Molecular biodiversity and population structure in common ash (Fraxinus excelsior L.) in Britain: implications for conservation.

Current forestry policy promotes the use of local seed for new plantings, on the assumption that local material may be better adapted to local conditions. However, landscape-scale genetic studies which are necessary to underpin conservation and breeding strategies are often lacking. We investigated molecular diversity in common ash (Fraxinus excelsior L.) sampled from 42 British and six French sites with microsatellites. Chloroplast haplotype H04 was the most common and widespread in Britain, although rare and localized individuals with H02 and H09 were also detected. In addition, three new chloroplast haplotypes were identified, and these were rare and highly localized. In terms of nuclear microsatellite markers, allelic richness differed between sites and decreased in an east to west direction. Differentiation between sites was often very low (mean F(ST) 0.025), indicating few differences between the majority of sites. There was a clear excess of homozygotes (mean H(O) 0.669, mean H(E) 0.818) and a relatively high F(IS) (mean 0.182), suggests a consistent level of inbreeding or a widespread Wahlund effect in many F. excelsior sites. Gene pool ancestry analysis suggested that the majority of British F. excelsior belongs to a single meta-population which covers mainland western and central Europe. Three northern and western sites diverged markedly from the dominant population, and may represent remnants of two late potential Ice Age refugia in northern Britain. The data provide new information which will aid development of appropriate conservation policies for ash and other wind pollinated tree species.

Contemporary pollen flow, characterization of the maternal ecological neighbourhood and mating patterns in wild cherry (Prunus avium L.).

Conversion of lowland woodland to agricultural land and resulting fragmentation in Britain has been ongoing since Neolithic times. To counteract this decline, plantations of native species, often based on non-British planting stock, have been established. This may ultimately be detrimental to the integrity of the native gene pool. We explore the genetic and ecological factors influencing the success of components of the local pollen pool, including the effect of a non-native planting on an ancient woodland population of wild cherry. Wild cherry exhibits gametophytic self-incompatibility (GSI) and vegetative reproduction, both of which may be determinants of paternal success. The majority (61%) of the successful pollen originated from within the study site with a maximum pollen transfer distance of 694 m. There was a distinct departure from random mating, with over half the successful pollen originating from trees which occur within 100 m of the mother tree. Self-incompatibility, clonality, tree size and proximity to the mother tree were all found to influence paternal success. Kinship of pollen gametes within a maternal progeny was highest when a mother tree was surrounded by a large number of ramets of a single, compatible clone consisting of large, adult trees. Although the contribution from the non-native plantation is currently low, it is likely that this will increasingly contribute to the progeny of the adjacent ancient population as it matures. The results clearly show that in self-incompatible species, such as P. avium, close neighbours may be pollinated by very different components of the local pollen pool.

Sevoflurane immediate preconditioning alters hypoxic membrane potential changes in rat hippocampal slices and improves recovery of CA1 pyramidal cells after hypoxia and global cerebral ischemia.

