Biomedical subjects

C S Robertson

Publications and source records attributed to C S Robertson.

At least 37 records · Page 2Linked to original sources

PubMed2000

Similarities between civilian gunshot wounds to the head and nongunshot head injuries.

BACKGROUND: This investigation compared the cerebral pathophysiologic status of gunshot wounds to the head (GSWH) with that of severe head injury of other causes (non-GSWH). METHODS: Data were collected prospectively from 71 GSWH and 541 non-GSWH patients. The two groups had similar demographic characteristics and injury severities. Cerebral metabolic parameters for each patient were averaged for the entire period of monitoring. These per-patient averages were compared between GSWH and non-GSWH groups. RESULTS: Median intracranial pressure was 21.4 mm Hg in GSWH patients vs. 16.7 mm Hg in non-GSWH patients (p < 0.001). Mean arterial pressures were similar, but the higher intracranial pressure in GSWH patients produced a lower median cerebral perfusion pressure. Cerebral blood flow, cerebrovascular resistance, cerebral metabolic rate of oxygen, average jugular venous oxygen saturation, and number of jugular venous desaturations did not differ significantly between the groups. Three-month outcome was death in 43% of GSWH patients and 32% of non-GSWH patients, persistent vegetative state or severe disability in 33% and 32%, respectively, and moderate disability or good recovery in 24% and 36%, respectively. These outcomes were not significantly different (p = 0.11). CONCLUSION: GSWH patients suffer global cerebral metabolic disturbances that are at least as severe as those seen in non-GSWH patients with injuries of comparable severity. This selected population of GSWH patients may enjoy outcomes comparable to those of non-GSWH patients if they are treated by the same aggressive protocols.

Adult↗

PubMed2000

Midline shift after severe head injury: pathophysiologic implications.

OBJECTIVE: To investigate the mechanism of the adverse effect of midline shift after severe traumatic brain injury. METHODS: This study compared averaged cerebral metabolic parameters of patients with midline shift > 5 mm (S) on initial computerized tomography scan to those of patients with shift < or = 5 mm (NS). The effect of an acute subdural hematoma (SDH) was determined by separating patients into those with and those without SDH and then re-examining the effect of shift in these subgroups. RESULTS: Four hundred fifty-four patients were studied. Cerebral metabolic rate of oxygen (CMRO2, in mL/100 g per min) was always lower with shift: 1.74 for SDH-S versus 2.21 for SDH-NS (p < 0.001), and 1.80 for non-SDH-S versus 2.24 for non-SDH-NS (p < 0.001). No other major effects of shift were seen in SDH patients. Among non-SDH patients, shift was associated with higher intracranial pressure (ICP): 23.1 mm Hg versus 16.3 mm Hg (p < 0.001). Other differences between shift and nonshift patients in the non-SDH group were due at least in part to interventions to treat the elevated ICP. CONCLUSION: Midline shift after severe traumatic brain injury is associated with reduced CMRo2, regardless of whether or not SDH is present. The deleterious effects of subdural blood may be related more to the mass effect of large SDHs than to the biochemical abnormalities caused by small amounts of blood in the subdural space.

Adult↗

PubMed2000

Brain nitric oxide changes after controlled cortical impact injury in rats.

Nitric oxide (NO) and the NO end products, nitrate and nitrite, were measured at the impact site after a 5-m/s, 3-mm deformation controlled cortical impact injury in rats. Immediately after the impact injury and the NO and microdialysis probes could be replaced, there was an increase from baseline in NO concentration of 83 +/- 16 (SE) nM, compared with 0.5 +/- 4 nM in the sham injured animals (P < 0.001). This marked increase in NO occurred at the time of the initial rise in blood pressure (BP) and intracranial pressure (ICP) in response to the injury. After the initial increase in BP and ICP, the BP decreased and stabilized at a value which was approximately 20 mmHg below the preinjury values, and ICP plateaued at an average value of 20 mmHg, compared with 8 mmHg in the sham-injured animals. This provided an average cerebral perfusion pressure of 40-50 mmHg, compared with 65-75 mmHg for the sham-injured animals. These values were relatively constant for the remainder of the 3-h monitoring period. The NO values also stabilized during this time period. By 1 h after the impact injury the NO concentration measured directly using the NO electrode had decreased from baseline values by an average value of 25 +/- 6 nM. NO concentration remained significantly lower than baseline values throughout the remainder of the 3-h monitoring period. The concentration of nitrate/nitrite in the dialysate fluid also decreased by an average value of 341 +/- 283 nM 20-40 min after the injury. Dialysate nitrite/nitrate concentrations remained less than the preinjury baseline values throughout the remainder of the 3-h monitoring period. Preinjury treatment with L-nitro-arginine methyl ester (L-NAME) blunted the injury-induced increase in NO and resulted in more severe immediate intracranial hypertension and more severe systemic hypotension at one hour after injury. Mortality was also 67% with L-NAME pretreatment, compared with 1% in untreated animals.

