Robert E. Anderson

Mayo Foundation for Medical Education and Research, Scottsdale, AZ, United States

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Publications (69)240.58 Total impact

  • Journal of Neurosurgery 11/2007; 107(4):887-97. DOI:10.3171/JNS-07/10/0887 · 3.23 Impact Factor
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    ABSTRACT: Cerebral blood flow (CBF) physiology is important to neurosurgeons who manage patients with cerebrovascular disease. The techniques to measure CBF and mathematical methods to calculate CBF have evolved over the past 50 years. These techniques have been refined to enable perioperative and intraoperative measurement of cerebral blood flow qualitatively and quantitatively. Some of the measurement techniques discussed in this chapter include PET, EEG, TCD, Xenon and thermal fusion.
    12/2004: pages 301-314;
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    ABSTRACT: The authors evaluated a new non-cross-linked, propylene oxide-treated, acellular collagen matrix for use as a dural substitute in rabbits. They then compared this material to a commonly used dural substitute as well as to native dura mater used during primary closure. Forty-six rabbits were randomly assigned to eight groups of five or six rabbits each. These groups differed according to the type of closure material that was used during surgery (native dura, control dural substitute, or experimental dural substitute) and the duration of convalescence. At the end of the experiment, the tightness of the duraplasty was assessed in each live rabbit by continuous infusion of fluid into the cistema magna until leakage was detected. The animals were killed and each specimen was sectioned and studied histologically. The authors found that the experimental dural substitute was safe in animals for this application, that it held sutures well, and that a watertight closure was usually achieved. There were fewer adhesions between the experimental material and neural tissue was less likely to adhere to the cranium than the control graft. Histological examination showed that the experimental material had slightly more spindle cells and vascularity than the control graft. The experimental graft material has several features that make it an attractive candidate for use as a dural substitute.
    Journal of Neurosurgery 01/2004; 99(6):1070-6. DOI:10.3171/jns.2003.99.6.1070 · 3.23 Impact Factor
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    ABSTRACT: The effects of interleukin (IL)-1beta on the cerebral vasculature are complex and incompletely understood. Many pathophysiological states in which inflammatory cascades have been implicated also have varying degrees of cerebral hypoperfusion. The purpose of this investigation was to examine the long-term effects of this proinflammatory cytokine and its antagonist on cerebral blood flow (CBF) following global cerebral hypoperfusion. Sprague-Dawley rats were randomly assigned to 12 groups and given continuous intracerebroventricular (ICV) infusions of IL-1beta, the IL-1 receptor antagonist (IL-1ra), or saline vehicle (control). Global cerebral hypoperfusion was produced by occlusion of both carotid arteries and one vertebral artery. Cerebral blood flow was measured at baseline and again after initiation of the infusions by performing a 133Xe clearance study. Prolonged ICV administration of IL-1beta resulted in a significant decrease in CBF compared with that in controls. Prolonged administration of the antagonist IL-1ra resulted in significant increases in CBF compared with that in both IL-1beta-treated animals and controls. This experiment demonstrates that long-term treatment with the proinflammatory cytokine IL-1beta adversely affects CBF.
    Journal of Neurosurgery 12/2003; 99(5):907-12. DOI:10.3171/jns.2003.99.5.0907 · 3.23 Impact Factor
  • Robert E Anderson, John L D Atkinson
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    ABSTRACT: Apnea and catecholamine surge have been known sequelae in the first few minutes of postexperimentally induced severe head injury for over a century. However, the intracranial pressure (ICP) response to these two pathophysiologic processes is poorly understood. We used the rat fluid percussion head injury model to study apnea and catecholamine surge separately and in combination on measured ICP response The three experimental groups of apnea, hypertensive surge, and both combined revealed significantly different ICP responses with markedly elevated pressures correlating closely with mean arterial blood pressure. ICP and mean arterial blood pressure correlate closely in the first few minutes after head injury in the absence of space-occupying hematomas, and may initiate pathophysiologic sequelae that can only be treated by earlier medical intervention at the scene.