Pretreatment with anesthetics before but not during hypoxia or ischemia can improve neuronal recovery after the insult. Sevoflurane, a volatile anesthetic agent, improved neuronal recovery subsequent to 10 min of global cerebral ischemia when it was present for 1 h before the ischemia. The mean number of intact hippocampal cornus ammonis 1 (CA1) pyramidal neurons in rats subjected to cerebral ischemia without any pretreatment was 17+/-5 (neurons/mm+/-S.D.) 6 weeks after the ischemia; naïve, non-ischemic rats had 177+/-5 neurons/mm. Rats pretreated with either 2% or 4% sevoflurane had 112+/-57 or 150+/-15 CA1 pyramidal neurons/mm respectively (P<0.01) 6 weeks after global cerebral ischemia. In order to examine the mechanisms of protection we used hypoxia to generate energy deprivation. Intracellular recordings were made from CA1 pyramidal neurons in rat hippocampal slices; the recovery of resting and action potentials after hypoxia was used as an indicator of neuronal survival. Pretreatment with 4% sevoflurane for 15 min improved neuronal recovery 1 h after the hypoxia; 90% of the sevoflurane-pretreated neurons recovered while none (0%) of the untreated neurons recovered. Pretreatment with sevoflurane enhanced the hypoxic hyperpolarization(-6.4+/-0.6 vs. -3.3+/-0.3 mV) and reduced the final level of the hypoxic depolarization (-39+/-6 vs. -0.3+/-2 mV) during hypoxia. Chelerythrine (5 muM), a protein kinase C/protein kinase M inhibitor, blocked both the improved recovery (10%) and the electrophysiological changes with 4% sevoflurane preconditioning. Two percent sevoflurane for 15 min before hypoxia did not improve recovery (0% recovery both groups) and did not enhance the hypoxic hyperpolarization or reduce the final depolarization during hypoxia. However if 2% sevoflurane was present for 1 h before the hypoxia then there was significantly improved recovery, enhanced hypoxic hyperpolarization, and reduced final depolarization. Thus we conclude that sevoflurane preconditioning improves recovery in both in vivo and in vitro models of energy deprivation and that preconditioning enhances the hypoxic hyperpolarization and reduces the hypoxic depolarization. Anesthetic preconditioning may protect neurons from ischemia by altering the electrophysiological changes a neuron undergoes during energy deprivation.

Thresholds of biodiversity and ecosystem function in a forest ecosystem undergoing dieback.

Ecological thresholds, which represent points of rapid change in ecological properties, are of major scientific and societal concern. However, very little research has focused on empirically testing the occurrence of thresholds in temperate terrestrial ecosystems. To address this knowledge gap, we tested whether a number of biodiversity, ecosystem functions and ecosystem condition metrics exhibited thresholds in response to a gradient of forest dieback, measured as changes in basal area of living trees relative to areas that lacked recent dieback. The gradient of dieback was sampled using 12 replicate study areas in a temperate forest ecosystem. Our results provide novel evidence of several thresholds in biodiversity (namely species richness of ectomycorrhizal fungi, epiphytic lichen and ground flora); for ecological condition (e.g. sward height, palatable seedling abundance) and a single threshold for ecosystem function (i.e. soil respiration rate). Mechanisms for these thresholds are explored. As climate-induced forest dieback is increasing worldwide, both in scale and speed, these results imply that threshold responses may become increasingly widespread.

The differential effects of volatile anesthetics on electrophysiological and biochemical changes during and recovery after hypoxia in rat hippocampal slice CA1 pyramidal cells.

Two volatile agents, isoflurane and sevoflurane have similar anesthetic properties but different potencies; this allows the discrimination between anesthetic potency and other properties on the protective mechanisms of volatile anesthesia. Two times the minimal alveolar concentration of an anesthetic is approximately the maximally used clinical concentration of that agent; this concentration is 2% for isoflurane and 4% for sevoflurane. We measured the effects of isoflurane and sevoflurane on cornus ammonis 1 (CA1) pyramidal cells in rat hippocampal slices subjected to 10 min of hypoxia (95% nitrogen 5% carbon dioxide) and 60 min of recovery. Anesthetic was delivered to the gas phase using a calibrated vaporizer for each agent. At equipotent anesthetic concentrations, sevoflurane (4%) but not isoflurane (2%), enhanced the initial hyperpolarization (6.7 vs. 3.4 mV), delayed the hypoxic rapid depolarization (521 vs. 294 s) and reduced peak hypoxic cytosolic calcium concentration (203 vs. 278 nM). While both agents reduced the final membrane potential at 10 min of hypoxia compared with controls, 4% sevoflurane had a significantly greater effect than 2% isoflurane (-24.4 vs. -3.5 mV). The effect of these concentrations of isoflurane and sevoflurane was not different for sodium, potassium or ATP concentrations at 10 min of hypoxia, the only difference at 5 min of hypoxia was that ATP was better maintained with 4% sevoflurane (2.2 vs. 1.3 nmol/mg). If the same absolute concentration (4%) of isoflurane and sevoflurane is compared then the cellular changes during hypoxia are similar for both agents and they both improve recovery. We conclude that an anesthetic's absolute concentration and not its anesthetic potency correlates with improved recovery of CA1 pyramidal neurons. The mechanisms of sevoflurane-induced protection include delaying and attenuating the depolarization and the increase of cytosolic calcium and delaying the fall in ATP during hypoxia.