Animals↗

PubMed1999

Simultaneous measurement of cortical potassium, calcium, and magnesium levels measured in head injured patients using microdialysis with ion chromatography.

Potassium, calcium and magnesium were measured in 3717 microdialysate samples in 43 patients with head injury experiencing refractory increased ICP, episodes of jugular venous oxygen desaturation and brain death. Cation analysis was performed with 'ion chromatography'. Potassium levels remained stable until severe physiological deterioration occurred, whereupon they increased 100-400%, usually associated with release of amino-acids including glutamate, aspartate, and taurine into the extracellular space. The magnesium and calcium levels remained unchanged, regardless of the severity of physiological deterioration.

Brain Injuries↗

PubMed1999

Validation of a controlled cortical impact model of head injury in mice.

A controlled cortical impact model of head injury was validated with mice. Mice were randomly assigned to moderate head injury, mild head injury, and sham injury groups. Beam balancing, open field activity, slant board inclination, grasp strength, and motor coordination were assessed prior to the injury and on days 1-5 postinjury. Morris water maze performance was evaluated on days 11-15 postinjury. Moderately head-injured mice took a significantly longer time to complete the motor coordination task and to find the hidden platform on the Morris water maze and had significantly fewer successful trials on both tasks than the mildly head-injured and sham-injured mice. Mildly head-injured and sham-injured mice performed similarly on both tasks. Contusion volume at the site of impact varied with severity of injury. Moderately head-injured mice had significantly larger contusions than mice with a mild head injury, and these mice in turn had significantly larger contusions than the sham-injured mice. Both moderately and mildly head injured mice had significantly fewer surviving cells in CA1 than the sham-injured mice but did not differ from each other in this regard. Although there was a group effect, only the mildly head-injured mice had significantly fewer surviving cells in CA3.

Animals↗

PubMed1999

Regional changes in cerebral extracellular glucose and lactate concentrations following severe cortical impact injury and secondary ischemia in rats.

Traumatic brain injury (TBI) causes the brain to be more susceptible to secondary insults, and the occurrence of a secondary insult after trauma increases the damage that develops in the brain. To study the synergistic effect of trauma and ischemia on brain energy metabolites, regional changes in the extracellular concentrations of glucose and lactate following a severe cortical impact injury were measured employing a microdialysis technique. Three microdialysis probes were placed in center of the impact site, in an area adjacent to the impact site, and in the contralateral parietal cortex, and perfused with artificial cerebrospinal fluid (CSF) at 2 microl/min. Rats were assigned to one of the following experimental groups (n = 7 per group): (1) combined impact injury and secondary insult, (2) impact injury with sham secondary insult, (3) sham impact with secondary insult, or (4) sham impact and sham secondary insult. The impact injury was produced with a pneumatic impactor (5 m/sec, 3-mm deformation). One hour following the impact injury, a secondary insult was produced by bilateral carotid occlusion for 1 h. The impact injury resulted in a three- to fivefold global increase in dialysate lactate concentrations, with a corresponding fall in dialysate glucose concentration by 50% compared to no change in lactate or glucose concentrations in sham-injured animals (p < .0001 for both lactate and glucose). The secondary insult resulted in a second increase in dialysate lactate and decrease in dialysate glucose concentration that was significantly greater in the animals that had suffered the impact injury than in the sham-injured animals. Ischemia and traumatic injury have synergistic effects on lactate accumulation and on glucose depletion in the brain that probably reflects persisting ischemia, but may also indicate mitochondrial abnormalities and inhibition of oxidative metabolism.

