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A W Unterberg

Publications and source records attributed to A W Unterberg.

At least 19 recordsLinked to original sources
PubMed2006

Granulocyte colony-stimulating factor does not affect contusion size, brain edema or cerebrospinal fluid glutamate concentrations in rats following controlled cortical impact.

INTRODUCTION: Granulocyte colony-stimulating factor (G-CSF) is an established treatment in the neutropenic host. Usage in head-injured patients at risk for infection may aggravate brain damage. In contrast, evidence of G-CSF neuroprotective effects has been reported in rodent models of focal cerebral ischemia. We investigated effects of G-CSF in acute focal traumatic brain injury (TBI) in rats. METHODS: Thirty-six male Sprague-Dawley rats were anesthetized with 1.2%) to 2.0% isoflurane and subjected to controlled cortical impact injury (CCII). Thirty minutes following CCII, either vehicle or G-CSF was administered intravenously. Animals were sacrificed 24 hours following CCII. Glutamate concentrations were determined in cisternal cerebrospinal fluid (CSF). Brain edema was assessed gravimetrically. Contusion size was estimated by 2,3,5-triphenyltetrazolium chloride staining and volumetric analysis. RESULTS: Dose-dependent leukocytosis was induced by infusion of G-CSF. Physiological variables were unaffected. Water content of the traumatized hemisphere and CSF glutamate concentrations were unchanged by treatment. Contusion volume was similar in all groups. CONCLUSIONS: A single injection of G-CSF did not influence cortical contusion volume, brain edema, or glutamate concentrations in CSF determined 24 hours following CCII in rats. G-CSF, administered 30 minutes following experimental TBI, failed to exert neuroprotective effects.

Animals↗
PubMed2005

Cerebral metabolism and intracranial hypertension in high grade aneurysmal subarachnoid haemorrhage patients.

We evaluated the effect of intracranial hypertension on cerebral metabolism in patients with high grade aneurysmal subarachnoid hemorrhage (SAH) using bedside cerebral microdialysis (MD). Thirty-six patients with SAH were studied and classified into two groups (intracranial pressure, ICP > 20 mmHg, n = 25) and (ICP < 20 mmHg, n = 11). ICP was monitored hourly using an intraventricular drainage (n = 36). The MD catheter was placed after aneurysm clipping into the vascular territory of interest and was perfused with Ringer's solution (0.3 microl/min). The MD samples were collected hourly for measurements of glucose, lactate, and glutamate (CMA 600, Sweden). Lactate/pyruvate ratio was also calculated. To calculate group specific differences, the 24 hours median values of the first 7 days after SAH were compared. Differences were considered statistically significant at P < 0.05. Patient groups were comparable for age, severity of SAH, Fisher's grade and duration of MD sampling. In patients with ICP > 20 mmHg from day 1 to 7 after SAH, extracellular concentrations of glucose were significantly lower, while the lactate/ pyruvate ratio was higher compared to SAH patients with normal ICP values. The differences between groups in glutamate levels was only significant on day 1 after SAH due to high inter-individual differences. We concluded that intracranial hypertension in associated with an anaerobic cerebral metabolism indicated cerebral ischemia in high grade SAH patients.

Brain↗
PubMed2005

Assessment of the relationship between age and continuous intracranial compliance.

The aim of this open, descriptive and prospective study was to determine if the new monitoring parameter "continuous intracranial compliance (cICC)" decreases with age in patients with traumatic brain injury (TBI). 30 patients with severe and moderate TBI (Glasgow Coma Scale score < or = 10) contributing to a European multicenter study, organized by the Brain-IT group, underwent computerized monitoring of blood pressure, intracranial pressure (ICP), cerebral perfusion pressure and cICC. Regression analyses of individual median ICP and median cICC versus patients' age revealed no significant dependency. Median cICC declined significantly with increasing ICP (when median ICP = 10, 20 and 30 mmHg, cICC = 0.64, 0.56 and 0.42 ml/mmHg respectively, p < 0.05). These three ICP groups were then subdivided according to age (0-20, 21-40, 41-60 and 61-80 years). Median cICC declined with age in both high ICP groups (median ICP = 20,30 mmHg). Percentage cICC values below a set pathological threshold of lower than 0.05 ml/mmHg across the four age groups were 28% (0-20 yrs), 59% (21-40 yrs), 60% (41-60 yrs) and 70% (61-80 yrs) respectively. The observed phenomenon of decreased intracranial volume challenge compensation with advancing age may contribute to the well-known fact of a worse outcome in elderly patients after TBI.