Desflurane improves the recovery of the evoked postsynaptic population spike from CA1 pyramidal cells after hypoxia in rat hippocampal slices.

Desflurane is a volatile anesthetic that allows rapid induction and emergence, reduces cerebral metabolism, and enhances tissue perfusion. We studied the effect of treatment with 4%, 6%, and 12% desflurane on hypoxic neuronal damage by comparing the size of the postsynaptic evoked population spike recorded from the cornu ammonis 1 (CA1) pyramidal cell layer of rat hippocampal slices before and 2 hours after a hypoxic insult. When the tissue was treated with 6% desflurane before, during, and after 3.5 minutes of hypoxia, recovery was significantly better in slices exposed to desflurane (37% +/- 9%) compared with untreated hypoxic slices (15% +/- 5%). A lower (4%) or higher (12%) concentration of desflurane did not significantly improve recovery after 3.5 minutes of hypoxia. In the period before hypoxia, 12% and 6% desflurane significantly increased the latency and decreased the amplitude of the postsynaptic population spike; 4% desflurane had a similar but nonsignificant effect on latency and amplitude. We conclude that 6% desflurane, a clinically useful concentration (1 minimal alveolar concentration), improved the recovery of postsynaptic evoked responses in rat hippocampal slices after 3.5 minutes of hypoxia. In vivo studies must be conducted to assess the potential clinical significance of 6% desflurane's neuroprotective activity.

Substantial heritable variation for susceptibility to Dothistroma septosporum within populations of native British Scots pine (Pinus sylvestris).

The threat from pests and pathogens to native and commercially planted forest trees is unprecedented and expected to increase under climate change. The degree to which forests respond to threats from pathogens depends on their adaptive capacity, which is determined largely by genetically controlled variation in susceptibility of the individual trees within them and the heritability and evolvability of this trait. The most significant current threat to the economically and ecologically important species Scots pine (Pinus sylvestris) is dothistroma needle blight (DNB), caused by the foliar pathogen Dothistroma septosporum. A progeny-population trial of 4-year-old Scots pine trees, comprising six populations from native Caledonian pinewoods each with three to five families in seven blocks, was artificially inoculated using a single isolate of D. septosporum. Susceptibility to D. septosporum, assessed as the percentage of non-green needles, was measured regularly over a period of 61 days following inoculation, during which plants were maintained in conditions ideal for DNB development (warm; high humidity; high leaf wetness). There were significant differences in susceptibility to D. septosporum among families indicating that variation in this trait is heritable, with high estimates of narrow-sense heritability (0.38-0.75) and evolvability (genetic coefficient of variation, 23.47). It is concluded that native Scots pine populations contain sufficient genetic diversity to evolve lower susceptibility to D. septosporum through natural selection in response to increased prevalence of this pathogen.

Rebound hypertension after sodium nitroprusside-induced hypotension.

Patients undergoing surgical procedures using sodium nitroprusside-induced hypotension were studied to determine the role of the renin-angiotensin system in the pathogenesis of rebound hypertension (RH) after discontinuing sodium nitroprusside (SNP) infusion. Retrospective observations documented RH in 9 of 12 patients (group I) with a systolic blood pressure (SBP) increase from 112 +/- 3.92 before SNP to 144 +/- 5.60 torr 10 min after SNP (p less than 0.001). In 12 patients (group II), plasma renin activity (PRA) rose from 950 +/- 432 to 3,611 +/- 1.874 pg/ml/hr (p less than 0.0005) during SNP and remained elevated (2,504 +/- 792 pg/ml/hr) 30 min after cessation of SNP. SBP rose from a control (pre-SNP) value of 112 +/- 5.24 to 129 +/- 8.52 torr after discontinuation of SNP (p less than 0.05). Significant PRA and SBP changes did not occur in a matched group of patients (group III) who did not receive SNP. That RH after cessation of SNP infusion was associated with persistent elevation of PRA leads us to suggest that RH may be attributable to the unopposed effects of the renin-angiotensin system after the rapid plasma disappearance of SNP.