Acidosis, Lactic↗

PubMed1999

Cerebral hemodynamic effects of pentobarbital coma in head-injured patients.

The purpose of this study was to examine the changes in cerebral hemodynamics of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variables were measured in 67 severely head-injured patients at the following times: before the loading dose of pentobarbital; after the loading dose of pentobarbital (average pentobarbital level 28.1+/-8.3 microg/mL); and 3 days later, when the peak pentobarbital level averaged 42.5+/-17.2 microg/mL. Intracranial pressure (ICP) and mean arterial blood pressure (MAP) were decreased by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, respectively. Cerebral perfusion pressure (CPP) was unchanged when the entire group was analyzed together. CBF, cerebral oxygen consumption (CMR(O)2), and arteriovenous oxygen difference (AVD(O)2) were significantly decreased after the loading dose of pentobarbital, by 20%, 31%, and 11%, respectively. The average cerebrovascular resistance (CVR) was increased by 20%. The change in CMR(O)2 with the loading dose of pentobarbital was closely related to the pretreatment value (n = 67, r2 = 0.65, p < .001). Thirty (45%) of the patients had a "good ICP response," with a reduction in ICP from 34+/-9 to 15+/-5 mm Hg after the initial loading dose of pentobarbital. Twenty-seven (40%) of the patients had a "partial ICP response," with ICP decreasing but still remaining above 20 mm Hg after the loading dose of pentobarbital. In the remaining 10 patients, ICP did not change or even increased after pentobarbital. In the 30 patients with a good ICP response, pretreatment CMR(O)2 and AVD(O)2 were greater before administration of pentobarbital, and CMR(O)2 and AVD(O)2 decreased more with the loading dose of pentobarbital, than in the patients with partial or no ICP response. The outcome was significantly better in the patients with a good or partial ICP response to pentobarbital, with 21% of these patients having a good recovery or moderate disability at 3 months after injury, compared with 100% persistent vegetative state or death in the nonresponders. In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, partly because their CMR(O)2 is already markedly reduced by the injury and partly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because hypotension limits the amount of barbiturates that can be given.

Adult↗

PubMed1999

Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis.

OBJECTIVE: To study cerebral glucose and lactate metabolism in head-injured patients using microdialysis. DESIGN: Prospective, nonrandomized, clinical study. SETTING: Neurosurgical intensive care unit in a university-affiliated county hospital. PATIENTS: One hundred twenty-six head-injured patients. INTERVENTIONS: Cerebral cortical neurochemical monitoring using microdialysis coupled with systemic hemodynamic and oxygenation monitoring, measurement of cerebral perfusion pressure and intracranial pressure, and measurement of global cerebral oxygenation using jugular venous oxygen saturation in all 126 patients. In selected cases, cerebral blood flow was also measured using cortical thermodilution probes in 33 patients, and regional cerebral oxygenation was measured using PO2 probes in 65 patients. MEASUREMENTS AND MAIN RESULTS: Elevated extracellular lactate, reduced glucose, and an elevated lactate/glucose ratio were observed with cerebral hypoxia and ischemia. Elevated lactate and an increased lactate/glucose ratio strongly correlated with death. Other more subtle alterations of lactate and glucose were seen early after injury that may reflect compensatory alterations in cerebral metabolism. CONCLUSIONS: Clinical neurochemical monitoring of glucose and lactate levels in the extracellular space of the cerebral cortex is technically feasible and provides insight into the bioenergetic status of the brain. Increased lactate and decreased glucose, indicating accelerated glycolysis, commonly occurred with cerebral ischemia or hypoxia, and increased anaerobic glycolysis in this setting is associated with a poor outcome.

Adult↗

PubMed1999

Prevention of secondary ischemic insults after severe head injury.

