Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

Benveniste, Helene; Kim, Katie R.; Hedlund, Laurence W.; Kim, John W.; Friedman, Allan H.

doi:10.3171/jns.2000.92.1.0100

Cited by 10 publications

(10 citation statements)

References 31 publications

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“…It is possible that acute changes in blood pressure (rather than prolonged hypertension) may be more important in haematoma expansion. Benveniste et al 59 examined ICH after a brain biopsy and found no difference in haemorrhage volume between SHR and WKY rats, but found increased haemorrhage in normotensive WKY rats subjected to acute increases in blood pressure.…”

Section: Mechanisms Of Brain Injury/therapeutic Approachesmentioning

confidence: 99%

Intracerebral haemorrhage: mechanisms of injury and therapeutic targets

Keep

Hua

2012

The Lancet Neurology

1,057

889

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Intracerebral haemorrhage (ICH) accounts for about 10–15% of all strokes. ICH is associated with high mortality and morbidity and there has been no successful Phase III clinical trial for this condition. The last six years has seen a great increase in the number of pre-clinical and clinical studies focused on ICH. There have been significant advances in the animal models available to study ICH and in our understanding of the mechanisms underlying brain injury following haemorrhage. This has led to the identification of several therapeutic targets that are now being pursued into clinical trials. These advances are described in this review in addition to information on past and current clinical trials. Many of the former were based on very limited pre-clinical data and possible guidelines on the nature of pre-clinical results that justify proceeding to the clinic are discussed.

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Section: Mechanisms Of Brain Injury/therapeutic Approachesmentioning

confidence: 99%

Intracerebral haemorrhage: mechanisms of injury and therapeutic targets

Keep

Hua

2012

The Lancet Neurology

1,057

889

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“…A rat study found acute BP elevation in either normotensive or hypertensive rats after ICH, which is associated with higher HE, more brain swelling, and worse neurological deficits (154, 155). Since acute ICH leads to activation of the adrenergic system, the role of antiadrenergic agents needs to be explored.…”

Section: Hematoma Expansionmentioning

confidence: 99%

Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing Controversies

Mittal

LacKamp

2016

Front. Neurol.

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Intracerebral hemorrhage (ICH) is a medical emergency, which often leads to severe disability and death. ICH-related poor outcomes are due to primary injury causing structural damage and mass effect and secondary injury in the perihemorrhagic region over several days to weeks. Secondary injury after ICH can be due to hematoma expansion (HE) or a consequence of repair pathway along the continuum of neuroinflammation, neuronal death, and perihemorrhagic edema (PHE). This review article is focused on PHE and HE and will cover the animal studies, related human studies, and clinical trials relating to these mechanisms of secondary brain injury in ICH patients.

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“…However, in one study we observed the opposite pattern; that is, systemic cooling provided greater protection as intervention delay increased from 1 to 12 hours after collagenase infusion (MacLellan et al, 2004). In that study, early cooling exacerbated bleeding, which likely occurred because cooling increased blood pressure, which itself worsens bleeding (Benveniste et al, 2000), and cooling may have also slowed clotting. As our focal cooling method does not notably affect blood pressure or body temperature Auriat et al, 2012), we had hoped that this method would be a safer alternative to systemic cooling.…”

Section: Discussionmentioning

confidence: 61%

Localized Hypothermia Aggravates Bleeding in the Collagenase Model of Intracerebral Hemorrhage

John

Dietrich

Colbourne

2015

Therapeutic Hypothermia and Temperature Management

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Animal studies testing whether therapeutic hypothermia is neuroprotective after intracerebral hemorrhage (ICH) have been inconclusive. In rodents, ICH is often produced in the striatum by infusing collagenase, which causes prolonged hemorrhaging from multiple vessels. Our previous data shows that this bleeding (hematoma) is worsened by systemic hypothermia given soon after collagenase infusion. In this study we hypothesized that localized brain hypothermia would also aggravate bleeding in this model (0.2 U of collagenase in 1.2 μL of saline). We also evaluated cooling after intrastriatal thrombin infusion (1 U in 30 μL of saline)-a simplified model of ICH thought to cause bleeding. Focal hypothermia was achieved by flushing cold water through an implanted cooling device attached to the skull underneath the temporalis muscle of adult rats. Previous work and data at this time shows this method cools the striatum to ∼33°C, whereas the body remains normothermic. In comparison to normothermic groups, cooling significantly worsened bleeding when instituted at 6 hours (∼94 vs. 42 μL, p=0.018) and 12 hours (79 vs. 61 μL, p=0.042) post-ICH (24-hour survival), but not after a 24-hour delay (36-hour survival). Rats were cooled until euthanasia when hematoma size was determined by a hemoglobin-based spectrophotometry assay. Cooling did not influence cerebral blood volume after just saline or thrombin infusion. The latter is explained by the fact that thrombin did not cause bleeding beyond that caused by saline infusion. In summary, local hypothermia significantly aggravates bleeding many hours after collagenase infusion suggesting that bleeding may have confounded earlier studies with hypothermia. Furthermore, these findings serve as a cautionary note on using cooling even many hours after cerebral bleeding.

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Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

Abstract: The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

Cited by 10 publications

References 31 publications

Intracerebral haemorrhage: mechanisms of injury and therapeutic targets

Intracerebral haemorrhage: mechanisms of injury and therapeutic targets

Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing Controversies

Localized Hypothermia Aggravates Bleeding in the Collagenase Model of Intracerebral Hemorrhage

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