The barbiturate thiopental reduces ATP levels during anoxia but improves electrophysiological recovery and ionic homeostasis in the rat hippocampal slice.

The barbiturate anesthetic thiopental enhances recovery of the evoked population spike recorded from rat hippocampal slices after short periods of anoxia. Thiopental reduces changes in sodium, potassium and calcium but enhances the fall in ATP levels during anoxia. The postsynaptic population spike recorded from the CA1 pyramidal cell region of the slices treated with thiopental (600 microM) recovered to 67% of the preanoxic amplitude after 3.5 min of anoxia. There was less recovery (24%) when a lower concentration of thiopental (250 microM) was used. Untreated slices recovered to only 10% of their preanoxic amplitude after 3.5 min of anoxia. Other studies have demonstrated that maintaining ATP levels during anoxia may be an important mechanism of protection. In contrast to those studies, thiopental was protective although it enhanced the fall of ATP levels after 3.5 min of anoxia in the CA1 region and after 3.5 and 5 min in the dentate region. Thus enhanced recovery of the population spike with thiopental is not due to its preservation of ATP levels. This result allows a clear separation of improved ATP levels during anoxia from other mechanisms of protection. We therefore looked for other mechanisms of protection. Sodium and potassium levels were measured after 10 min of anoxia. In untreated tissue, sodium levels in the slice rose and potassium levels fell significantly. In thiopental-treated tissue, changes in sodium and potassium caused by anoxia and by veratridine under normoxic conditions were significantly reduced. During anoxia calcium-45 uptake increases; thiopental significantly reduces this uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of blocking sodium influx on anoxic damage in the rat hippocampal slice.

The in vitro rat hippocampal slice was used to study the effect of tetrodotoxin, a sodium channel blocker, on anoxic damage. Tetrodotoxin improved recovery of the evoked population spike after anoxia and reduced the fall in adenosine 5'-triphosphate during anoxia. Electrophysiological responses to perforant pathway stimulation were recorded in the dentate granule cell layer before, during and after 10 min of anoxia, with and without tetrodotoxin. Preincubation with tetrodotoxin permitted recovery of the evoked population spike to 43 +/- 10% (mean +/- standard error) in the post-anoxic period; this compared to 3 +/-3% recovery in untreated tissue (P less than 0.005). Similar studies of the CA1 pyramidal cells, which are more sensitive to anoxia, showed that tetrodotoxin improved recovery of the postsynaptic response after 5 min of anoxia. The recovery was 69 +/- 15% of its pre-anoxic level when treated with tetrodotoxin. This compares to no recovery in untreated tissue (P less than 0.005). Biochemical studies demonstrated a significantly reduced fall in adenosine 5'-triphosphate levels during levels in the dentate granule cell layer fell to 1.4 nM/mg dry wt, whereas following treatment with tetrodotoxin they only fell to 2.2 nM/mg. Since it required only 5 min of anoxia to damage the CA1 pyramidal cells, adenosine 5'-triphosphate levels were measured in this region after 5 min of anoxia. Adenosine 5'-triphosphate levels in the CA1 region fell to 2.2 nM/mg in untreated tissue after 5 min of anoxia, compared to 2.9 nM/mg in the tetrodotoxin-treated tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Lidocaine attenuates apoptosis in the ischemic penumbra and reduces infarct size after transient focal cerebral ischemia in rats.