Adolescent↗
PubMed2005

The antioxidant effect of N-acethylcysteine on experimental contusion in rats.

N-acethylcysteine (NAC) is known to have direct and indirect antioxidant abilities. We investigated the potential protective effect of NAC on ICP, brain edema and contusion volume after Controlled Cortical Impact (CCI) injury. A moderate CCI injury was induced on the left hemisphere in 48 Sprague Dawley rats. The animals were treated with intraperitoneal injection of NAC (163 mg/kg/KG) or physiological saline. Measurements of intracranial pressure (ICP) were performed and brains were removed at 24 hours. Gravimetric analysis of post-traumatic edema and morphometric measurements (TTC staining) of contusion volume were carried out in 24 animals, respectively. ICP measurements increased significantly over time with no significant differences between both groups. The relative difference in water content in NAC treated animals (1.45 +/- 0.1%) did not differ significantly versus placebo (1.47 +/- 0.2%). The contusion volume was diminished by 19% in the NAC group (53.52 +/- 5.3 mm3) versus placebo (66.28 +/- 4.7 mm3) without showing statistical significance. The antioxidant properties of NAC did not affect intracranial pressure or posttraumatic brain edema formation, although the moderate reduction of contusion volume might reveal beneficial effects on focal contusion.

Acetylcysteine↗
PubMed2005

The use of neuronavigation in transnasal transsphenoidal pituitary surgery.

BACKGROUND: Recurrent pituitary adenomas and localisation of microadenomas potentially cause difficulties during transsphenoidal pituitary surgery. Neuronavigation might improve tumour removal in such cases. METHODS: Between 12/98 and 04/01 transnasal transsphenoidal adenomectomies were performed in 152 patients at our department. In 16 of these patients neuronavigation was chosen as a means of safely approaching the tumour and improving the efficacy of tumour localisation and removal. Mean age of the 7 female and 9 male patients was 51.8 +/- 13.7 years. Patients were subdivided according to the underlying pathology, i. e. microadenomas (n = 8, mean diameter: 5.75 +/- 2.1 mm), and recurrent adenomas (n = 8). The imaging of adenomas was achieved in preoperatively obtained 1 mm transversely reconstructed magnetic resonance sections from a dynamic enhanced 3D-FFE sequence (Gyroscan 1.5 Tesla, Philips). Contour-guided surgery via a transnasal transsphenoidal approach to the sella region was performed using the MKM navigation microscope (Zeiss). RESULTS: Endocrinologic studies revealed secretion of growth hormone (GH), ACTH, and follicle stimulating hormone (FSH) in 5, 4, and 1 patient, respectively. The remaining 7 adenomas did not secrete any hormones. All pituitary tumours were accurately localised by neuronavigation. In all recurrent macroadenomas, the tumours were rapidly and safely approached through the scarred tissue and the tumour volume was significantly reduced. Neither intraoperative nor postoperative complications occurred in these patients. In hormone-secreting pituitary tumours with far lateral localisation, endocrinologic abnormalities were corrected in 5 patients, while hormone secretion was significantly decreased in 3 patients. In 1 patient with histologically verified adenoma, hormone secretion did not significantly change following surgical removal. CONCLUSIONS: Neuronavigation in pituitary surgery is of use in only a small number of cases. Nevertheless, we suggest that contour-guided, transsphenoidal adenomectomy may prove helpful in approaching recurrent adenomas and localising lateral microadenomas.

Acromegaly↗
PubMed2005

Acute haemorrhage into a microcystic meningioma leading to cerebral herniation.

