The association between FLAIR vascular hyperintensities and outcomes in patients with border zone infarcts treated with medical therapy may vary with the infarct subtype.

RATIONALE AND OBJECTIVES: Fluid-attenuated inversion recovery vessel hyperintensities (FVHs) reflect the haemodynamic state and may aid in predicting the prognosis of border zone (BZ) infarct patients. This study was to explore the relationship between FVHs and functional outcomes for different BZ infarct subtypes following medical therapy administration. MATERIALS AND METHODS: Consecutive patients with ischemic stroke were retrospectively enrolled and classified into internal BZ (IBZ) infarct, cortical BZ (CBZ) infarct and mixed-type infarct patients. FVHs were quantified using the FVH-Alberta Stroke Program Early CT Score (ASPECTS) system, and the scores were used to divide the patients into low-FVH (0-3) and high-FVH (4-7) groups. The FVH location and the cerebrovascular stenotic degree were recorded. Logistic regression was performed to identify risk factors for poor outcomes (modified Rankin scale score ≥3). RESULTS: A total of 207 BZ infarct patients (IBZ, n = 130; CBZ, n = 52; mixed-type, n = 25) were included. The FVH score was positively correlated with cerebrovascular stenosis (r = 0.332, P < 0.001) in all patients. A high FVH score was associated with poor outcomes in all (OR 2.568, 95% CI (1.147 to 5.753), P = 0.022) and in CBZ infarct patients (OR 9.258, 95% CI 1.113 to 77.035), P = 0.040). FVH-diffusion-weighted imaging (DWI) mismatch was not significantly associated with outcomes in the entire patient group or in any subgroup. CONCLUSIONS: A high FVH score is associated with poor long-term outcomes in patients with CBZ infarcts but not in those with IBZ or mixed-type infarcts.

[Muscarinic receptors modulate the mRNA expression of NMDA receptors in brainstem and the release of glutamate in periaqueductal grey during morphine withdrawal in rats].

The antisense approach and RT-PCR were used to study the effects of muscarinic receptors on the scores of morphine-withdrawal syndrome and the expression of NMDA receptor subtypes (NR(1A) and NR(2A)) mRNA in rat spinal cord and brainstem. The concentrations of glutamate in periaqueductal grey (PAG) of morphine-withdrawal rats were determined by capillary electrophoresis with laser-induced fluorescence detection. The data showed that the NR(1A) and NR(2A) mRNA levels were increased significantly in the spinal cord and brainstem 1 h after the injection of naloxone (4 mg/kg, i.p.) in morphine-dependent rats. Moreover, in morphine-dependent rats pretreated (i.p.) with scopolamine (0.5 mg/kg), or pirenzepine (10 mg/kg), MK801 (0.125 mg/kg), L-N-nitroarginine methylester (10 mg/kg) 30 min before naloxone injection, the NR(1A) and NR(2A) mRNA levels were significantly lower than those of 1 h morphine-withdrawal rats. Intrathecal injection of NR(1A) or M(2) receptor antisense oligonucleotides (A-oligo, 4 microg/per rat) 24 h prior to naloxone challenge could block the morphine withdrawal symptoms including wet dog shaking, irritability, salivation, diarrhea, chewing and weight loss. Meanwhile, in morphine-dependent rats the NR(1A) mRNA levels in the spinal cord and brainstem were down-regulated by intrathecal injection of M(2) receptor A-oligo. The glutamate concentrations in PAG microdialysis were increased to a maximal level 15 min after naloxone injection. The glutamate response was inhibited by pretreatment with M(2) receptor A-oligo but not by M(1) A-oligo. The results suggest that the expression of NMDA receptors and the release of glutamate in brainstem are involved in the processes of morphine withdrawal and that the NMDA receptor expression is possibly regulated by the muscarinic receptors during morphine withdrawal.

[mRNA expression of muscarinic receptors in spinal cord and brainstem in morphine dependent rats].

AIM: To observe mRNA expression of muscarinic acetylcholine receptors in spinal cord and brainstem in morphine dependent or withdrawal rats. METHODS: The mRNA expression level of m1, m2, m3, m4 and m5 were determined by RT-PCR, the beta-actin mRNA expression was used as internal control. RESULTS: The mRNA level of m1, m2, m3, m4 and m5 in spinal cord and m1 and m2 in brainstem were increased significantly during morphine dependence, and the levels of m1, m2, m3 and m4 in spinal cord and m1 in brainstem were decreased 1 h after the injection of naloxone (4 mg.kg-1, i.p.) in morphine dependent rats. Either scopolamine (0.5 mg.kg-1) or pirenzepine (10 mg.kg-1) was shown to significantly decrease the morphine withdrawal symptoms in rats. The levels of m1, m2, m3 and m5 in spinal cord were increased by pretreatment with pirenzepine and the levels of m2, m3 and m4 in spinal cord were increased by pretreatment with scopolamine. CONCLUSION: The adaptive expression of muscarinic receptors at spinal and supraspinal levels play important role in mediating morphine dependence and withdrawal in rats.