Lidocaine is a local anesthetic and antiarrhythmic agent. Although clinical and experimental studies have shown that an antiarrhythmic dose of lidocaine can protect the brain from ischemic damage, the underlying mechanisms are unknown. In the present study, we examined whether lidocaine inhibits neuronal apoptosis in the penumbra in a rat model of transient focal cerebral ischemia. Male Wistar rats underwent a 90-min temporary occlusion of middle cerebral artery. Lidocaine was given as an i.v. bolus (1.5 mg/kg) followed by an i.v. infusion (2 mg/kg/h) for 180 min, starting 30 min before ischemia. Rats were killed and brain samples were collected at 4 and 24 h after ischemia. Apoptotic changes were evaluated by immunohistochemistry for cytochrome c release and caspase-3 activation and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) for DNA fragmentation. Cytochrome c release and caspase-3 activation were detected at 4 and 24 h after ischemia and DNA fragmentation was detected at 24 h. Double-labeling with NeuN, a neuronal marker, demonstrated that cytochrome c, caspase-3, and TUNEL were confined to neurons. Lidocaine reduced cytochrome c release and caspase-3 activation in the penumbra at 4 h and diminished DNA fragmentation in the penumbra at 24 h. Lidocaine treatment improved early electrophysiological recovery and reduced the size of the cortical infarct at 24 h, but had no significant effect on cerebral blood flow in either the penumbra or core during ischemia. These findings suggest that lidocaine attenuates apoptosis in the penumbra after transient focal cerebral ischemia. The infarct-reducing effects of lidocaine may be due, in part, to the inhibition of apoptotic cell death in the penumbra.

Treatment of intraoperative hypertensive emergencies in patients with intracranial disease.

In patients with neuropathologic processes leading to disturbed cerebrovascular autoregulation, sudden increases in arterial blood pressure may lead to a sudden elevation in cerebral blood flow and intracranial pressure. Therefore, sudden increases in arterial pressure should be assiduously avoided in the perioperative period. Hypertensive episodes may occur at any time during anesthesia, but are more likely to occur (1) during laryngoscopy and intubation, (2) at the time of skin incision, (3) at extubation, and (4) during awakening. In patients with cardiovascular disease, such hypertensive episodes may also cause deterioration of the cardiovascular situation. Catecholamines are the principal mediators of such intraoperative hypertensive reactions. There are 2 options available to the anesthesiologist: (1) attempt to suppress this response after it has occurred, or (2) prevent its occurrence at the outset. Treatment of hypertension often relies on agents that relax vascular smooth muscle. In patients with compromised intracranial compliance, however, cerebral vasodilation must be avoided because it leads to an increase in cerebral blood volume. This, in turn, may raise intracranial pressure and result either in herniation of brain contents or a decrease in cerebral perfusion pressure leading to brain ischemia. Different pharmacologic means of preventing or suppressing such intraoperative hypertensive reactions are reviewed. Many of the drugs reviewed resulted in adverse effects that could preclude their use in patients with reduced intracranial compliance. Alpha- and beta-adrenergic receptor blockers can safely be administered to such patients.

Methods for studying the effect of anesthetics on anoxic damage in the rat hippocampal slice.

The rat hippocampal slice was used as a model system to study the effects of anesthetics on anoxic damage. Thiopental, but not isoflurane, allowed recovery of the postsynaptic population spike evoked from the dentate granule cells. Creatine preincubation protected both dentate granule and CA1 pyramidal cells against anoxic damage. Calcium-free, 10 mM magnesium artificial cerebrospinal fluid (ACSF) was shown to protect CA1 pyramidal cells against anoxic damage. The presynaptic population spike recovered to its preanoxic amplitude after anoxia even under conditions where the postsynaptic population spike demonstrated no recovery. Thus the hippocampal slice is a useful system for studying the effects of anesthetics and other pharmacological agents on anoxic damage.

Effect of small changes in temperature on CA1 pyramidal cells from rat hippocampal slices during hypoxia: implications about the mechanism of hypothermic protection against neuronal damage.