Low-grade (WHO level I) meningiomas are slow-growing, benign tumours typically presenting with unspecific symptoms (e.g. headache), seizures, cranial nerve compression and neuropsychological symptoms determined by location and size of the lesion. Haemorrhagic onset and sequelae are rare, and have been described infrequently. This is a case of a 50-year-old male presenting with signs of tentorial herniation secondary to hyperacute intratumoural haemorrhage (ITH) into a previously undiagnosed meningioma. Emergency surgical decompression and exstirpation of the lesion helped to achieve a favourable outcome. ITH has been described in all including benign intracranial neoplasms. Factors associated with a higher risk for haemorrhage in meningiomas are discussed. Though haemorrhages associated with meningiomas have been reported, ITH into low-grade meningiomas leading to herniation remains a rarity. Bearers of known lesions and their treating physicians who opt for conservative or delayed treatment should be aware of this remote complication.

Acute Disease↗
PubMed2004

Differential effects of prolonged isoflurane anesthesia on plasma, extracellular, and CSF glutamate, neuronal activity, 125I-Mk801 NMDA receptor binding, and brain edema in traumatic brain-injured rats.

BACKGROUND: Volatile anesthetics reduce neuronal excitation and cerebral metabolism but can also increase intracellular water accumulation in normal and injured brains. While attenuation of neuronal excitation and glutamate release are beneficial under pathological conditions, any increase in edema formation should be avoided. In the present study we investigated duration-dependent effects of the commonly used isoflurane/nitrous oxide (N2O) anesthesia on EEG activity, specific NMDA receptor binding, extracellular, CSF, and plasma glutamate, and cerebral water content in brain-injured rats subjected to short (30 minutes) or prolonged (4 hours) anesthesia. METHODS: Before controlled cortical impact injury (CCI), during prolonged (4-8 hours) or short anesthesia (7.5-8 hours after CCI), and before brain removal, changes in neuronal activity were determined by quantitative EEG analysis and glutamate was measured in arterial plasma. Brains were processed to determine acute and persisting changes in cerebral water content and 125I-Mk801 NMDA receptor binding at 8 and 32 hours after CCI, i.e., immediately or 24 hours after short or prolonged anesthesia. During prolonged anesthesia glutamate was measured via microdialysis within the cortical contusion. CSF was sampled before brain removal. FINDINGS: Prolonged isoflurane (1.8 vol%) anesthesia significantly increased EEG activity, plasma, cortical extracellular, and CSF glutamate, cortical and hippocampal 125I-Mk801 NMDA receptor binding, and cerebral water content in brain-injured rats. These changes were partially reversible within 24 hours after prolonged anesthesia. At 24 hours, CSF glutamate was significantly reduced following long isoflurane anesthesia compared to rats previously subjected to short anesthesia despite an earlier significant increase. Conclusions. The partially reversible increases in EEG activity, 125I-Mk801 NMDA receptor binding, cerebral water content, plasma and CSF glutamate appear important for physiological, pathophysiological, and pharmacological studies requiring prolonged anesthesia with isoflurane. Increases in extracellular cortical and plasma glutamate could contribute to acute aggravation of underlying tissue damage.

Anesthetics, Inhalation↗
PubMed2004

Neuronal activity and cortical perfusion determined by quantitative EEG analysis and laser doppler flowmetry are uncoupled in brain injured rats.

Following traumatic brain injury uncoupling of metabolism from perfusion, reflected by an increase in cellular activity in face of reduced perfusion contributes to secondary tissue damage. Standard autoradiographic techniques employed to study metabolism and perfusion are limited by the inability to perform longitudinal investigations. Therefore, the aims of this study were to investigate if metabolic uncoupling can be studied by applying noninvasive and non-radioactive methods. For this, quantitative EEG analysis and laser Doppler flowmetry were employed to determine changes in EEG activity as a global measure of neuronal activity and pericontusional cortical perfusion during the early phase following controlled cortical impact injury (CCII). In eight rats changes in neuronal activity and pericontusional cortical perfusion were determined before, at 4 and 24 hours after CCII. Neuronal activity was significantly increased by 40% at 4 hours after CCII followed by a significant decrease by 60% at 24 hours compared to pre-trauma levels. Pericontusional cortical perfusion was significantly reduced by 45% and 18% at 4 and 24 hours after CCII. respectively. Non-radioactive methods like quantitative EEG analysis and laser Doppler flowmetry can be used to reveal underlying uncoupling of EEG activity from cortical perfusion which is mostly sustained in the early phase following CCII.

Anesthesia Recovery Period↗
PubMed2004

Edema and brain trauma.

