently removed from the facial artery, and the external carotid artery was ligated at its origin. During air injection, mean arterial blood pressure was observed and recorded. SSEPs and physiological data were recorded at 5, 15, 30, 45, 60, 90, and 120 minutes after air injection.
The methohexital infusion was discontinued 2 hours after air injection. The arterial catheter, cranial screws, and cortical thermocouple were removed. Incisions in the scalp, groin, and neck were closed and infiltrated with a total of 3 mL of 0.5% lidocaine. The animals were extubated when they regained spontaneous ventilation and protective airway reflexes, usually 10 to 20 minutes after discontinuation of methohexital. After extubation, animals received 50% oxygen by mask. Neurological status was assessed 3 hours after air injection (approximately 1 hour after extubation). Approximately 5 hours after air embolism, animals were returned to their cages, where food and water were available. Animals underwent a final neurological evaluation 24 hours after air injection. They were then reanesthetized with 5% isoflurane in oxygen and killed by pentobarbital overdose (150 mg/kg IV).
We chose a relatively slow stimulation rate, wide filter settings, and a long recording time to maximize detection of evoked responses. The stimulus was 0.25 milliseconds in duration at a supramaximal voltage, delivered at 1.4 Hz. Sixty-four responses were averaged with a Grass model 10 evoked response system with band-pass filters of 0.3 and 10 000 Hz. High-amplitude electric artifact was automatically rejected. The analog signal was converted to digital data by an A-D board interfaced with an IBM AT computer for subsequent analysis. The amplitude of the primary cortical deflection was measured from the trough of the first major negative deflection (N1, occurring typically at approximately 13 milliseconds) and the peak of the next positive deflection (P2, occurring typically at approximately 28 milliseconds). The latencies of N1 and P2 were recorded for each animal before air embolism; postembolism amplitude measurements were made from those points. The amplitude of the N1-P2 complex was expressed as a percentage of the baseline value for each animal.
The neurological scoring system used was a modification of that described by Baker et al16 (Table 1
). The best possible neurological score equaled zero, and the worst possible neurological score equaled 97. Withdrawal responses in hindlimbs were not tested because of possible nerve damage during isolation of the femoral artery. The neurological examiner was aware that animals had undergone an operative procedure but was unaware of group assignment.
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Data are reported as mean±SD. Jonckheere's nonparametric trend test was used to assess the presence of a dose-response relationship between dose of air and SSEP amplitude.17 We used a nonparametric test because SSEPs were not normally distributed. Tied values were counted in favor of the null hypothesis to ensure that the reported probability value exceeded the actual value. To test whether SSEP amplitudes correlated with neurological scores, we used Kendall's one-sided nonparametric correlation coefficient (b) between SSEP amplitude at 2 hours and neurological impairment at 3 hours.18 We used this correlation coefficient because we had no a priori reason to specify a linear relationship between the two measurements. A curve relating the two measurements was calculated by means of locally weighted least-squares regression, with a tension of 0.5.19 The one-sided Mann-Whitney test was used to assess whether SSEP at 2 hours was greater among animals that survived to 24 hours than among those that died.
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Results |
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There were no important differences among groups in any systemic variable at any point throughout the experiment (Table 2
).
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Increasing dose of air was associated with greater neurological impairment at 3 hours (Fig 1). Likewise, there was a dose-response relationship between dose of air and SSEP amplitude at 2 hours (P=.00003) (Fig 2). SSEP amplitudes at 2 hours were inversely correlated with neurological impairment scores at 3 hours (=-0.71, P<.0001). A curve was drawn to improve visualization of the relationship between the measurements (Fig 3). The correlation between the 2-hour SSEP amplitude and 3-hour neurological score was independent of the neurological score. In other words, the correlation between poor (high) neurological scores and SSEPs was equal to the correlation between good (low) neurological scores and SSEPs (Fig 3).
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Somatosensory amplitudes over time, expressed as a percentage of baseline, are shown in Fig 4. SSEP amplitude generally increased over time in groups that received air. The correlation between SSEP amplitude and 3 hour neurological score improved over time. The correlation between SSEP amplitude and neurological score was nearly as good at 1 hour as it was at 2 hours after air embolism (Fig 4).
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By 24 hours, rabbits had either recovered neurologically (scores 
16) or were dead. SSEP amplitudes at 2 hours were less in animals that died (11±16%; n=9) than in those that survived to 24 hours (53±20%; n=9) P=.0008 (Fig 5).