    The Journal of trauma 04/2003; 54(3):550-4. DOI:10.1097/01.TA.0000047049.64695.69 · 2.96 Impact Factor
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    Bernard A Coert, Robert E Anderson, Fredric B Meyer
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    ABSTRACT: The purpose of this study was to test the hypothesis that the efficacy of 7-nitroindazole (7-NI), a selective neuronal nitric oxide (NO) synthase (NOS) inhibitor, is pH dependent in vivo during focal cerebral ischemia. Wistar rats underwent 2 h of focal cerebral ischemia under 1% halothane anesthesia. 7-NI, 10 and 100 mg/kg in 0.1 ml/kg DMSO, was administered 30 min before occlusion. Ischemic brain acidosis was manipulated by altering serum glucose concentrations. Confirmation of the effects of these serum glucose manipulations on brain intracellular pH (pH(i)) was confirmed in a group of acute experiments utilizing umbelliferone fluorescence. The animals were euthanized at 72 h for histology. 7-NI significantly (P < 0.05) reduced infarction volume in both the normoglycemic by 93.3% and hyperglycemic animals by 27.5%. In the moderate hypoglycemic animals, the reduction in infarction volume did not reach significance because moderate hypoglycemia in itself dramatically reduced infarction volume. We hypothesize that a mechanism to explain the published discrepancies on the effects of neuronal NOS inhibitors in vivo may be due to the effects by differences in ischemic brain acidosis on the production of NO.
    AJP Heart and Circulatory Physiology 02/2003; 284(1):H151-9. DOI:10.1152/ajpheart.00580.2002 · 4.01 Impact Factor
  • Robert E Anderson, Fredric B Meyer
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    ABSTRACT: It has been demonstrated in many studies that intracellular brain acidosis during cerebral ischemia is a significant factor in perpetuating the cycle of cellular dysfunction leading to neuronal injury. The purpose of this study was to determine whether preischemic administration of alkalotic agents could reduce neuronal injury after focal cerebral ischemia. Fifteen fasted rabbits under 1.0% halothane anesthesia were randomized into three groups: Group 1 rabbits were ischemic controls (n = 5) that underwent 4 hours of focal cerebral ischemia. Groups 2 and 3 rabbits underwent a paradigm similar to that of Group 1, except that they were pretreated with either sodium bicarbonate or Carbicarb at similar buffering capacities. Intracellular brain pH (pH(i)), regional cortical blood flow (rCBF), and intrinsic reduced nicotinamide adenine dinucleotide (NADH) fluorescence were measured with in vivo fluorescence imaging. At the end of each experiment, infarct volume expressed as a percentage of hemispheric volume was measured by triphenyltetrazolium chloride staining. Preischemic alkalinization did not alter brain pH(i), rCBF, or NADH fluorescence. After 4 hours of ischemia, brain pH(i), rCBF, NADH fluorescence, and infarct volume measured 6.40 +/- 0.09 (mean +/- standard error), 11 +/- 2 ml/100 g/min, 165 +/- 8% of baseline control, and 37 +/- 3% in ischemic controls, respectively. In Group 2 animals treated with sodium bicarbonate, brain pH(i), rCBF, NADH fluorescence, and infarct volume improved significantly (P < 0.05, analysis of variance) to 6.74 +/- 0.08, 24 +/- 6 ml/100 g/min, 137 +/- 6% of baseline control, and 22 +/- 4%, respectively. Group 3 Carbicarb animals demonstrated improvements in brain pH(i), rCBF, and NADH fluorescence, with a significant reduction in infarct volume. These findings suggest that pretreatment with alkalinizing agents may be a useful intervention to provide intraoperative cerebral protection from ischemic injury.
    Neurosurgery 11/2002; 51(5):1256-65; discussion 1265-6. DOI:10.1097/00006123-200211000-00022 · 3.03 Impact Factor
  • Bernard A Coert, Robert E Anderson, Fredric B Meyer
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    ABSTRACT: A nitric oxide (NO) donor that has been successfully used in the treatment of myocardial infarction, 3-morpholinosydnonimine (SIN-1), may be a potential neuroprotective agent. Production of NO in brain microsomes is dependent on the pH. The purpose of this study was to determine the efficacy of SIN-1 and its dependence on pH in vivo during periods of focal cerebral ischemia. At 0.1 or 1 mg/kg, SIN-1 was administered to 54 Wistar rats 30 minutes before a 2-hour period of focal cerebral ischemia under moderate hypo-, normo-, and hyperglycemic conditions. Measurements of brain intracellular pH (pHi); regional cortical blood flow, and the redox state of nicotinamide adenine dinucleotide were obtained in three additional animals to confirm the effects of the serum glucose manipulations. The animals were killed at 72 hours after the ischemic period to obtain infarction volumes. Administration of SIN-1 significantly reduced infarction in normoglycemic animals and, to a lesser extent, in hyperglycemic animals, indicating that SIN-1 was less effective under hyperglycemic conditions. At either dose SIN-1 had no significant effect on infarction volume in moderately hypoglycemic animals because moderate hypoglycemia in itself significantly (p < 0.005) reduced infarction volume. The NO donor SIN-1 may be a useful intraoperative cerebral protective agent. Furthermore, it is hypothesized that a mechanism that could explain the published discrepancies regarding the effects of NO donors in vivo may be affected by differences in ischemic brain acidosis.
