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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 2/3 of all patients with thrombosis of the superior sagittal sinus (SSS) develop signs of increased ICP and/or brain oedema (BE). The time of onset and the spectrum of symptoms in SSS thrombosis vary extremely. This variability might be caused by differences in pathomechanism like BE and rise of ICP, parameters studied in the present contribution. 10 domestic pigs received a standardized occlusion of the SSS with two different balloon types (spherical and cylindrical). They were monitored for several systemic and intracranial pressures. After 4 hours of occlusion the brains were examined for BE (Evans blue, water content). They were compared with those of 4 sham-operated control animals. 4 animals underwent cerebral angiography. Within 4 hours ICP rose to 60 mm Hg in the group with the spherical balloon. Normal ICP of 5-10 mm Hg was seen in the group with the cylindrical balloon and in the sham-operated controls. The water content of the white matter was elevated in both occlusion groups differing significantly from the control group. Haemorrhagic infarction of the frontal parts of the cerebrum occurred in animals with concomitant obliteration of bridging and cortical veins. We conclude from our experiments that SSS occlusion may initiate a multitude of possible pathomechanisms depending on the involvement of bridging veins, cortical veins and inner brain veins.
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PMID:Brain oedema and intracranial pressure in superior sagittal sinus balloon occlusion. An experimental study in pigs. 208 3

We studied brain water self diffusion in pseudotumour cerebri by MR-imaging using single spin echo pulse sequences with pulsed magnetic field gradients of different magnitude. The methods is based on the fact that the movement of water molecules is restricted in brain tissue and that accumulation of water in the brain tissue will enhance the self diffusion of water. In order to evaluate the brain water content in pseudotumour cerebri we compared the water self diffusion coefficient in various regions of the brain in pseudotumour patients with that of healthy controls. Ten patients with pseudotumour cerebri were studied. All had increased ICP and increased resistance to CSF outflow. All patients had normal conventional MR spin echo images without focal lesions and a normal sized ventricular system. All patients had abnormal diffusion images showing increased water diffusion. Some patients had in particular increased diffusion in the periventricular regions, others in the whole brain. The diffusion coefficients in all brain regions of interest were significantly higher in patients than in controls. The findings suggest that patients with pseudotumour cerebri have a convective transependymal flow of water causing an interstitial brain oedema and in addition an intracellular brain water accumulation.
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PMID:Brain water accumulation in pseudotumour cerebri demonstrated by MR-imaging of brain water self-diffusion. 208 39

It has been considered that mannitol reduces a raised intracranial pressure effectively by improving pressure volume relationship. The objective of this study is to determine how the pressure volume status is changed by a bolus mannitol administration with using several biomechanical parameters (intracranial pressure, pressure volume index, and intracranial elastance). Our data indicated that mannitol changed the PVI more sensitively than ICP and elastance. "Estimated Intracranial Volume Change (EICVC)" has been newly defined during mannitol infusion on the basis of PVI and ICP change. EICVC for first 30 minutes-period at which the intracranial pressure most vigorously decreased was only about 5 ml in volume. The temporal course of EICVC and ICP were not different, thus, it could account for the change of ICP properly. However, the temporal course of PVI indicating the intracranial venous blood pooling, can not be explained only by EICVC since the PVI has been changed more rapidly than any other parameters. Therefore, we speculated that the ratio of intracranial components could be more largely altered by mannitol than the net of intracranial volume change. The fundamental mechanism of ICP reduction by mannitol is possibly the brain water movement into venous circulation.
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PMID:[PVI in analyzing pressure volume relationship--effect of a bolus mannitol administration]. 212 Nov 96

The effect of THAM on brain oedema parameters was initially investigated in animals with cold brain lesions; THAM was then used in head injury patients, ICP, SAP and CPP were analyzed. In the experiments with rats after freezing lesion, THAM was compared to equivalent doses of Na-bicarbonate. The animals were artificially respirated and sacrificed 6 h after trauma. THAM did significantly reduce water (wet-dry weight technique) and sodium contents in both hemispheres, whereas bicarbonate was ineffective. The potassium contents were even preserved at almost normal levels. In 80 patients receiving alternatively THAM (18-36 g/100-200 ml/1-2h), mannitol (20%, 125-250 ml/20-40 min) or sorbitol (40%, 70-140 ml/20-40 min), the ICP rapidly decreased following THAM infusion. The maximal fall in ICP (33%) was equal to that with mannitol and sorbitol. The slope of ICP decrease was equal with THAM and Mannitol but steeper with sorbitol. With THAM, however, the effect on ICP lasts longer than with osmotherapy. The EEG improved more rapidly after THAM. As shown by blood plasma values, the action of THAM is not based on osmotic effects. The increases in pH and especially in base excess suggest an intracerebral buffering. The encouraging results with THAM require a randomized clinical trial after severe head injury which is presently prepared.
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PMID:A comparative analysis of THAM (Tris-buffer) in traumatic brain oedema. 212 78

Continuous measurement of CBV and CBF by means of laser-Doppler flowmetry was performed to analyze the temporal profile of cerebrovascular response to water accumulation in an infusion model of brain oedema. Using this method, the effect of mannitol on CBV was also examined to determine how mannitol improves the intracranial pressure-volume relationship. The results show that: (1) The presence of an oedema generator elicits a continuous reduction of CBV and a transient reduction of CBF. With cessation of this mechanical force of oedema production, CBV and CBF return to control levels. (2) Mannitol increases CBV and PVI. The improvement of PVI might be due to an increase in CBV as well as ICP reduction.
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PMID:Effect of mannitol on intracranial pressure-volume status and cerebral haemodynamics in brain oedema. 212 81

