The effects of mannitol and urea on cerebral hemodynamics and cerebrospinal fluid pressure

Goluboff, Bernard; Shenkin, Henry A.; Haft, Harold

doi:10.1212/wnl.14.10.891

Cited by 51 publications

(9 citation statements)

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“…Mannitol is commonly used to induce a transient hyperosmotic state, and the effect of glucose injection mimics that of mannitol 17 even though glucose is rapidly transported into the brain and metabolized. Intravenous mannitol injection can decrease blood viscosity, 18 lower intracranial pressure, 19 and increase PacOj. 2021 Direct application of hyperosmotic solutions to the surface of the brain causes pial artery dilation.…”

Section: Resultsmentioning

confidence: 99%

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

Duckrow¹,

Beard²,

Brennan³

1987

Stroke

146

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The presence of hyperglycemia prior to stroke or cardiac arrest can increase neuronal damage caused by brain ischemia. Acute hyperglycemia shows this effect in animal models of stroke. However, chronic hyperglycemia and chronic hyperglycemia with additional acute elevation of blood glucose are more common premorbid states for stroke patients. The effect of chronic hyperglycemia on regional cerebral blood flow (rCBF) is unclear but blood flow changes may play a role in this ischemic cell damage. We measured rCBF in awake restrained rats that had chronic hyperglycemia induced by treatment with streptozotocin. This was compared to that measured in rats made acutely hypergh/cemic by injecting glucose into the peritoneal space. rCBF was measured in 17 brain regions using [ u C]iodoantipyrine. During chronic hyperglycemia, when plasma glucose was 29 ^.m/ml, rCBF was decreased and a regional distribution of this effect was noted; 9 hindbrain regions showed a mean flow decrease of 14% while forebraln regions demonstrated less flow reduction. Acute elevation of plasma glucose during normoglycemia or superimposed on chronic hyperglycemia produced flow reductions of 7% for each 10 /xm/mJ increment in plasma glucose up to 60 /xm/ml. Both chronic and acute hyperglycemia are associated with decreased rCBF and the mechanism for this effect does not appear to adapt to chronic hyperglycemia. (Stroke 1987; 18:52-58) C LINICAL studies suggest that hyperglycemia is a risk factor for stroke 1 and that it increases brain injury during stroke or cardiac arrest.2 "4In animal models of stroke, acute hyperglycemia before ischemia increases mortality 3 and the number of neurons that die. 6 "* After transient ischemia, hyperglycemia increases and prolongs postischemic hyperemia 89 and enhances the heterogeneity of reperfusion. 10However, in normal animals an acute elevation of plasma glucose is associated with decreased regional cerebral blood flow (rCBF). 10 " This effect could limit compensatory blood flow mechanisms during an ischemic event.In clinical situations hyperglycemia, whether iatrogenic or the result of stroke itself, 12 is seldom as acute or as severe as that induced in animal models of stroke. Also, diabetics are frequently exposed to acute increases in blood glucose superimposed on a background of chronic hyperglycemia. Little is known about the effect of chronic hyperglycemia on rCBF. For these reasons we measured rCBF in awake restrained rats that had a moderate chronic hyperglycemia produced by treatment with streptozotocin. We found that chronic hyperglycemia was associated with decreased rCBF. Also, a specific regional distribution of this effect was noted with hindbrain regions manifesting CBF decreases during chronic hyperglycemia. Materials and Methods The isotope 4-iodo|7V-methyl-14 C]antipyrine, 53 mCi/mmol, was obtained from Amersham, Arlington Heights, El. Streptozotocin, 2-deoxy-2-([methylnitrosoamino]carbonyl)-amino(-

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Section: Resultsmentioning

confidence: 99%

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

Duckrow¹,

Beard²,

Brennan³

1987

Stroke

146

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“…Prolonged edema from brain ischemia can cause life-threatening brain herniation of the vital structures. The clinical administration of mannitol and glycerol is restricted to the early stage of stroke, before blood-brain barrier breakdown, and exhibits the major drawbacks, such as rebound intracranial pressure or increase in cerebral volume with the secondary edema (Goluboff et al, 1964;Larsson et al, 1976). Very limited drug candidates have been evaluated targeting brain edema during stroke.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Neuroprotective Effects of Biphalin, an Opioid Receptor Agonist, in a Model of Focal Brain Ischemia

