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

Kassell, Neal F.; Baumann, Kent W.; Hitchon, Patrick W.; Gerk, Mary K.; Hill, Todd; Sokoll, Martin D.

doi:10.1161/01.str.13.1.59

Cited by 48 publications

(12 citation statements)

References 15 publications

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“…22 All of these factors would increase rCBF, and increases have been measured in humans with glioma," in normal baboons, 20 and in dogs. 21 However, in animals this flow increase has been transient, and a more persistent decrease in CBF has been noted after 20 minutes." 21 Mechanisms for this decrease have not been postulated.…”

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

View full text Add to dashboard Cite

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“…In healthy volunteers, intravenous infusion of hypertonic dextrose or NaCl solutions has been found to increase forearm blood flow as a result of a decrease in resistance [35] . Similarly, intravascular infusion of hypertonic solutions has been shown to increase cerebral blood flow [36,37] . Sasaki and co-workers suggested that hypertonic solutions produce non-specific vasodilation of cerebral arteries by inhibiting the influx of external Ca 2+ rather than the release of intracellularly stored Ca 2+ [38] .…”

Section: Discussionmentioning

confidence: 99%

Potentiation of EDHF-mediated relaxation by chloride channel blockers

et al. 2010

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Aim: To investigate the involvement of Cl -channels in endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in rat mesenteric arteries. Methods: Cl -channel and K ir channel activities were studied using whole-cell patch clamping in rat mesenteric arterial smooth muscle cells. Isometric tension of arterial rings was measured in organ chambers. Results: The volume-activated Cl -current in rat mesenteric arterial smooth muscle cells was abolished by Cl -channel blockers NPPB or DIDS. The EDHF-mediated vasorelaxation was potentiated by NPPB and DIDS. The EDHF response was diminished by a combination of apamin and charybdotoxin, which agreed with the hypothesis that EDHF response involves the release of K + via the Ca 2+ -activated K + channels in endothelial cells. The elevation of K + concentration in bathing solution from 1.2 mmol/L to 11.2 mmol/L induced an arterial relaxation, which was abolished by the combination of BaCl 2 and ouabain. It is consistent to the hypothesis that K + activates K + /Na + -ATPase and inward rectifier K + (K ir ) channels, leading to the hyperpolarization and relaxation of vascular smooth muscle. The K + -induced relaxation was augmented by NPPB, DIDS, or withdrawal of Cl -from the bathing solution, which could be reversed by BaCl 2 , but not ouabain. The potentiating effect of Cl -channel blockers on K + -induced relaxation was probably due to the interaction between Cl -channels and K ir channels. Moreover, the K + -induced relaxation was potentiated when the arteries were incubated in hyperosmotic solution, which is known to inhibit volume-activated Cl -channels. Conclusion: The inhibition of Cl -channels, particularly the volume-activated Cl -channels, may potentiate the EDHF-induced vasorelaxation through the K ir channels.

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“…The first effect of mannitol is rheological. An immediate expansion of intravascular volume lowers the hematocrit and blood viscosity while increasing cerebral blood flow and cerebral oxygenation which lead to vasoconstriction and decrease in ICP 5,12,17) . The second effect is an osmotic effect to shift brain tissue water into the intravascular space and reduce cerebral extracellular free water by the establishment of an osmotic gradient along the blood-brain barrier 6,7) .…”

Section: Discussionmentioning

confidence: 99%

“…Osmotic therapy with mannitol is effective in reducing ICP by its rheological and osmotic effects 5,7,12,17) . Theoretically, its osmotic effect is produced in the brain with an intact blood-brain barrier (BBB) and extravasation of mannitol through a disrupted BBB may exacerbate vasogenic brain edema.…”

Section: Introductionmentioning

confidence: 99%