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  • 1
    ISSN: 1619-1560
    Keywords: Myocardial infarction ; Blood pressure variability ; Arterial blood pressure ; Autonomic nervous function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the study was to assess non-invasively circadian blood pressure rhythm as well as the influence of parasympathetic function 2 and 6 weeks after acute myocardial infarction treated with beta-blocking agents. Twenty-four patients with uncomplicated first myocardial infarction, and aged less than 60 years, underwent ambulatory blood pressure recordings every 15 min during the day (0900–2100 h) and every 30 min during the night (2100–0900 h), 2 and 6 weeks after infarction. The deep breathing test (6 breaths/min) was performed on each occasion. Normal circadian blood pressure rhythm was maintained with a nocturnal decline of 10 to 15%. Both for systolic and diastolic blood pressure a moderate increase was obtained after 6 weeks (107.8 ± 9.2 mmHg vs. 111.8 ± 10.3 mmHg; NS and 64.9 ± 4.5 mmHg vs. 68.8 ± 6.5 mmHg;p 〈 0.05). The respective blood pressure variations were significantly higher at that time (10.0 ± 2.4 mmHg vs. 13.6 ± 4.2 mmHg;p 〈 0.001 and 7.9 ± 1.7 mmHg vs. 11.7 ± 3.5 mmHg,p 〈 0.001). There was a close correlation (r=0.60,p 〈 0.005) between 24-h diastolic blood pressure variability and the results of the parasympathetic function test (deep breathing) 2 weeks after infarction. We conclude that the circadian blood pressure rhythm persists after acute myocardial infarction. The correlation between blood pressure variability and parasympathetic function early after infarction suggests a role for vagal control in post-infarction blood pressure variability.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 14 (1999), S. 253-263 
    ISSN: 1573-7365
    Keywords: Antisense Oligodeoxynucleotide ; Seizure ; GABA-Transaminase ; Cocaine ; Pentylenetetrazol ; GABA Antisense oligodeoxynucleotide ; Seizure ; GABA-Transaminase ; Cocaine ; Pentylenetetrazol ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanism of action of many anticonvulsive agents is to increase the function of the GABAergic system. Inhibition of GABA-Transaminase (GABA-T), the degradative enzyme for GABA, increases GABA levels in the brain. In this study, antisense oligodeoxynucleotides (ASO) targeted at the start codon region of GABA-Transaminase mRNA were used to modify seizure activity. Mice were treated, by intracerebroventricular injection, with antisense oligos or appropriate controls. At various times after treatment, the animals were challenged with cocaine (70 mg/kg, i.p.) and observed for seizure activity. At 15 hours after treatment, 1.152 and 1.44 nmol antisense oligo blocked cocaine-induced seizures. There was no effect of antisense oligo 8 or 36 hours after treatment. In addition, treatment with 7.2 nmol antisense oligo prevented pentylenetetrazol-induced seizures. These data demonstrate the modulation of seizure threshold using antisense oligodeoxynucleotides to GABA-T.
    Type of Medium: Electronic Resource
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