Comparison of the anticonstrictor action of dihydropyridines (nimodipine and nicardipine) and Mg2+ in isolated human cerebral arteries

Alborch, Enrique; Salom, Juan B.; Perales, Alfredo; Torregrosa, Germán; Miranda, Francisco Javier Noya; Alabadí, JoséA.; Jover, Teresa

doi:10.1016/0014-2999(92)90289-g

Cited by 43 publications

(22 citation statements)

References 23 publications

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“…In addition, there was no indirect effect of serum Mg +2 on the NS. This finding can be explained by the effect of Mg +2 in the dilatation of vasoconstricted intracranial arteries, as was observed in previous studies [1,2,13,14,20]. Since the large cerebral arteries are bathed in CSF, it is possible that a high Mg +2 concentration may cause a direct dilatation of the large vessels and so reduce the vasoconstritive effect in the early stages after the stroke.…”

Section: Discussionmentioning

confidence: 65%

Cerebrospinal fluid magnesium level as a prognostic factor in ischaemic stroke

Lampl

Geva

Gilad

et al. 1998

Journal of Neurology

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Magnesium has been reported to have a dilatatory effect on cerebral arteries. Reduction of extracellular Mg+2 has been shown to be directly correlated with the intensity of cerebral spasm. A neuroprotective effect of magnesium in stroke has also been hypothesized. The aim of our study was to examine the Mg+2 levels in serum and cerebrospinal fluid (CSF) in the early stage of stroke and to evaluate the correlation between Mg+2 levels and the development of neurological deficits. Between 1986 and 1994, 96 patients who had a stroke of 24- to 48-h duration were enrolled in the study. Serum and CSF levels of magnesium were checked on admission, 2448 h after the onset of stroke. Using a neurological score, the neurological deficit was assessed on the 1st day, 1 and 4 weeks later. Computed tomography (CT) was performed after 1 week, and the volume and location of infarction were calculated and measured. Statistical analysis was performed for cortical and subcortical patients separately, using Spearman correlation and multiple linear and logistic regression analyses. Significant correlation was found between CSF Mg+2 and the size of the infarct (P < 0.0001). There was no correlation between serum Mg+2 and CSF Mg+2 levels. Regression analysis demonstrated an increase in the values of the Mathew Neurological Score with higher CSF Mg+2 levels. This association remained true after other factors such as age, associated heart disease, diabetes and infarction size had been taken into account by the regression model. The results confirm that there is a relationship between a low Mg+2 concentration in CSF during the first 48 h after onset of ischaemic stroke and the intensity of the neurological deficit. The therapeutic consequence of this finding may have some importance.

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Section: Discussionmentioning

confidence: 65%

Cerebrospinal fluid magnesium level as a prognostic factor in ischaemic stroke

Lampl

Geva

Gilad

et al. 1998

Journal of Neurology

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“…5 There are several potential mechanisms of neuroprotection, which include noncompetitive NMDA receptor blockade, 10 enhanced regional cerebral blood flow to areas of focal ischemia, 6 antagonism of voltage-gated calcium ion channels, 7 and more favorable recovery of cellular energy metabolism after restoration of perfusion. In addition, magnesium infusions have improved neurological recovery after MCAO 28 ; have been neuroprotective in spinal cord ischemia 29,30 and isolated white matter anoxia 2 ; and have shown potent anticonstrictor effects against relevant mediators, including endothelin-1, angiotensin II, 31 prostaglandin F 2 ␣, serotonin, 32 and excitatory amino acids. 33 Systemic infusion of magnesium reversed basilar artery vasoconstriction in a rat model of subarachnoid hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Dose Optimization of Intravenous Magnesium Sulfate After Acute Stroke

Muir

Lees

1998

Stroke

101

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Background and Purpose-Parenterally administered MgSO 4 is neuroprotective in standard animal models of focal cerebral ischemia and in many other paradigms of brain injury. Previous small clinical trials in stroke patients have explored the safety and tolerability of different infusion regimens. This study was undertaken to optimize the regimen for a multicenter trial. Methods-Within 24 hours of the onset of clinically diagnosed stroke, patients were randomized to receive placebo or one of three intravenous MgSO 4 infusions: a loading infusion of 8, 12, or 16 mmol, followed by 65 mmol over 24 hours. Cardiovascular parameters, serum magnesium concentrations, and blood glucose concentrations were determined. Outcome at 30 and 90 days was recorded. Results-Twenty-five patients were recruited and treated at a mean time of 20 hours after stroke. No tolerability problems were identified. No effects of magnesium on heart rate, blood pressure, or blood glucose were evident. Serum magnesium concentrations rose to target levels most rapidly in the highest loading infusion group and were maintained in all groups for at least 24 hours. Conclusions-MgSO 4 infusions that rapidly elevate the serum magnesium concentration to potentially therapeutic levels are well tolerated and have no major hemodynamic effects in patients with acute stroke. The 16-mmol loading infusion achieved target serum concentrations most rapidly and has been chosen for further trials. (Stroke. 1998;29:918-923.)

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“…Therefore, Mg 2+ may prevent excess Ca 2+ influx and release of Ca 2+ more powerfully than the organic Ca 2+ channel blockers which act on voltage-operated membrane channels. The vasodilating effects of Mg 2+ have been studied previously and it was shown that although Mg 2+ can cause significant vasodilatation it is three to five orders of magnitude less potent than the organic Ca 2+ channel blockers [12,15,28]. As Mg 2+ also possesses unique and potentially useful Ca 2+ 28,29,30], it seemed more reasonable to study MgSO4 in a traumatic brain-injury model instead of cerebral vasospasm or ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…The vasodilating effects of Mg 2+ have been studied previously and it was shown that although Mg 2+ can cause significant vasodilatation it is three to five orders of magnitude less potent than the organic Ca 2+ channel blockers [12,15,28]. As Mg 2+ also possesses unique and potentially useful Ca 2+ 28,29,30], it seemed more reasonable to study MgSO4 in a traumatic brain-injury model instead of cerebral vasospasm or ischemia. In previous studies, it was stated that excess Mg 2+ markedly inhibited lactate production and high-energy phosphate breakdown during anoxia [9,31].…”

Section: Discussionmentioning

confidence: 99%