OBJECTIVE: The purpose of this study was to compare the effects of two acute-care management strategies on the frequency of jugular venous desaturation and refractory intracranial hypertension and on long-term neurologic outcome in patients with severe head injury. DESIGN: Randomized clinical trial. SETTING: Level I trauma hospital. PATIENTS: One hundred eighty-nine adults admitted in coma because of severe head injury. INTERVENTIONS: Patients were assigned to either cerebral blood flow (CBF)-targeted or intracranial pressure (ICP)-targeted management protocols during randomly assigned time blocks. In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and PaCO2 was kept at approximately 35 torr (4.67 kPa). In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa) was used to treat intracranial hypertension. MEASUREMENTS AND MAIN RESULTS: The CBF-targeted protocol reduced the frequency of jugular desaturation from 50.6% to 30% (p = .006). Even when the frequency of jugular desaturation was adjusted for all confounding factors that were significant, the risk of cerebral ischemia was 2.4-fold greater with the ICP-targeted protocol. Despite the reduction in secondary ischemic insults, there was no difference in neurologic outcome. Failure to alter long-term neurologic outcome was probably attributable to two major factors. A low jugular venous oxygen saturation was treated in both groups, minimizing the injury that occurred in the ICP-targeted group. The beneficial effects of the CBF-targeted protocol may have been offset by a five-fold increase in the frequency of adult respiratory distress syndrome. CONCLUSIONS: Secondary ischemic insults caused by systemic factors after severe head injury can be prevented with a targeted management protocol. However, potential adverse effects of this management strategy may offset these beneficial effects.

Adolescent↗

PubMed1999

Comparison of jugular venous oxygen saturation and brain tissue Po2 as monitors of cerebral ischemia after head injury.

OBJECTIVE: To compare the characteristics of jugular venous oxygen saturation (Sjvo2) and brain tissue Po2 (Pbto2) as monitors for cerebral ischemia after severe head injury. Sjvo2 has been useful as a monitor for cerebral ischemia, but it is limited by its inability to identify regional cerebral ischemia. Pbto2 may be superior to Sjvo2 for this purpose, because oxygenation in localized areas of the brain can be monitored. DESIGN: Sjvo2 and Pbto2 were successfully monitored in 58 patients with severe head injury. The changes in Sjvo2 and Pbto2 were compared during ischemic episodes. SETTING: Neurosurgical intensive care unit of a level I trauma center. MEASUREMENTS AND MAIN RESULTS: During the monitoring period, which averaged 90 hrs/patient, there were 54 episodes during which Sjvo2 decreased to <50% and/or Pbto2 decreased to <8 torr. Two of these episodes were caused by an infarction in the area of the Po2 probe, leaving 52 episodes of global hypoxia/ischemia that were identified by one of the two monitors. The sensitivities of the two monitors for detecting ischemia, using the thresholds of 50% and 8 torr for Sjvo2 and Pbto2, respectively, were similar. The Sjvo2 catheter detected 69.7% of the episodes and the Pbto2 catheter detected 63.5% of the episodes. In most of the remaining episodes, both probes reflected a decrease in oxygenation, but not to levels below the defined thresholds. The major differences in the two measures of oxygenation included the following: a) Sjvo2 more consistently reflected a reduction in oxygenation during hyperventilation; b) Pbto2 was affected more by changes in arterial Po2; and c) during severe global ischemia, Pbto2 decreased to 0 and remained at 0, whereas Sjvo2 initially decreased but then increased again as cerebral blood flow ceased, and the only blood in the jugular bulb was of extracerebral origin. CONCLUSIONS: The two monitors provide complimentary information, and neither monitor alone identifies all episodes of ischemia. The best strategy for using these monitors is to take advantage of the unique features of each monitor. Sjvo2 should be used as a monitor of global oxygenation; but Pbto2 should be used as a monitor of local oxygenation, ideally with the catheter placed in an area of the brain that is vulnerable to ischemia but that may be salvageable with appropriate treatment.

Adult↗

PubMed1999

Cerebral hemodynamic effects of phenylephrine and L-arginine after cortical impact injury.

