PubMed · 9442946
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D McKelvey. 1998. Using the fentanyl patch.. https://pubmed.ncbi.nlm.nih.gov/9442946/
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BACKGROUND: Chronic in vivo treatment with nitroglycerin (NTG) induces tolerance to nitrates and cross-tolerance to nitrovasodilators and endothelium-derived nitric oxide (NO). We previously identified increased vascular superoxide formation and reduced NO bioavailability as one causal mechanism. It is still controversial whether intracellular downstream signaling to nitrovasodilator-derived NO is affected as well. METHODS AND RESULTS: We therefore studied the effects of 3-day NTG treatment of rats and rabbits on activity and expression of the immediate NO target soluble guanylyl cyclase (sGC) and on the cGMP-activated protein kinase I (cGK-I). Tolerance was induced either by chronic NTG infusion via osmotic minipumps (rats) or by NTG patches (rabbits). Western blot analysis, semiquantitative reverse transcription-polymerase chain reaction, and Northern blot analysis revealed significant and comparable increases in the expression of sGC alpha(1) and beta(1) subunit protein and mRNA. Studies with the oxidative fluorescent dye hydroethidine revealed an increase in superoxide in the endothelium and smooth muscle. Stimulation with NADH increased superoxide signals in both layers. Although cGK-I expression in response to low-dose NTG was not changed, a strong reduction in vasodilator-stimulated phosphoprotein (VASP) serine239 phosphorylation (specific substrate of cGK-I) was observed in tolerant tissue from rats and rabbits. Concomitant in vivo and in vitro treatment with vitamin C improved tolerance, reduced oxidative stress, and improved P-VASP. CONCLUSIONS: We therefore conclude that increased expression of sGC in the setting of tolerance reflects a chronic inhibition rather than an induction of the sGC-cGK-I pathway and may be mediated at least in part by increased vascular superoxide.
OBJECTIVE: The aim of the present study was to evaluate how hormone replacement therapy (HRT) could influence the course of primary headaches in postmenopausal women. METHODS: Fifty patients presenting for clinical evaluation of menopausal status and suffering from headache were enrolled. The observational period lasted 7 months during which women filled in a diary with the clinical characteristics of headache attacks (frequency, days with headache, severity) and the analgesic use (no. of analgesic/month). Climacteric symptoms and both anxiety and depression were also measured. At the first visit the patients were divided into two groups: those suffering from migraine without aura (MwA) and those suffering from episodic tension-type headache (ETTH) and separately randomized. After a month of run-in period, they received two different HRT regimen, either: (1) transdermal estradiol 50 mcg every 7 days for 28 days plus medroxyprogesterone acetate (MAP) 10 mg/day from 15th to 28th day, or (2) oral conjugated estrogens 0.625 mg/day for 28 days plus MAP 10 mg/day for the last 14 days. Follow up evaluations were planned after 1, 3 and 6 months of treatment. RESULTS: While we did not observe any significance change regarding headache parameters in ETTH patients during both transdermal and oral treatment, the course of migraine was significantly affected by the route of HRT. Both frequency of attacks (F = 8.5; P < 0.000) and days with headache (F = 6.9; P < 0.000) significantly increased during HRT in the subgroup assuming oral formulation. On the contrary, no changes in the same parameters were found in the group taking transdermal treatment. Moreover, while severity of migraine was unaffected by HRT, analgesic consumption was significantly increased in the subgroup on oral treatment (F = 6.3; P = 0.001). CONCLUSIONS: HRT significantly affects the course of headache in postmenopausal migraine sufferers. Indeed, while the clinical pattern of ETTH remained stable throughout the observational period, patients suffering from MwA worsened their symptoms within the first 3 months of treatment. In particular, the oral route of administration significantly worsened migraine in comparison to the transdermal route.
OBJECTIVE: To determine the efficacy and safety of percutaneous ethanol injection (PEI) for the treatment of hyperthyroidism caused by bilateral hyperplastic thyroid nodules in cats. DESIGN; Prospective study. ANIMALS: 7 cats. PROCEDURE: Hyperthyroidism was diagnosed on the basis of clinical signs and increased serum total thyroxine (TT4) concentrations. The presence of 2 cervical thyroid nodules was confirmed by use of ultrasonography and technetium Tc 99m albumin thyroid scans. After the death of 1 cat that received PEI in both thyroid nodules at the same time, the protocol was changed to injecting ethanol into 1 nodule at a time, with at least 1 month between injections. Clinical signs, serum TT4 concentrations, serum ionized calcium concentrations, laryngeal function, findings on ultrasonographic examinations of the ventral cervical region, and results of thyroid scans were monitored. RESULTS: Serum TT4 concentrations transiently decreased in all 6 cats (into the reference range in 5 of 6 cats) within 4 days of the first staged ethanol injection. Each subsequent injection resulted in a transient decrease in serum TT4 concentration. The longest period of euthyroidism was 27 weeks. Adverse effects included Horner's syndrome, dysphonia, and laryngeal paralysis. One cat died of unrelated causes. One cat underwent bilateral thyroidectomy, 2 cats were treated with methimazole, and 2 cats that had increased serum TT4 concentrations were not treated further, because they remained clinically normal. CONCLUSIONS AND CLINICAL RELEVANCE: Percutaneous ethanol ablation of bilateral thyroid nodules as a treatment for cats with hyperthyroidism is not recommended. This treatment is not as efficacious as the medical and surgical treatments presently used.