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury (TBI) as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" due to blood-brain barrier (BBB) disruption resulting in extracellular water accumulation and "cytotoxic/cellular" due to sustained intracellular water collection. A third type, "osmotic" brain edema is caused by osmotic imbalances between blood and tissue. Rarely after TBI do we encounter a "hydrocephalic edema/interstitial" brain edema related to an obstruction of cerebrospinal fluid outflow. Following TBI, various mediators are released which enhance vasogenic and/or cytotoxic brain edema. These include glutamate, lactate, H(+), K(+), Ca(2+), nitric oxide, arachidonic acid and its metabolites, free oxygen radicals, histamine, and kinins. Thus, avoiding cerebral anaerobic metabolism and acidosis is beneficial to control lactate and H(+), but no compound inhibiting mediators/mediator channels showed beneficial results in conducted clinical trials, despite successful experimental studies. Hence, anti-edematous therapy in TBI patients is still symptomatic and rather non-specific (e.g. mannitol infusion, controlled hyperventilation). For many years, vasogenic brain edema was accepted as the prevalent edema type following TBI. The development of mechanical TBI models ("weight drop," "fluid percussion injury," and "controlled cortical impact injury") and the use of magnetic resonance imaging, however, revealed that "cytotoxic" edema is of decisive pathophysiological importance following TBI as it develops early and persists while BBB integrity is gradually restored. These findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence.

Acidosis, Lactic↗
PubMed2003

Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO2.

The objective of the present study was to test the new continuous intracranial compliance (cICC) device in terms of data quality, relationship to intracranial pressure (ICP) and brain tissue oxygenation (PtiO2). A total of 10 adult patients with severe traumatic brain injury underwent computerized monitoring of arterial blood pressure, ICP, cerebral perfusion pressure, end-tidal CO2, cICC and PtiO2 providing a total of 1726 h of data. (1) The data quality assessed by calculating the 'time of good data quality' (TGDQ, %), i.e. the median duration of artefact-free time as a percentage of total monitoring time reached 98 and 99% for ICP and PtiO2, while cICC measurements were free of artefacts in only 81%. (2) Individual regression analysis showed broad scattered correlation between cICC and ICP ranging from low (r = 0.05) to high (r = 0.52) correlation coefficients. (3) From 225 episodes of increased ICP (ICP > 20 mmHg > 10 min), only 37 were correctly predicted by a preceding decline in cICC to pathological values (< 0.5 ml/mmHg). (4) In all episodes of cerebral hypoxia (PtiO2 < 10 mmHg > 10 min), cICC was not pathologically altered. Based on the present results, we conclude that the current hardware and software version of the cICC monitoring system is unsatisfactory concerning data quality, prediction of increased ICP and revelance of cerebral hypoxic episodes.

Adult↗
PubMed2003

Metabolic changes during impending and manifest cerebral hypoxia in traumatic brain injury.

The objective was to measure metabolic changes monitored by bedside microdialysis during impending and manifest hypoxia in traumatic brain injury. In 41 patients, a PtiO2-catheter (Licox; 1/min) was placed into non-lesioned frontal white matter together with a microdialysis catheter (CMA, hourly). Data were analysed for identification of episodes of impending (PtiO2 < 10 - 15 mmHg > 5 min) and manifest cerebral hypoxia (PtiO2 < 10 mmHg, > 5 min). In 69% of patients hypoxic episodes occurred, most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, glutamate was increased (p = 0.03), while the energy metabolites remained stable. Manifest hypoxia was reflected by significant increases of glutamate (p = 0.007) and lactate (p = 0.044), but normal lactate-pyruvate ratios. We conclude that hyperventilation had a potential adverse effect on cerebral metabolism and was most frequently associated with cerebral hypoxia. A PtiO2 < 10 mmHg can induce metabolic changes with increase of glutamate and lactate. The presence of anaerobic cerebral metabolism probably depends on duration and severity of the hypoxic episode.

Adolescent↗
PubMed2002

Intracranial compliance as a bed-side monitoring technique in severely head-injured patients.

