Effects of Magnesium Treatment in a Model of Internal Capsule Lesion in Spontaneously Hypertensive Rats

Abstract

Background and Purpose-The study aim was to assess the effects of magnesium sulfate (MgSO 4 ) administration on white matter damage in vivo in spontaneously hypertensive rats. Methods-The left internal capsule was lesioned by a local injection of endothelin-1 (ET-1; 200 pmol) in adult spontaneously hypertensive rats. MgSO 4 was administered (300 mg/kg SC) 30 minutes before injection of ET-1, plus 200 mg/kg every hour thereafter for 4 hours. Infarct size was measured by T2-weighted magnetic resonance imaging (day 2) and histology (day 11), and functional recovery was assessed on days 3 and 10 by the cylinder and walking-ladder tests. Results-ET-1 application induced a small, localized lesion within the internal capsule. Despite reducing blood pressure, MgSO 4 did not significantly influence infarct volume (by magnetic resonance imaging: median, 2.1 mm 3 ; interquartile range, 1.3 to 3.8, vs 1.6 mm 3 and 1.2 to 2.1, for the vehicle-treated group; by histology: 0.3 mm 3 and 0.2 to 0.9 vs 0.3 mm 3 and 0.2 to 0.5, respectively). Significant forelimb and hindlimb motor deficits were evident in the vehicle-treated group as late as day 10. These impairments were significantly ameliorated by MgSO 4 in both cylinder (left forelimb use, PϽ0.01 and both-forelimb use, PϽ0.03 vs vehicle) and walking-ladder (right hindlimb score, PϽ0.02 vs vehicle) tests. Conclusions-ET-1-induced

Lasting Pure-Motor Deficits after Focal Posterior Internal Capsule White-Matter Infarcts in Rats

“…In one study, 12 motor deficits were limited to a modest twofold increase in foot-faults, and sensory deficits were more prominent, possibly due to the lesion placement in anterior dorsal internal capsule. In another study in hypertensive rats, 13 lesions were smaller, and motor deficits were once again very mild (cylinder test asymmetry index~1.5) and limited to the forelimb (walking ladder test score~5.3 on a scale of 0 worst to 6 best). Both studies followed the animals for only 2 weeks or less; therefore, persistence of the deficits was not demonstrated.…”

“…13 After the injection, the needle was left in place for additional 10 minutes to avoid backflow. The burr hole was sealed with bone wax (Ethicon, Somerville, NJ, USA).…”

“…11 The ET-1 model has been used to produce capsular lesions in rats. 12,13 However, deficits have been mild and short-lasting, limiting the usefulness of such models for recovery paradigms.…”

Exendin-4-Loaded PLGA Microspheres Relieve Cerebral Ischemia/Reperfusion Injury and Neurologic Deficits through Long-Lasting Bioactivity-Mediated Phosphorylated Akt/eNOS Signaling in Rats

“…26 Anesthesia was induced with 5% Exendin-4-loaded PLGA microspheres and stroke C-T Chien et al halothane and maintained with 1.5% halothane. Control and DM rats treated with vehicle, Ex-4, or PEx-4 24 hours after CAO were intubated and mechanically ventilated at a rate of 60 breaths/minute.…”

A Rat Model of Photothrombotic Capsular Infarct with a Marked Motor Deficit: A Behavioral, Histologic, and microPET Study

“…Although many studies of therapeutic strategies have been performed using cortical infarct models, only a few studies have investigated subcortical capsular infarcts (SCIs), owing to a lack of pertinent rodent models for capsular infarct. [6][7][8] Specifically, to investigate motor deficits and their recovery after a stroke, a portion of the motor pathway from the motor cortex to the medullary pyramid should be selectively destroyed or modified to create animal models that have motor impairment. However, most of these models involve damage within the gray matter of the cortex, and only a few studies have attempted to damage the white matter to develop a stroke model.…”