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  • 1
    ISSN: 1432-1238
    Keywords: Key words Cerebral blood flow ; CPP management ; Intracranial pressure ; Pressure autoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To ascertain if norepinephrine can be used as part of the cerebral perfusion pressure (CPP) management to increase arterial blood pressure (MAP) without causing cerebral hyperemia after severe head injury (HI).¶Design: Prospective, interventional study.¶Setting: Intensive care unit in a university hospital.¶Patients: Twelve severely HI patients; median Glasgow Coma Scale was 6 (range 3–8).¶Interventions: CPP management ( = 70 mmHg). Pressure autoregulation (assessed by norepinephrine infusion) was defined intact if %CPP/%CVR ≤ 2.¶Results: Cerebral blood flow (CBF: Xe133 inhalation technique), jugular bulb oxygen saturation (SjO2) and transcranial Doppler (TCD) were recorded during the test. Norepinephrine increased CPP by 33 % ( ± 4). Autoregulation was found to be intact in ten patients and defective in two. In the ten patients with preserved autoregulation, CBF decreased from 31 ± 3 to 28 ± 3 ml/100 g/min; in the two patients with impaired autoregulation CBF increased respectively from 16 to 35 and from 21 to 70 ml/100 g/min. SjO2 did not change significantly from baseline. TCD remained within the normal range.¶Conclusions: During CPP management norepinephrine can be used to increase MAP without potentiating hyperemia if pressure autoregulation is preserved. The assessment of pressure autoregulation should be considered as a guide for arterial pressure-oriented therapy after HI.
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  • 2
    ISSN: 0942-0940
    Keywords: Blood brain barrier ; cerebral blood flow ; intracranial pressure ; arachidonic acid ; brain oedema ; evoked potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema. The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15–20 mm2) by intravenously administered Evans Blue dye 2%. Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO2 reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms. The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.
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  • 3
    ISSN: 0942-0940
    Keywords: Brain edema ; blood brain barrier ; serum protein ; evoked potential ; glioma ; cerebral blood flow ; permeability factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO2 reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymor-phonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes. These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.
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  • 4
    ISSN: 0942-0940
    Keywords: Head injury ; cerebral perfusion pressure ; arterial hypotension ; raised intracranial pressure ; outcome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A group of 74 patients with head injury (54 severe, 17 moderate and 3 minor) had continuous monitoring of both arterial and intracranial pressure with computer-based registration of these pressures, cerebral perfusion pressure and other vairables. In 60 patients cerebral perfusion pressure CPP fell below 60 mm Hg for periods of 5 minutes or longer. The distribution over time of these reductions in CPP during up to 12 days of monitoring was studied, and each episode of reduced CPP was attributed to a fall in arterial pressure, an increase in intracranial pressure, or both. Two clusters of reduced CPP were found, one during the first 24 hours of monitoring, when reduced CPP was mainly caused by a reduction in arterial pressure, and the other at 5 or 6 days after injury, when reduced CPP was due mainly to an increase in intracranial pressure. There was a significant correlation between low CPP due to reduced arterial pressure and the Injury Severity Score (p〈0.001), suggesting that resuscitative measures may have been less than optimal in these cases. There was also significant correlation between the duration of low CPP and low arterial pressure and an adverse outcome from injury as assessed at 6, 12 and 24 months after injury (p〈0.001). It is recommended that in patients with severe and significant head injury who require monitoring, this should include both arterial and intracranial pressure, be continued for at least 6 days, that cerebral perfusion pressure should be displayed and recorded, and that particular attention is paid to detecting and correcting even small reductions in arterial pressure, especially those that reduce CPP below 60 mm Hg.
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  • 5
    ISSN: 0942-0940
    Keywords: Bradykinin ; intracranial pressure ; evoked potentials ; cerebral blood flow ; brain edema ; blood brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 μL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 μL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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  • 6
    ISSN: 1432-1238
    Keywords: Key words Cerebral perfusion pressure ; Intracranial pressure ; Mean arterial pressure ; Endothelium ; Pressure autoregulation ; Cerebral blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To investigate the role of the endothelin system in pressure autoregulation of cerebral blood flow (CBF) in rats.¶Design: We tested pressure autoregulation by increasing cerebral perfusion pressure (CPP; mean arterial pressure–intracranial pressure) with norepinephrine (0.08 μg · kg−1· min−1 for 30 min) twice in ten anesthetized normocapnic rats. The first test was performed without (control test) and the second test after administration of the combined endothelin ETA/B receptor antagonist, bosentan, i. v. (30 mg/kg; drug test). CBF was measured by the hydrogen clearance technique.¶Results: During the control test, norepinephrine infusion increased CPP by 21 ± 2 (23 ± 2 %) mmHg (mean ± SEM; p 〈 0.001) and CBF by 3.6 ± 3.1 (6 ± 8 %) ml/100 g/min (p = 0.5, Fig. 1); during the drug test, norepinephrine infusion increased CPP by 18 ± 1 (20 ± 2 %) mmHg (p 〈 0.001) and CBF by 15.8 ± 4.1 (46 ± 13 %) ml/100 g/min (p = 0.004). Mean arterial pressure was not affected by bosentan infusion (p = 0.2). PaC02 levels were stable during the tests (40.2 ± 1.4 mmHg).¶Conclusions: The endothelin system is involved in cerebral pressure autoregulation in a rodent model in vivo. The role of this system under pathophysiologic conditions such as subarachnoid hemorrhage, where basal vascular tone and its regulation may be altered, remains to be defined.
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