Small reductions in temperature have been shown to improve neurologic recovery after ischemia. We have examined the effect of temperature on biochemical and physiological changes during hypoxia using rat hippocampal slices as a model system. The postsynaptic population spike recorded from the CA1 pyramidal cell region of slices subjected to 7 min of hypoxia with hypothermia (34 degrees C) recovered to 73% of its prehypoxic level; slices subjected to the same period of hypoxia at 37 degrees C did not recover. After 7 min of hypoxia ATP fell to 48% of its prehypoxic concentration at 34 degrees C and 30% at 37 degrees C. Potassium fell to 86% during 7 min of hypoxia with hypothermia, this compares to a fall to 58% at 37 degrees C. The increase in sodium after 7 min of hypoxia was also attenuated by hypothermia (133% vs. 163% of its prehypoxic concentration). When the hypoxic period was shortened to 3 min (37 degrees C) the population spike recovered to 94%. If the temperature was increased to 40 degrees C there was only 7% recovery of the population spike after 3 min of hypoxia. With hyperthermia (40 degrees C), ATP fell to 33% after 3 min of hypoxia, this compares to 81% at normothermia. Potassium fell to 76% after 3 min of hypoxia with hyperthermia, this compares to 91% at 37 degrees C. Sodium concentrations increased with hyperthermia before hypoxia, at 3 min of hypoxia there was no significant difference between the hyperthermic and normothermic tissue; there was a large increase in sodium with hyperthermia after 5 min of hypoxia (209% vs. 146%). We conclude that the improved recovery after hypothermic hypoxia is at least in part due to the attenuated changes in ATP, potassium and sodium during hypoxia and that the worsened recovery with hyperthermia is due to an exacerbation of the change in ATP, potassium and sodium concentrations during hypoxia.

Anesthetic protection against anoxic damage in the rat hippocampal slice.

Evoked population spikes were recorded from the dentate granule cell layer of hippocampal slices obtained from adult rats. These slices were subjected to short periods of anoxia in the presence of different anesthetics. The recovery of the population spike after anoxia was compared across treatments. Little or no recovery was found after 10 min of anoxia when no anesthetic (4 +/- 4%), 1.5% isoflurane (5 +/- 5%), or 15% isoflurane (0 +/- 0%) was present during the anoxic periods. However, the population spike did recover to 81 +/- 7% of its preanoxic amplitude within 1 h after the anoxia if thiopental 160 mg/liter was present in the perfusate during the anoxia. Fifteen percent isoflurane and 160 mg/liter thiopental were equipotent in reducing the amplitude of the evoked population spike before anoxia but only thiopental protected against the damage after 10 min of anoxia. Our results suggest that the blocking of the evoked population spike by thiopental is not the sole mechanism of its protection against anoxic damage. Isoflurane (1.5%) was able to provide a small degree of protection against shorter periods (7 min) of anoxia.

Anoxia reduces depolarization induced calcium uptake in the rat hippocampal slice.

Veratridine-induced depolarization caused a large increase in Ca uptake in the rat hippocampal slice (30.2 vs. 9.0 nM/mg dry weight). This uptake was reduced to 18.4 nM/mg when veratridine was combined with anoxia. When compared with veratridine exposure alone, the combination of anoxia and veratridine increased intracellular Na (460 vs. 380 microM/g), decreased intracellular K (30 vs. 40 microM/g) and decreased ATP levels (0.1 vs. 0.8 nM/mg). The changes in Na, K, and ATP should enhance net Ca uptake, yet Ca uptake was reduced. This suggests an effect of anoxia to block Ca channels. In summary anoxia attenuates depolarization-induced Ca uptake. This may represent a mechanism by which neurons are partially protected against anoxic damage which could be more severe if depolarization-induced Ca uptake was not limited.

Intramedullary pressure in syringomyelia: clinical and pathophysiological correlates of syrinx distension.