A recently developed monitoring technology makes an on-line assessment of intracranial compliance (ICC) possible. Aims of our research: 1. Course and values of ICC (critical threshold: < 0.5 ml/mmHg) in episodes of pathological intracranial pressure (ICP) (> 20 mmHg) and reduced cerebral oxygenation (brain tissue PO2 (PtiO2) < 10 mmHg). 2. Mean ICC in different ages. 3. Relationship between ICC and outcome. 4. Evaluation of ICC as routine monitoring parameter by calculation of s.c. time-of-good-data-quality (TGDQ). Computer data assessment of 7 patients with severe closed head-injury was performed providing 830 hours of data. TGDQ resulted from the formula: TGDQ (%) = artifact free time (min) x 100 (%)/total monitoring time (min). Outcome was assessed 6 months posttrauma (Glasgow Outcome Score (GOS). 1. Analysis revealed 43 episodes of pathologically elevated ICP and 39 of critical ICC. In 17 cases overlapping periods were found. In 9 of these ICC preceded ICP. Reduced cerebral oxygenation was neither related with high ICP nor low ICC. 2. ICC was found to be age-related. At a cut-off-point of 20 mmHg in ICP, ICC in children (< or = 16 years) was 0.9, in adults (17-60 years) 0.7 and in elderly (> 60 years) 0.6 ml/mmHg. 3. Adverse outcome was indicated best by high ICP (up to 45% of monitoring time) followed by low ICC (up to 41% of monitoring time). 4. TGDQ in ICC was 72% compared to 95% in ICP and 98% in PtiO2. In predicting adverse outcome, ICP was equal to ICC. The different ICC in each age class points to the need of age-adjusted thresholds. Further refinements of ICC technology are needed to improve ICC data quality and therefore become a useful tool in neuromonitoring.

Adolescent↗
PubMed2002

Neuronal activity determined by quantitative EEG and cortical microdialysis is increased following controlled cortical impact injury in rats.

Following brain injury increased glutamate release is linked to sustained neuronal activation resulting in excitotoxic tissue damage. Isoflurane anesthesia has been shown to decrease electroencephalographic (EEG) activity and extracellular (e.c.) glutamate, possibly attenuating excitotoxic tissue damage. However, based on clinical experience EEG activity can fluctuate despite stable isoflurane concentrations. Therefore, the aims of this study were to investigate the impact of neuronal activity assessed by quantitative EEG on e.c. glutamate during isoflurane anesthesia following controlled cortical impact injury (CCII). In 10 rats balanced anesthesia using isoflurane was induced at 4 hours after CCII. Under steady-state conditions maintaining isoflurane at 1.8 vol%, EEG was recorded for 3 hours. During this period, e.c. glutamate was sampled in the pericontusional cortex by microdialysis. Despite maintaining isoflurane at 1.8 vol%, neuronal activity expressed as low frequency EEG power showed marked fluctuations. Spontaneous increases in neuronal activity coincided with elevated e.c. glutamate levels and vice versa. Overall, EEG power correlated significantly with pathologically elevated e.c. glutamate levels (n = 58; R2 = 0.54; p < 0.05). Despite unchanged isoflurance concentrations fluctuations in neuronal activity were reflected by altered EEG power and e.c. glutamate concentrations. Therefore, neuronal activity needs to be considered for the interpretation of e.c. glutamate levels.

Animals↗
PubMed2002

Norepinephrine is superior to dopamine in increasing cortical perfusion following controlled cortical impact injury in rats.

Following traumatic brain injury catecholamines are routinely applied to increase cerebral perfusion. To date, it remains controversial if infusion of catecholamines is associated with diminished cerebral perfusion due to catecholamine-mediated vasoconstriction. The aims of the present study were to investigate the effects of norepinephrine and dopamine on cortical perfusion and brain edema following controlled cortical impact injury (CCII) in rats. Four hours after CCII, rats (n = 22) received either norepinephrine or dopamine with the aim of increasing MABP to 120 mm Hg for 90 minutes. Control rats were given NaCl. Cortical perfusion was measured before, during, and after catecholamine infusion using Laser Doppler flowmetry. Brain swelling was determined directly after the study period (8 hrs after CCII). Following CCII cortical perfusion was reduced by 40% compared to pre-trauma values in all rats. Parallel to the increases in MABP, cortical perfusion was significantly elevated under norepinephrine and dopamine, respectively (p < 0.05). Despite similar MABP values this increase was mostly sustained under norepinephrine. In control rats cortical perfusion remained diminished. Brain swelling was similar in all groups. Both norepinephrine and dopamine significantly increased cortical perfusion following CCII. Norepinephrine, however, was superior to dopamine in CBF. Based on increased CBF and unchanged brain swelling catecholamine-mediated vasoconstriction does not seem to occur under the present study design.