OBJECTIVE: To determine the effects of a pressor agent (phenylephrine and L-arginine) on the abnormal cerebral hemodynamics and on neurologic outcome after a severe cortical impact injury in rats. DESIGN: Prospective, randomized study. SETTING: University laboratory. SUBJECTS: Male Long-Evans rats, weighing 300 to 400 g, fasted overnight. INTERVENTIONS: The animals were anesthetized with isoflurane, and a severe cortical impact injury (velocity, 5 m/sec; deformation, 3 mm) was produced in the right parietal cortex. Five minutes after impact injury, one of the following three treatments were infused: 1 mL saline intravenously for 10 mins, 300 mg/kg L-arginine in 1 mL saline intravenously for 10 mins, or 0.3 microg/kg/min phenylephrine intravenously for 3 hrs. Mean arterial pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flow (LDF) at the impact site and in the contralateral parietal cortex were monitored for 3 hrs after the impact injury. Histologic examination of the brain was performed at 2 wks after injury in a separate group of L-arginine- and saline-treated animals. MEASUREMENTS AND MAIN RESULTS: The immediate response to the impact injury was an increase in ICP, and a decrease in mean arterial pressure, CPP, and LDF. In the saline-treated animals, LDF decreased to <25% of the baseline values at the impact site and stayed at that level for the entire 3-hr monitoring period. On the contralateral side, LDF decreased initially and recovered gradually to approximately 50% of the preimpact baseline value. Infusion of both phenylephrine and L-arginine increased LDF back to near-baseline levels. However, phenylephrine increased ICP significantly, whereas ICP with L-arginine did not change. L-arginine treatment reduced the contusion volume from a median value of 5.28 mm3 to 0.63 mm3. CONCLUSIONS: Phenylephrine increased cerebral blood flow (CBF) by increasing CPP. L-arginine, however, increased CBF without changing CPP. The improvement in CBF was accompanied by a decrease in neurologic injury. Although the pressor agents are used currently to increase CBF after traumatic brain injury, other strategies may also increase CBF without the potential adverse effects of induced hypertension.

Animals↗

PubMed1999

Cerebrovascular reactivity to CO(2) and hypotension after mild cortical impact injury.

Cerebrovascular reactivity to CO(2) or hypotension was studied in vivo and in vitro [pressurized arteries ( approximately 82 micrometer) and arterioles ( approximately 30 micrometer)] at 1 h after mild controlled cortical impact (CCI) injury in rats. The cortical perfusion response [assessed using laser-Doppler flowmetry (LDF)] to altered CO(2) was diminished (up to 81%) after mild CCI injury. The responses to CO(2) alterations in arteries and arterioles isolated from the injured cortex were similar to responses in vessels isolated from sham-injured animals. After mild CCI injury, the autoregulatory response to hypotension (measured using LDF) was maintained or even enhanced, depending on the method used to measure the response. Vessels isolated from the injury site showed a response to changes in pressure similar to that in vessels isolated from sham-injured rats. We conclude that mild CCI injury produces complicated alterations in cerebrovascular control. Whereas the autoregulatory response to hypotension was maintained or even enhanced, the in vivo vascular response to CO(2) was severely compromised. The altered response to CO(2) was not caused by an intrinsic vascular perturbation but rather an altered milieu after mild CCI injury.

Animals↗

PubMed1999

The consequences of traumatic brain injury on cerebral blood flow and autoregulation: a review.

In this decade, the brain argueably stands as one of the most exciting and challenging organs to study. Exciting in as far as that it remains an area of research vastly unknown and challenging due to the very nature of its anatomical design: the skull provides a formidable barrier and direct observations of intraparenchymal function in vivo are impractical. Moreover, traumatic brain injury (TBI) brings with it added complexities and nuances. The development of irreversible damage following TBI involves a plethora of biochemical events, including impairment of the cerebral vasculature, which render the brain at risk to secondary insults such as ischemia and intracranial hypertension. The present review will focus on alterations in the cerebrovasculature following TBI, and more specifically on changes in cerebral blood flow (CBF), mediators of CBF including local chemical mediators such as K+, pH and adenosine, endothelial mediators such as nitric oxide and neurogenic mediators such as catecholamines, as well as pressure autoregulation. It is emphasized that further research into these mechanisms may help attenuate the prevalence of secondary insults and therefore improve outcome following TBI.

Animals↗

PubMed1999

Elevated jugular venous oxygen saturation after severe head injury.

