The pathophysiology of experimental brain edema

Hossmann, Konstantin‐Alexander

doi:10.1007/bf01780838

Cited by 29 publications

(19 citation statements)

References 48 publications

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“…An important modulator of focal ischemic injury is brain edema which can be differentiated into two phases: An early cytotoxic type of edema, followed after some time by a late vasogenic type of edema (for review see Hossmann, 1989;Rosenberg, 1999;Rosand and Schwamm, 2001). The cytotoxic type of edema is threshold dependent.…”

Section: Brain Edemamentioning

confidence: 99%

Pathophysiology and Therapy of Experimental Stroke

2006

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1. Stroke is the neurological evidence of a critical reduction of cerebral blood flow in a circumscribed part of the brain, resulting from the sudden or gradually progressing obstruction of a large brain artery. Treatment of stroke requires the solid understanding of stroke pathophysiology and involves a broad range of hemodynamic and molecular interventions. This review summarizes research that has been carried out in many laboratories over a long period of time, but the main focus will be on own experimental research. 2. The first chapter deals with the hemodynamics of focal ischemia with particular emphasis on the collateral circulation of the brain, the regulation of blood flow and the microcirculation. In the second chapter the penumbra concept of ischemia is discussed, providing a detailed list of the physiological, biochemical and structural viability thresholds of ischemia and examples of how these thresholds can be applied for imaging the penumbra. The third chapter summarizes the pathophysiology of infarct progression, focusing on the role of peri-infarct depolarisation, the multitude of putative molecular injury pathways, brain edema and inflammation. Finally, the fourth chapter provides an overview of currently discussed therapeutic approaches, notably the effect of mechanical or thrombolytic reperfusion, arteriogenesis, pharmacological neuroprotection, ischemic preconditioning and regeneration. 3. The main emphasis of the review is placed on the balanced differentiation between hemodynamic and molecular factors contributing to the manifestation of ischemic injury in order to provide a rational basis for future therapeutic interventions.

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Section: Brain Edemamentioning

confidence: 99%

Pathophysiology and Therapy of Experimental Stroke

2006

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“…This important clinical complication is caused by 'noxious factors' that directly affect the function of brain cells resulting in brain swelling and a reduction of the intercellular space. During cytotoxic oedema the blood-brain barrier functions are not influenced (Betz et al 1989;Hossmann, 1989). There is an uptake of sodium and a loss of potassium by the brain cells, leading to an increase in K+ concentration of brain interstitial fluid (Hossmann, Sakaki & Zimmermann, 1977;Hansen, Gjedde & Siemkowicz, 1980).…”

Section: Str _7etch-acti }'A Ted Ca4tion Channelsmentioning

confidence: 99%

Stretch‐activated non‐selective cation channels in the antiluminal membrane of porcine cerebral capillaries.

Popp

Hoyer

Meyer

et al. 1992

The Journal of Physiology

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SUMMARY1. Single stretch-activated (SA) channels have been studied in isolated brain capillary endothelial cells as well as in the antiluminal membrane of intact porcine cerebral capillaries using the patch-clamp recording technique.2. The SA channels were found to be cation selective and permeable to Nat, K+, Ba2+ and Ca2 . 3. With monovalent cations in the patch pipette, the channels showed inward rectification in cell-attached patches with a single-channel conductance of 37 pS at negative and 24 pS at positive clamp potentials.4. With either 70 mM-Ca2+ or Ba2+ in the patch pipette, the current-voltage relation was linear with slope conductances of 16 and 19 pS, respectively.5. Mean channel open probability increased with increasing pressure and with depolarizing clamp potentials.6. Cell swelling induced by hypotonic shock activated the SA channels in cellattached experiments.7. The SA channel may be involved in cell volume or blood flow regulation. The contribution of these channels to the regulation of cerebrospinal salt and water content, especially in brain oedema, is discussed.

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“…Thus, the values were stable above the threshold for maintenance of normal cortical blood flow. 8 There was no significant difference in neurological outcome among groups (data not shown). Table 1 demonstrates the infarct sizes expressed as a percentage of the total crosssectional area at the level photographed.…”

Section: Resultsmentioning

confidence: 85%

Lack of effect of PN 200-110 on neuronal injury and neurological outcome in middle cerebral artery-occluded rats.

Marinov

Wassmann

1991

Stroke

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We evaluated the influence of a continuous intravenous infusion of 0.24 mg/kg PN 200-110 started 20 minutes before the induction of ischemia and continued for 2 hours on infarct size, histopathology, and neurological outcome in middle cerebral artery-occluded rats treated with PN 200-110 (n=8), placebo (n=7), or saline (n=8). Neurological examination was performed 24 hours after occlusion. We quantified infarct size by 2,3,5-triphenyl-tetrazolium chloride, hematoxylin and eosin, and Nissl staining and by computerized analysis of tracings of the infarcted areas and evaluated neuronal injury at the infarct periphery. The different types of ischemic cell damage were quantified by direct visual counting. We found no differences among saline-, placebo-, and PN 200-110-treated rats regarding infarct size, amount of neuronal alteration, and neurological outcome. Our results indicate the lack of a significant protective effect of this drug in experimental focal ischemia. (Stroke 1991^22:1064-1067) I n a search for effective cerebroprotective agents for use in neurosurgical practice, we became interested in dihydropyridine calcium antagonists. In another experimental study, 1 we demonstrated the therapeutic efficacy of nimodipine in lessening the extent of focal ischemia and the severity of peri-infarct neuronal injury. We explained these beneficial effects predominantly by the vasoactive properties of the drug, which increases cerebral blood flow (CBF) in the penumbra zone to above the ischemic threshold. Despite existing controversies regarding the mechanisms of the anti-ischemic action of calcium channel blockers, their most probable role is in restoration of tissue perfusion at the infarct periphery, rather than in protection of the neuronal cell by preventing Ca 2+ overload. 2 -6 On the other hand, some calcium antagonists are considered dangerous since they may worsen postischemic brain edema in experimental conditions by increasing the blood flow threshold for ion homeostasis (impaired membrane protection) and by increasing blood flow. Received December 5, 1990; accepted April 4, 1991. brain edema by using a new dihydropyridine calcium antagonist, PN 200-110. 1112 In this study we evaluated the cerebroprotective properties of this drug. Materials and MethodsWe permanently occluded the right middle cerebral artery (MCA) in 23 male Fischer-344 rats weighing 250-300 g by means of microsurgical transcTanial exploration and coagulation. 13 The MCA trunk was occluded by microbipolar coagulation from a point proximal to the origin of the lateral striate artery to 1 mm beyond where the vessel crosses the olfactory striae.14 The animals were anesthetized with 50 mg/kg i.m. ketamine HC1 and 2 mg/kg i.m. xylazine. The left femoral artery and vein were cannulated with polyethylene catheters to allow continuous blood pressure monitoring, arterial blood sampling, and drug administration. Animals were maintained at normothermia by external heating.Isradipine was donated by Sandoz AG, Nurenberg, FRG. Based on practical expe...

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The pathophysiology of experimental brain edema

Cited by 29 publications

References 48 publications

Pathophysiology and Therapy of Experimental Stroke

Pathophysiology and Therapy of Experimental Stroke

Stretch‐activated non‐selective cation channels in the antiluminal membrane of porcine cerebral capillaries.

Lack of effect of PN 200-110 on neuronal injury and neurological outcome in middle cerebral artery-occluded rats.

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