    Journal of Neurosurgery 10/2002; 97(4):914-21. DOI:10.3171/jns.2002.97.4.0914 · 3.23 Impact Factor
  • Robert E Anderson, Fredric B Meyer
    Methods in Enzymology 02/2002; 352:482-94. · 2.19 Impact Factor
  • Robert E. Anderson, Fredric B. Meyer
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    ABSTRACT: The role of gender difference and estrogen in ischemic cerebrovascular events is controversial. Evidence is lacking as to whether or not there are significant gender differences in the incidence and outcome of stroke in the clinical setting. Recent clinical epidemiological studies have demonstrated that there is no significant association between the use of hormonal replacement therapy and the risk of stroke. However, several animal studies have shown that there are gender differences in stroke outcome and that exogenous administered estrogens are neuroprotective. In this study, the influence of gender differences and the effects of synthetic and non-synthetic estrogens were examined in a model of focal cerebral ischemia using 210 male, intact female, and ovariectomized female rats. All animals underwent 3 h of middle cerebral artery and bilateral common carotid artery occlusion. After 72 h, the rats were sacrificed and stained for histological assessment of infarction. There were no gender differences in infarction volume. Intravenous administration of either low or high dose 17 beta-estradiol or tibolone did not alter infarct volume. Subcutaneous administration of low and high dose 17beta-estradiol using 7-day release pellets did not alter infarct volume. Low dose tibolone using implanted 7-day release pellets did not alter infarct volume. However, high dose tibolone using implanted 7-day release pellets significantly (P<0.05) reduced infarct volume only in ovariectomized female rats. These results demonstrate that estrogen therapy has no effect on infarction volume following severe focal cerebral ischemia.
    Brain Research 10/2000; 878(1-2):88-97. DOI:10.1016/S0006-8993(00)02713-X · 2.83 Impact Factor
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    Bert A Coert, Robert E Anderson, Fredric B Meyer
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    ABSTRACT: Alterations in polyamine metabolism during and after global or focal cerebral ischemia can produce a multiplicity of effects on brain such as modification in mitochondria calcium buffering capacity, exacerbating glutamate-mediated neurotoxicity, and impairment of the blood-brain barrier. In this study, the endogenous polyamine spermine was administered intravenously 30 min prior to temporary focal cerebral ischemia in rats induced by clipping of the left middle cerebral and bilateral common carotid arteries for 3 h. Three days after removal of the microclips, intracardiac perfusion with 2% 2,3,5-triphenyl tetrazolium chloride was performed. Coronal slices were cut, photographed, and examined for cortical infarct volume. Spermine reduced infarct volume in a dose-dependent fashion. This study demonstrates that the use of polyamines may be considered as a powerful tool in prevention of ischemic tissue damage following focal cerebral ischemia.
    Neuroscience Letters 04/2000; 282(1-2):5-8. DOI:10.1016/S0304-3940(00)00856-9 · 2.06 Impact Factor
  • Robert E Anderson, Fredric B Meyer
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    ABSTRACT: The interaction between nitric oxide (NO.) and focal cerebral ischemia is multifaceted. Experiments have shown that inhibition of nitric oxide synthase (NOS) either ameliorates or exacerbates focal cerebral ischemia. Recent in vitro experiments have shown that NOS activity is pH-dependent. Previous work from this laboratory has demonstrated that N(G)-nitro-L-arginine-methyl-ester (L-NAME) mitigated cerebral ischemia independent from regional cerebral blood flow (rCBF) changes during moderate focal cerebral ischemia. This study examined the effects of L-NAME inhibition on brain pH(i), rCBF, and NADH redox state during 3 h of severe focal cerebral ischemia. Fifteen fasted rabbits under 1.5% halothane were equally divided into three groups: ischemic controls and two drug groups receiving either 1.0 or 10 mg/kg L-NAME intravenously 30 min prior to ischemia. In the ischemic controls, brain pH(i) declined from 6.95+/-0.04 to 6.60+/-0.05, rCBF declined from 48+/-7 to 10+/-3 ml/100 g/min, and NADH fluorescence increased by 149+/-15% 3 h after onset of ischemia (p<0.01 for all three parameters). L-NAME at either dose did not significantly alter these values. Infarct volume was not significantly different between both the L-NAME treated groups and the ischemic control group. This data suggests that during severe focal cerebral ischemia, NO. mechanisms of injury have a less important punitive role. One possible explanation is that the severity of acidosis secondary to anaerobic metabolism during severe focal cerebral ischemia attenuates NOS activity.