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Discussion |
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In previous work with this air embolism model, we used 24-hour neurological outcome to demonstrate a protective effect of heparin.15 In that study we chose neurological examination as the end point in part because of the lack of data demonstrating a correlation between SSEP and neurological outcome. We chose a 24-hour neurological examination (rather than an earlier time point) to avoid residual anesthetic effect. In the present study we clearly observed a residual anesthetic effect. Animals that received no cerebral arterial air were still neurologically abnormal at 3 hours, with scores ranging from 4 to 41. Our concern with an early examination was that a residual anesthetic effect might decrease neurological differences among groups. However, in the present study, despite the influence of residual anesthetic, we demonstrated a dose relationship between dose of intracarotid air and neurological impairment. Additionally, in pilot work we observed that animals with greater 3-hour neurological impairment scores tended to die before the 24 neurological examination. Because a number of factors may influence operative mortality in addition to neurological injury, we elected to make comparisons at 3 hours.
There was a relatively large dispersion of neurological scores within each air dose group, suggesting a varying degree of injury within dose groups. This finding is reasonable when one considers that the distribution and subsequent clearance of air within the cerebral vasculature probably varies among individuals. In a similar fashion, SSEP amplitudes varied widely among individuals within dose groups (Fig 2
). Nevertheless, despite the relatively high degree of variability of both SSEP amplitude and neurological score among individuals, we observed a striking correlation between SSEP amplitude at 2 hours and both short-term (3-hour) neurological examination and 24-hour mortality. This finding supports the theory that after cerebral air embolism, electrophysiological measures and functional outcome correspond. At no dose of air was the relationship between SSEP amplitude and neurological examination score better or worse (Fig 3). In other words, the correlation appeared to be the same at all degrees of neurological impairment. Therefore, we conclude that SSEP amplitude may be a reasonable surrogate for neurological examination as a measure of outcome in this model of cerebral air embolism.
While SSEP amplitude has not been reported to correlate with neurological outcome in any animal model of cerebral injury, changes in SSEP have been studied in a number of animal models of cerebral ischemia. Branston et al20 found in baboons that local cerebral blood flow (CBF) below 16 mL·100 g-1·min-1 resulted in a decrease in SSEP amplitude and that CBF below 10 to 12 mL·100 g-1·min-1 abolished evoked responses altogether. In subsequent studies, these and other investigators observed that the recovery of SSEP amplitude after temporary middle cerebral artery (MCA) occlusion correlated with higher occlusion (residual) CBF and greater immediate postocclusion tissue oxygen content.21 22 However, after ischemia (ie, during reperfusion) the association between SSEPs and CBF was lost. CBF returned to or exceeded the preischemic value despite persistently abnormal SSEPs. Other investigators have likewise demonstrated differential effects of cerebral air embolism on CBF and SSEPs, with loss of the CBF/SSEP relationship after injury.23 24 Thus, it would appear that SSEPs provide information concerning the adequacy of CBF provided that neuronal injury has not already occurred.
Because SSEPs are a summation of neuronal responses to repeated stimuli, postischemic SSEP amplitude might be expected to better correlate with neuronal viability or function rather than with substrate availability per se. Intracellular pH and high-energy phosphate concentration might be used as a measure of "neuronal cellular health." Indeed, in dogs, Nishijima and colleagues25 observed that rapid normalization of intracellular pH was a sensitive predictor of electrophysiological recovery after a short period of global ischemia. In subsequent work, recovery of evoked response amplitude was observed to be independent of high-energy phosphate concentration,26 suggesting that persistent acidosis during reperfusion can contribute to postischemic electrophysiological deficit despite adequate ATP recovery.
To our knowledge, the only study examining the relationship between the return of SSEP amplitude and histological neuronal injury after permanent focal ischemia was performed by Steinberg and colleagues.27 They measured SSEPs in 15 cats undergoing permanent MCA occlusion. In seven cats there was no recovery of SSEPs over time (6 hours). These animals had moderate to severe ischemic neuronal changes, ranging from 21% to 64% (mean, 39%) of the total ipsilateral cortex. In the remaining eight cats, although there was complete loss of SSEP amplitude with occlusion, there was considerable recovery of SSEP amplitude during the subsequent 6 hours of the study. This second group of animals, which had some return of SSEPs, had ischemic areas ranging from 4% to 14% (mean, 9%) of the total ipsilateral cortex. Thus, some recovery of evoked potential was associated with less histological ischemic change than no recovery. However, there was no correlation between either maximum SSEP amplitude or SSEP amplitude at the end of the experiment and histological grade. While these authors readily acknowledge that their study was too small to avoid a type II error, return of SSEP amplitude may indeed be a poor measure of resultant neurological injury after MCA occlusion. The difference between the findings of Steinberg and colleagues and those of the present experiment may be explained by pathophysiological differences between cerebral ischemia induced by MCA occlusion and that produced by air emboli.