Shah²,

Wang³

et al. 2011

J Pharmacol Exp Ther

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Approximately 795,000 people experience a new or recurrent stroke in the United States annually. The purpose of this study was to assess the protective effect of a nonselective opioid receptor agonist, biphalin, in brain edema and infarct damage by using both in vitro and in vivo models of stroke. In an in vivo model of ischemia, biphalin significantly decreased edema (66.6 and 58.3%) and infarct (52.2 and 56.4%) ratios in mouse transient (60-min occlusion/24-h reperfusion) and permanent (6 h) middle cerebral artery occlusion models, respectively. Biphalin administration also showed decreased neurodegeneration in hippocampal, cortical, and striatal brain tissue after ischemia, evidenced by reduced Fluoro-Jade C staining. In addition, biphalin improved neurological function after stroke injury evidenced by neurological score and locomotor activity evaluation. Biphalin significantly decreased penumbral expression of Na ϩ , K ϩ , 2Cl Ϫ cotransporter (NKCC) and the translocation of the conventional isoforms of protein kinase C (PKC). It also reversed the activation of PKC-induced cell volume increase during ischemia in primary neuronal cell cultures exposed to 1 h of oxygen glucose deprivation. These data suggest that opioid receptor activation provides neuroprotection during stroke, and a possible explanation of this mechanism could be the inhibition of NKCC function via the regulation of PKC-dependent cell signaling.

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“…The changes in clinical condition are usually attributed to CBF increasing above ischemic thresholds as a result of lowered intracranial pressure (ICP) and increased perfusion pressure. 7 However, the underlying mechanisms are undoubtedly more complicated. Mannitol has been demonstrated to increase CBF in brain injured animals and man without altering cerebral perfusion pressure, 3 …”

Section: Discussionmentioning

confidence: 99%

“…18 In normal subjects with intact autoregulation, these factors alone may not increase CBF. However, mannitol is also associated with an increase in CMR0 2 , 7 an increase in arterial PCOj, hemodilution, and decreased blood viscosity. 12 The reason that the increase in CBF observed in this study was smaller than that reported by others may, at least in part, be due to the efforts we made to compensate for the transient increase in arterial PC0 2 which occurred shortly after administration of the mannitol.…”

mentioning

confidence: 98%

The effects of high dose mannitol on cerebral blood flow in dogs with normal intracranial pressure.

Kassell¹,

Baumann²,

Hitchon³

et al. 1982

Stroke

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SUMMARY In normal dogs, bolus administration of a very high dose of mannitol (2 gm/kg) resulted in a small, transient increase in cerebral blood flow (CBF) of approximately 8 percent lasting less than 10 minutes followed by a significant reduction in CBF of approximately 20 percent lasting at least three hours. The increase in CBF may in part be related to changes in cardiovascular and hematological parameters. No explanation is available for the reduction below control values but, since urine losses were not replaced in these animals, changes in the state of hydration may have been responsible. It appears that the increase in CBF resulting from mannitol administered by bolus infusion are of neither sufficient magnitude nor duration to explain the protective effect observed in other studies where cerebral blood flow was reduced below ischemic levels. This suggests then, that either the effect of mannitol on CBF is quantitatively different when flow is reduced to critical levels or that the protective effect observed when the cerebral circulation is compromised is based upon a different mechanism than augmentation of flow. Further studies on the effect of mannitol on CBF in ischemic situations, where the cerebral circulation is compromised, are required.

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The effects of mannitol and urea on cerebral hemodynamics and cerebrospinal fluid pressure

Cited by 51 publications

References 0 publications

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

Characterization of Neuroprotective Effects of Biphalin, an Opioid Receptor Agonist, in a Model of Focal Brain Ischemia

The effects of high dose mannitol on cerebral blood flow in dogs with normal intracranial pressure.

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