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 microliters/hr for 3 hrs) of saline, bradykinin (10(-4) to 10(-6) M), arachidonic acid (10(-2) to 10(-3) M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance). ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (++), 20% protein ( ) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.
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PMID:The contribution of secondary mediators to the etiology and pathophysiology of brain oedema: studies using a feline infusion oedema model. 212 86

The water-extractable component of snuff (snuff extract) inhibits the replication of herpes simplex virus (HSV) by suppressing the synthesis of viral DNA. This process probably causes HSV to be oncogenic. To further understand the mechanism of inhibitory action of snuff extract on HSV replication, the effect of snuff extract on the synthesis of viral DNA and proteins in type 1 HSV (HSV-1) infected cells was investigated. Snuff extract inhibited the synthesis of viral DNA and altered the production of certain classes of viral proteins. The syntheses of ICP4, a viral alpha-protein, and ICP8, a beta-protein, were not generally reduced by noncytotoxic concentrations of snuff extract (where ICP = infected cell polypeptide). However, snuff extracts significantly inhibited the production of ICP gC (glycoprotein C), a gamma 2-protein, and the inhibition was in a concentration-dependent fashion: the higher the concentration of snuff extracts, the greater the inhibition. Based on the fact that the production of alpha- and beta-proteins is absolutely necessary for and precedes the viral DNA synthesis and that viral gamma 2-proteins are mostly produced by the newly synthesized viral DNA, it is concluded that snuff extract inhibits HSV-1 DNA replication directly rather than indirectly via the alteration of viral protein synthesis.
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PMID:Effect of snuff extract on the replication and synthesis of viral DNA and proteins in cells infected with herpes simplex virus. 215 33

The effects of sepsis on intracellular Na+ concentration ([Na+]i) and glucose metabolism were examined in rat red blood cells (RBCs) by using 23Na- and 2H-nuclear magnetic resonance (NMR) spectroscopy. Sepsis was induced in 15 halothane-anesthetized female Sprague-Dawley rats by using the cecal ligation and perforation technique; 14 control rats underwent cecal manipulation without ligation. The animals were fasted for 36 h, but allowed free access to water. At 36 h postsurgery, RBCs were examined by 23Na-NMR by using dysprosium tripolyphosphate as a chemical shift reagent. Human RBCs from 17 critically ill nonseptic patients and from 7 patients who were diagnosed as septic were also examined for [Na+]i. Five rat RBC specimens had [Na+]i determined by both 23Na-NMR and inductively coupled plasma-atomic emission spectroscopy (ICP-AES). For glucose metabolism studies, RBCs from septic and control rats were suspended in modified Krebs-Henseleit buffer containing [6,6-2H2]glucose and examined by 2H-NMR. No significant differences in [Na+]i or glucose utilization were found in RBCs from control or septic rats. There were no differences in [Na+]i in the two groups of patients. The [Na+]i determined by NMR spectroscopy agreed closely with measurements using ICP-AES and establish that 100% of the [Na+]i of the RBC is visible by NMR. Glucose measurements determined by 2H-NMR correlated closely (correlation coefficient = 0.93) with enzymatic analysis. These studies showed no evidence that sepsis disturbed RBC membrane function or metabolism.
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PMID:Sepsis does not alter red blood cell glucose metabolism or Na+ concentration: a 2H-, 23Na-NMR study. 230 34

Earlier studies by our laboratories indicated that severe fluid percussion injury in cats results in the development of significant brain edema. In this study we measured the spatial distribution of edema developed after both central and lateral modes of impact with the objective of determining the degree to which the edema volume may contribute to ICP elevation and neurologic deterioration. All animals developed a marked increase in tissue water, particularly in the brainstem. In laterally injured cats, the increase in brainstem water equaled the edema produced supratentorially. Adding the increase of brainstem edema and the edema volume of the supratentorial compartment, we found an average water increase of 1.125 cc in survivors and 2.492 cc in nonsurvivors. This represents a significant volume increase when it is considered that the average PVI of the normal cat is approximately 0.9 cc (6). However, we observed that the PVI was reduced soon after injury and at a time when it has been reported that water content was near normal levels (7). Taking these studies in concert, we believe that the early reduction in PVI is most probably due to vascular swelling. The developing edema further contributes to reductions in PVI, thus setting the stage for elevated ICP and the tissue impaction observed in nonsurvivors.
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PMID:Comparative studies of edema produced by fluid percussion injury with lateral and central modes of injury in cats. 239 17

These results show that infusion edema produces a significant increase in brainstem tissue water similar to the distribution seen after traumatic injury. The increased brainstem water of 0.24 cc is equivalent to a brainstem volume rise of 7.26% and was sufficient to cause a marked reduction in the PVI and sustained elevation of the ICP. Despite the ICP rise, somatosensory and brainstem potentials are only mildly affected and return to normal within 8 hr. The fact that severe fluid percussion injury results in obliteration of BAER immediately after impact would suggest that the neurologic deterioration seen in the fluid percussion model of injury is due to direct structural damage of the tissue, which was received at the moment of impact, and not to the compressive effect of the developing brainstem edema at levels achieved in these experiments (7.62% swelling). As in other mechanical models, edema results in secondary compression of the tissue and contributes to the general brain swelling, which if unabated could lead to tentorial herniation and death. In these infusion studies, we must conclude that in some cases, mild secondary compression was sufficient to affect other control centers and produce systemic failure at levels of edema that do not result in alteration of evoked potentials. This might explain the deaths of those animals that occurred during the infusion period in which brainstem potentials remained intact.
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PMID:Contribution of brainstem edema to neurophysiologic deterioration in the cat infusion edema model. 239 32


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