    Brain Research 03/2000; 856(1-2):220-6. DOI:10.1016/S0006-8993(99)02435-X · 2.83 Impact Factor
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    Jonathan A. Friedman, Robert E. Anderson, Fredric B. Meyer
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    ABSTRACT: Understanding the physiological mechanisms of cerebral blood flow (CBF) is of great importance to neurosurgeons engaged in the management of patients with cerebrovascular disease. Over the past 50 years, techniques to measure CBF and mathematical methods to calculate CBF have evolved substantially. For the cerebrovascular surgeon, intraoperative CBF monitoring is an important adjunct in certain intra- and extracranial procedures. The authors review current techniques in use for the intraoperative measurement of CBF.
    Neurosurgical FOCUS 02/2000; 9(5):e4. DOI:10.3171/foc.2000.9.5.4 · 2.14 Impact Factor
  • Robert E. Anderson, William K. Tan, Fredric B. Meyer
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    ABSTRACT: Within the ischemic penumbra, there is a heterogeneous development of cortical intracellular acidosis that is associated with selective neuronal injury. This experiment, which used a rabbit model of moderate focal cerebral ischemia, examined the time course for changes in intracellular brain pH, cortical blood flow, capillary bed density, and mitochondrial function in the ischemic penumbra. After cortical annotation of regions of intracellular acidosis in the ischemic penumbra, the animals underwent transcardiac carbon black perfusion for measurement of capillary bed density. Analysis of variance and Pearson's correlation coefficients were used to determine the relationship between capillary bed density, brain intracellular pH, mitochondrial function, and cortical blood flow. Thirty minutes after the onset of ischemia, cortical blood flow declined from 46+/-2 to 22+/-1 mL/100gm/min (P<.01) in all groups. The overall cortical intracellular brain pH measured 6.78+/-.01 compared with a preischemic value of 6.98+/-.01 (P<.05). Within this moderately ischemic cortex, there were small regions (1,000 to 45,000 mum(2)) of increased acidosis, meauring 6.68+/-.01, not associated with focal changes in cortical blood flow, occurring within 15 minutes of ischemia and persisting throughout the ischemic period. Capillary bed density progressively declined with ongoing ischemia occurring after the development of acidosis. For example, capillary bed density in preischemic controls was 338+/-6/mm(2), whereas after 1 hour of ischemia, it measured 147+/-12/mm(2), at 3 hours 97+/-23/mm(2), and at 6 hours 92+/-16/mm(2). Mitochondrial function was reduced coinciding with the decrease in capillary bed density. These data support the hypothesis that cortical acidosis in the ischemic penumbra facilitates the development of perfusion defects that subsequently lead to mitochondrial dysfunction.
    Journal of Stroke and Cerebrovascular Diseases 11/1999; 8(6):368-79. DOI:10.1016/S1052-3057(99)80044-5 · 1.99 Impact Factor
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    Bert A. Coert, Robert E. Anderson, Fredric B. Meyer
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    ABSTRACT: A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions. Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, N(G)-nitro-L-arginine-methyl-ester (L-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-1-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-i um-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally in dimethyl sulfoxide (DMSO) 60 minutes before ischemia was induced. Two ischemic control groups, to which either saline or DMSO was administered, were also included in this study. Seventy-two hours after flow restoration, the animals were perfused with tetrazolium chloride for histological evaluation. Cortical infarction volume was significantly reduced by 71% in the group treated with 1 mg/kg L-NAME when compared with the saline-treated ischemic control group (27.1+/-37 mm3 compared with 92.5+/-26 mm3, p < 0.05). The NOS inhibitor 7-NI significantly reduced cortical infarction volume by 70% and by 92% at doses of 10 and 100 mg/kg: 35.2+/-32 mm3 (p < 0.05) and 9+/-13 mm3 (p < 0.005), respectively, when compared with the DMSO-treated ischemic control group (119+/-43 mm3). There was no significant difference between the saline-treated and DMSO-treated ischemic control groups. Treatment with NO donors did not significantly alter cortical infarction volume. These results support an important role for NO in ischemic neurotoxicity and indicate that neuronal NOS inhibition may be valuable in reducing cortical injury in patients suffering temporary focal cerebral ischemia during neurovascular procedures.