Cortical SSEP signals are derived from a population of cortical neurons receiving sensory afferents from thalamic relay neurons. As such, cortical SSEPs are dependent on the functional integrity of both cortical and subcortical elements. Interruption along any point in the afferent sensory pathway would result in a loss of the specific evoked response. In the case of cerebral air embolism, injured neurons are widely dispersed.12 13 Consequently, some of the neurons of the evoked potential neuronal pathway are affected, while other members of the population are preserved, resulting in a net signal of lesser amplitude. Because of the wide distribution of cerebral arterial air embolism, neurons involved in the SSEP pathway may be affected to roughly the same extent as all other neuronal populations. If so, cortical SSEP amplitude might be expected to correlate with overall neurological status. In this experiment we observed such a relationship. We found the magnitude of SSEP disturbance and neurological impairment to correlate extremely well over the entire range of outcomes. This finding suggests that as the dose of air increased, the percentage of the affected neurons involved in SSEP generation increased in roughly the same proportion as non-SSEP neurons.
In summary, we have demonstrated a dose effect of intracarotid air embolism on neurological injury, measured by either return of SSEP amplitude or neurological examination. Additionally, we have demonstrated a good correlation between SSEP amplitude at 2 hours and neurological impairment score at 3 hours in rabbits who have undergone cerebral air embolism.
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Acknowledgments |
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This study was supported in part by the Foundation for Anesthesia Education and Research with a grant from Arrow International.
Received February 5, 1996; revision received May 16, 1996; accepted June 18, 1996.
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References |
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Ryu K, Hindman B, Reasoner D, Dexter F. Heparin reduces neurological impairment after cerebral arterial air embolism in the rabbit. Stroke. 1996;27:303-310.
16.
Baker AJ, Zornow MH, Grafe MR, Scheller MS, Skilling SR, Smullin DH, Larson AA. Hypothermia prevents ischemia-induced increases in hippocampal glycine concentrations in rabbits. Stroke. 1991;22:666-673.
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Jonckheere AR. A distribution-free K-sample test against ordered alternatives. Biometrika. 1954;41:133-143.
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Matsumiya N, Koehler RC, Traystman RJ. Consistency of cerebral blood flow and evoked potential alterations with reversible focal ischemia in cats. Stroke. 1990;21:908-916.
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Editorial Comment
Department of Neurosurgery Research LaboratoriesUniversity of Texas at HoustonHealth Science CenterHouston, Tex
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferencesIntroduction References |
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Reasoner et al have provided an extensive analysis of the relationship between changes in somatosensory evoked potentials (SSEPs) and neurological outcome in rabbits subjected to a cerebral air embolism. The investigators report that SSEP amplitudes at 2 hours were inversely correlated with neurological impairment scores at 3 hours and that SSEP amplitudes at 2 hours were less in animals that died than those that survived at 24 hours. On the basis of these observations, the investigators conclude that "SSEP amplitude may be a reasonable surrogate for neurological examination as a measure of outcome in this model of cerebral air embolism." While their data clearly suggest that SSEPs may be important adjunctive measures of outcome after cerebral air embolism, it seems still premature to use SSEPs as an exclusive surrogate for neurological examinations, especially when outcomes are assessed at later time points after cerebral air embolism. It is not surprising that SSEP amplitudes at 2 hours were inversely correlated with neurological assessments conducted 1 hour later. Correlations between SSEP and mortality at 24 hours must also be viewed cautiously since, as the authors recognize, a number of factors may influence mortality in addition to neurological injury. Unfortunately, while these investigators have previously used neurological outcome at 24 hours to demonstrate a protective effect of heparin,1R 24-hour assessments were not possible in the present study since rabbits had either recovered neurologically or were dead by 24 hours after injury. Thus, while the research lays a firm foundation for studies of the potential usefulness of SSEPs as surrogate measures of neurological outcome, additional studies examining correlations between SSEPs and neurological outcomes at later time points are important before SSEPs can be reliably used as surrogate measures in this model system.
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1R. Ryu K, Hindman B, Reasoner D, Dexter F. Heparin reduces neurological impairment after cerbral arterial air embolism in the rabbit. Stroke.. 1996;27:303-310.
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