Animals↗
PubMed2002

Cortical hypoperfusion precedes hyperperfusion following controlled cortical impact injury.

Impaired cerebral perfusion contributes to tissue damage following traumatic brain injury. In this longitudinal study persistence of reduced cortical perfusion employing laser doppler flowmetry was investigated following controlled cortical impact injury (CCII). Before, 30 minutes, 6, 24, and 48 hours after CCII, perfusion in pericontusional cortex was determined by moving a laser doppler probe in 50 x 0.2 mm steps over the traumatized hemisphere in 5 rats. Arterial blood gases and mean arterial blood pressure were monitored. Mean arterial blood pressure and arterial blood gases remained stable during the entire experiments. At 30 minutes and 6 hours following CCII, cortical perfusion was significantly diminished by 24% and 43% (p < 0.05), respectively compared to pre-trauma levels. At 24 and 48 hours after CCII, pericontusional blood flow was significantly increased by 64% and 123%. Cortical hypoperfusion found within the early phase following trauma is reversible and precedes a long lasting phase of hyperperfusion. Changes in tissue mediators (endothelin, acidosis, NO) could account for these findings.

Animals↗
PubMed2002

Detection of secondary insults by brain tissue pO2 and bedside microdialysis in severe head injury.

We evaluated bedside cerebral on-line microdialysis for early detection of cerebral hypoxia in patients with traumatic brain injury. 24 severely head injured patients (Glasgow Coma Score < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring using the LICOX (GMS mbH, Germany) microcatheter device. The catheter was placed into the non-lesioned frontal white matter within 32.2 (7-48) hrs post injury. The microdialysis catheter (CMA 100, Sweden) was placed close to the PtiO2 probe via a 2- or 3-way skull screw, connected to a pump and perfused with Ringer solution (0.3 microliter/min). The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate-ratio and glutamate (CMA 600, Sweden). We identified 252 episodes of impending hypoxia (PtiO2 < 15 mm Hg; 11,810 minutes) and 38 episodes of cerebral hypoxia (PtiO2 < 10 mm Hg; 1996 minutes). Before cerebral hypoxia, glucose decreased significantly. Glutamate was unchanged when no hypoxia or impending hypoxia occurred but increased 3-4 fold before a hypoxic episode appeared. We conclude that early metabolic detection of cerebral hypoxia before a critical decrease in brain tissue PtiO2 is seen and possibly allows earlier changes in treatment (e.g. reduction of hyperventilation therapy).

Adolescent↗
PubMed2002

Temporal profiles of extracellular nitric oxide metabolites following aneurysmal subarachnoid hemorrhage.

The temporal profile of nitric oxide metabolite concentrations i.e. nitrite and nitrate (NOx) was investigated in brain parenchyma of patients following aneurysmal subarachnoid hemorrhage (SAH). In a subset of ten patients (7F/3M, age: 47 +/- 14 yrs) included in a prospective clinical trial on neurochemical intensive-care monitoring, microdialysis (MD) probes (CMA70, Sweden) were implanted at time of aneurysm surgery. Samples from patients clipped electively (n = 3) were considered "normal" in regard to SAH patients (n = 7). MD was performed for 162 +/- 63 hrs. NOx was measured off-line using a highly sensitive, fluorometric assay (2-3-diaminonaphtalene, DAN). NOx concentrations determined from electively operated patients averaged 36.7 +/- 9.6 microM (n = 59, pooled data). Regardless of the development of delayed ischemic neurological deficits (DIND), SAH patients showed a specific temporal profile of NOx consisting of an initial peak followed by an exponential decay. In detail, NOx decreased from initial values of 46.2 +/- 34.8 microM to 23.5 +/- 9.0 microM on day 6-7 after SAH (p < 0.05). Following SAH extracellular concentrations of NO metabolites decrease over time. This is in agreement with hypothetical NO scavenging by products of hemolysis. However, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.

Adult↗