OBJECT: The aim of this study was to investigate the incidence of elevated (> or = 75%) jugular venous oxygen saturation (SjvO2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury. METHODS: Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO2 (Group III) if their mean SjvO2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively. A high SjvO2 occurred in 19.1% of patients. There was no consistent relationship between SjvO2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO2). In Group I, the outcomes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome. CONCLUSIONS: Posttraumatic elevation of SjvO2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.

Adult↗

PubMed1998

Comparison of the myogenic response in rat cerebral arteries of different calibers.

The myogenic response, the characteristic of blood vessels to contract with increasing pressure, was studied at three different locations along the middle cerebral artery (MCA) vascular tree. We hypothesized that smaller caliber vessels would have a more pronounced myogenic response at lower pressures than larger diameter arteries, corresponding to pressures normally experienced in vivo. Cerebral vessels (MCAs, branches of the MCA, and penetrating arterioles) were isolated from male rats, cannulated with glass micropipettes, and pressurized. Changes in diameter were measured as the transmural pressure was increased from 20-100 mmHg. The MCAs, which had a resting diameter of 202 +/- 10 micron (n = 9) at 50 mmHg, showed its greatest myogenic response between 60-100 mmHg (8+/-2% constriction, n = 9, p < 0.001). The penetrating arterioles [58 +/- 4 micron (n = 8) at 50 mmHg], on the other hand, showed its greatest myogenic response between 20-60 mmHg (10 +/- 4% constriction, n = 8, p < 0.05). Branches of the MCA [118 +/- 14 micron (n = 8) at 50 mmHg] showed a slight constriction over the entire pressure range (5 +/- 9% constriction between 20-100 mmHg, p=ns). Our results suggest that the myogenic response appears to be best developed in the range of pressures found during physiological conditions for a given vessel in the MCA territory. This characteristic is fundamental in the overall control of cerebrovascular resistance.

Animals↗

PubMed1998

Catecholamine assays in a rat model for autonomic dysreflexia.

OBJECTIVE: To determine if norepinephrine (NE) levels increased during autonomic dysreflexia (AD) hypertension in spinal cord injured rats. DESIGN: Prospective, randomized study of three groups of eight rats that underwent C8 spinal cord transection. Two days postoperatively, catecholamine samples were collected from the animals as follows: group 1 without preoperative chemical sympathectomy using 6-hydroxydopamine (6-OH DA) or induced AD; group 2 with induced AD; and group 3, preoperative chemical sympathectomy with 6-OH DA and induced AD. SETTING: Basic science research laboratory in an academic institution. PARTICIPANTS: Sprague-Dawley male rats weighing 300g. INTERVENTION: Three episodes of induced AD hypertension with bowel distension for 1 minute. RESULTS: Results showed a significant difference between groups 1 and 2, 2 and 3, and 1 and 3 (p=.0002, ANOVA, Y1/2, post hoc Tukey). The mean NE levels in groups 1, 2, and 3 were 465+/-400 ng/mL, 1,328+/-1,116 ng/mL, and 31+/-61 ng/mL, respectively. CONCLUSION: NE increased during AD in the spinal cord injured rat. NE levels were effectively blocked by 6-OH DA when AD was induced. Knowledge of catecholamine levels in this process may assist in determining both pathophysiology and potential pharmacologic treatment options in future human studies.

Animals↗

PubMed1998

Metabolic changes in the brain during transient ischemia measured with microdialysis.

Forty-four patients with severe head injury were monitored for episodes of cerebral ischemia using jugular venous oxygen saturation (sjvO2), brain tissue pO2 (ti-pO2), and a microdialysis probe. The concentration of lactate and glucose were measured in the microdialysate. A total of 10 episodes of global ischemia were observed. The characteristic pattern of a simultaneous decrease in sjvO2 and brain ti-pO2 with an increase in the concentration of lactate occurred in all 10 patients. In addition, 3 episodes of regional ischemia were observed. Although brain ti-pO2 decreased to very low values and the concentration of lactate increased in the microdialysate, sjvO2 remained unchanged. Brain ti-pO2 adds another dimension to our cerebral monitoring by allowing the detection of regional cerebral ischemia.

Adult↗

PubMed1998

Effect of glucose administration on contusion volume after moderate cortical impact injury in rats.

Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.

Animals↗