    Journal of Neurosurgery 02/1999; 90(2):332-8. DOI:10.3171/jns.1999.90.2.0332 · 3.23 Impact Factor
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    ABSTRACT: During focal cerebral ischemia, the ischemic penumbra or border-zone regions of moderate cortical blood flow reductions have a heterogeneous development of intracellular cortical acidosis. This experiment tested the hypotheses that (1) this acidosis is secondary to glucose utilization and (2) this intracellular acidosis leads to recruitment of potentially salvageable tissue into infarction. Brain pHi, regional cortical blood flow, and NADH redox state were measured by in vivo fluorescent imaging, and infarct volume was assessed by triphenyltetrazolium chloride histology. Thirty fasted rabbits divided into 6 groups of 5 each were subjected to 4 hours of permanent focal ischemia in the presence of hypoglycemia ( approximately 2.8 mmol/L), moderate hyperglycemia ( approximately 11 mmol/L), and severe hyperglycemia (>28 mmol/L) under either normoxia or moderate hypoxia (PaO2 approximately 50 mm Hg). Preischemic hyperglycemia led to a more pronounced intracellular acidosis and retardation of NADH regeneration than in the hypoglycemia groups under both normoxia and moderate hypoxia in the ischemic penumbra. For example, 4 hours after ischemia, brain pHi in the severe hyperglycemia/normoxia group measured 6.46, compared with 6.84 in the hypoglycemia/normoxia group (P<0.01), and NADH fluorescence measured 173% compared with 114%. Infarct volume in the severe hyperglycemia/normoxia group measured 35.1+/-6.9% of total hemispheric volume, compared with 13.5+/-4.2% in the hypoglycemia/normoxia group (P<0.01). Hyperglycemia significantly worsened both cortical intracellular brain acidosis and mitochondrial function in the ischemic penumbra. This supports the hypothesis that the evolution of acidosis in the ischemic penumbra is related to glucose utilization. Furthermore, the observation that hypoglycemia significantly decreased infarct size supports the postulate that cortical acidosis leads to recruitment of ischemic penumbra into infarction.
    Stroke 01/1999; 30(1):160-70. DOI:10.1161/01.STR.30.1.160 · 6.02 Impact Factor
  • John L. D. Atkinson, Robert E. Anderson, Michael J. Murray
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    ABSTRACT: Background: Apnea is a known response of concussive head injury. Hypoxic or ischemic brain injury has been documented in a high percentage of severe head injury deaths. The respiratory response after head injury remains poorly defined, however, and its contribution to hypoxic or ischemic mechanisms after severe head injury is unknown. Methods: Eighteen anesthetized but spontaneously breathing rats were subjected to fluid percussion head injury of varying severities. Respiratory rate and volume of air were recorded before and after injury with a Hans Rudolph/Varadyne pneumotach differential pressure transducer and graphically measured. Postmortem inspection of the brains was performed. Results: Apnea and subsequent respiratory dysfunction are directly proportional to the magnitude of energy delivered to the brain. Higher energy results in a dysfunctional or absent respiratory response, probably attributable to failure or disorganized function of the medullary respiratory center. Conclusion: This study for the first time graphically depicts the respiratory response after head injury. Higher energy delivered to the brain directly correlates with a markedly abnormal respiratory response that probably contributes significantly to subsequent hypoxic or ischemic brain injury. The absence of the space-occupying hematoma or gross parenchymal disruption suggests that in the clinical setting many of these patients may otherwise have survivable head injury if rescued by early ventilatory assistance.