OBJECTIVE: The pathophysiological effects of syrinx distension are incompletely understood. Although it is generally assumed that the accumulation of fluid within syrinx cavities can contribute to neurological dysfunction, there are no reports describing intramedullary pressure in syringomyelia. The purpose of the current study was to measure syrinx pressures in patients with progressive clinical deterioration and to correlate these data with neurological deficits and intraoperative physiological findings. METHODS: Intramedullary fluid pressure was measured manometrically in 32 patients undergoing syrinx shunting procedures. The data were correlated with syrinx morphology, intraoperative somatosensory evoked potentials, laser Doppler measurements of local spinal cord blood flow (six patients), and neurological findings before and after syrinx decompression. RESULTS: Syrinx pressures recorded under atmospheric conditions ranged from 0.5 to 22.0 cm H2O (mean = 7.7 cm). There was a significant elevation of the cardiac pulse (mean = 0.7 cm H2O) and the respiratory pulse (mean = 1.1 cm H2O) that was consistent with raised cerebrospinal fluid pressure. Syrinx pressures decreased to subatmospheric levels after surgical drainage. In 18 of 24 patients with predrainage somatosensory evoked potential abnormalities, syrinx decompression produced a consistent reduction of N20 latencies (mean change = 0.49 ms +/- 0.094 SE right, P = 0.002; 0.61 ms +/- 0.089 SE left, P = 0.001) and a similar but less consistent increase in N20 amplitudes (mean change = 0.17 mV +/- 0.103 SE right, P = 0.115; 0.31 mV +/- 0.097 SE left, P = 0.027). Measurements of local spinal cord blood flow revealed very low baseline values (mean = 12.2 arbitrary units +/- 13.9 standard deviation), which increased to intermediate levels (mean = 144.7 arbitrary units +/- 42.6 standard deviation) after syrinx decompression. Patients with syrinx pressures greater than 7.7 cm H2O tended to have more rapidly progressive symptoms, exhibited greater improvements after shunting, and had a higher incidence of postoperative dysesthetic pain. CONCLUSION: The current study is the first to measure intramedullary pressure in a human disease. Evidence is presented that distended syringes are associated with varying levels of raised intramedullary pressure that can accentuate or induce neurological dysfunction by the compression of long tracts, neurons, and the microcirculation. Symptoms referrable to raised intramedullary pressure are potentially reversible by syrinx decompression.

Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions.

Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 +/- 1.85 to 27.61 +/- 3.33 torr (p greater than 0.0005) and cerebral perfusion pressure decreased from 89.32 +/- 3.5 to 43.23 +/- 4.60 torr (p less than 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.

Intracranial pressure during nitroglycerin-induced hypotension.

Nitroglycerin was given intravenously to five anesthetized, hyperventilated (PaCO2 25 to 30 torr) patients during craniotomy, to facilitate surgery by creating a relatively bloodless field, and to decrease the potential need to blood transfusion. A subarachnoid screw and an indwelling radial artery catheter were inserted to monitor intracranial pressure (ICP) and mean arterial pressure (MAP). As MAP decreased from 10.4 +/- 4.0 (SE) to 69.0 +/- 1.8 torr, ICP increased from 14.2 +/- 0.7 (SEM) to 30.8 +/- 1.1 torr. Cerebral perfusion pressure decreased from 90.2 +/- 3.6 (SEM) to 38.2 +/- 2.3 torr (p < 0.0005). We attribute this nitroglycerin-induced ICP increase to capacitance vessel dilation within the relatively noncompliant cranial cavity, with subsequent cerebral blood volume increase.

The persistence of a misconception about vision after educational interventions.

Children and adults, like many ancient philosophers, believe that seeing involves emissions from the eye. Several experiments tested the strength of these "extramission" beliefs to determine whether they, like other scientific misconceptions, are resistant to educational experiences. Traditional college-level education had little impact. Presenting a simplified lesson, stressing visual input, and a lesson directly counteracting the vision misconception had an impact, but for older participants the effect was evident only on short-term tests. Despite some gain due to learning, overall the results demonstrated the robustness of extramission beliefs.