    The Journal of Trauma Injury Infection and Critical Care 01/1998; 45(5):941-945. DOI:10.1097/00005373-199811000-00016
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    Luca Regli, Mark C. Held, Robert E. Anderson, Fredric B. Meyer
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    ABSTRACT: This experiment examined the effects of nitric oxide (NO) synthase inhibition on brain intracellular pH, regional cortical blood flow, and NADH fluorescence before and during 3 h of focal cerebral ischemia using in vivo fluorescence imaging. Thirty fasted rabbits under 1% halothane were divided into four treatment groups receiving N omega-nitro-L-arginine methyl ester (L-NAME) intravenously at 20 min prior to ischemia (0.1, 1, and 10 mg/kg and 1 mg/kg + 5 mg/kg L-arginine) and two control groups (nonischemic and ischemic). In ischemic controls, brain pH(i), declined to 6.73 +/- 0.03 at 30 min and remained acidotic through the remainder of the ischemic period. In the 0.1 mg/kg group, brain pH(i) fell after 30 min of ischemia to 6.76 +/- 0.05 (p < 0.05), but then improved progressively despite occlusion. In the 1 mg/kg group, brain pH(i), remained normal despite middle cerebral artery (MCA) occlusion. In the 10 mg/kg group and in the combined L-NAME + L-arginine group, pH(i) fell after 30 min of ischemia to 6.81 +/- 0.03 (p < 0.05) and remained acidotic. During occlusion, regional cortical blood flow dropped in a dose-dependent manner. After 3 h of ischemia, regional cortical blood flow was 33.9 +/- 10.9 and 25.1 +/- 8.9 ml/100 g/min at doses of 0.1 and 10.0 mg/kg, respectively, L-NAME treatment did not significantly alter the increased NADH fluorescence that accompanied occlusion. This study shows that L-NAME can prevent intracellular brain acidosis during focal cerebral ischemia independent from regional cortical blood flow changes. This experiment suggests that NO is involved in pH(i) regulation during focal cerebral ischemia.
    Journal of Cerebral Blood Flow & Metabolism 09/1996; 16(5):988-95. DOI:10.1097/00004647-199609000-00024 · 5.34 Impact Factor
  • Luca Regli, Robert E. Anderson, Fredric B. Meyer
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    ABSTRACT: The use of intermittent reperfusion versus straight occlusion during neurovascular procedures is controversial. This experiment studied the effects of intermittent reperfusion and single occlusion on intracellular brain pH (pHi), regional cerebral or cortical blood flow, and nicotinamide adenine dinucleotide (NADH) fluorescence during temporary focal ischemia. Twenty fasted rabbits under 1.0% halothane anesthesia were divided into four groups: (1) nonischemic controls, (2) 60 minutes of uninterrupted focal ischemia, (3) 2 x 30-minute periods of focal ischemia separated by a 5-minute reperfusion, and (4) 4 x 15-minute periods of focal ischemia separated by three 5-minute reperfusion periods. Focal ischemia was produced by occlusion of both the middle cerebral and ipsilateral anterior cerebral arteries. After the final occlusion, there was a 3-hour reperfusion period in all groups. Regional cerebral and cortical blood flow, brain pHi, and NADH fluorescence were measured with in vivo panoramic fluorescence imaging. During occlusion, regional cerebral and cortical blood flows and NADH fluorescence values were not different among the groups. Brain pHi was significantly lower in the 4 x 15-minute group compared with the 1 x 60-minute group (6.57 +/- 0.02 versus 6.73 +/- 0.06; P < .03) but not significant when compared with the 2 x 30-minute group. During the short reperfusion periods, all parameters returned to normal except for NADH fluorescence levels, which remained elevated. During the postischemic final reperfusion period, there was a mild brain alkalosis of approximately 7.1 in all groups. There were no significant differences in NADH fluorescence among groups during the final reperfusion. Regional cerebral and cortical blood flow returned to near normal values in all groups. This study demonstrates that intermittent reperfusion during temporary focal ischemia has different effects on the intracytoplasmic and the intramitochondrial compartments: worsening of brain cytoplasmic pHi but no significant differences in the oxidation/reduction level of mitochondrial NADH.
    Stroke 09/1995; 26(8):1444-51; discussion 1451-2. DOI:10.1161/01.STR.26.8.1444 · 6.02 Impact Factor

Publication Stats

1k Citations
240.58 Total Impact Points

Institutions

  • 1999–2003
    • Mayo Foundation for Medical Education and Research
      • Department of Neurosurgery
      Scottsdale, AZ, United States
    • Graduate School USA
      Washington, Washington, D.C., United States
  • 1975–2003
    • Mayo Clinic - Rochester
      • Department of Neurosurgery
      Rochester, Minnesota, United States