2007
DOI: 10.1016/j.smrv.2006.03.006
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Opioids, sleep architecture and sleep-disordered breathing

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Cited by 251 publications
(196 citation statements)
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References 51 publications
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“…One such possibility could be increased generalized anxiety or a more anxious response to medical equipment in these patients. Our data also show that nearly 20% of patients with CompSAS used opioids, agents known to be associated with central sleep apnea and altered respiratory control [24]. Opioid use could potentially be a risk factor for the development of CompSAS, though the mechanism is not understood; on the other hand, opioids are known to suppress PLMS.…”
Section: Discussionmentioning
confidence: 55%
“…One such possibility could be increased generalized anxiety or a more anxious response to medical equipment in these patients. Our data also show that nearly 20% of patients with CompSAS used opioids, agents known to be associated with central sleep apnea and altered respiratory control [24]. Opioid use could potentially be a risk factor for the development of CompSAS, though the mechanism is not understood; on the other hand, opioids are known to suppress PLMS.…”
Section: Discussionmentioning
confidence: 55%
“…Genel olarak opiyatların kullanımının REM uykusunu ve yavaş dalga uykusunu azaltarak, uyanıklığı artırarak uykuyu önemli ölçüde bozduğu; 8,19 eroin kullanımının, morfin ve metadon kullanımına göre REM uyku süresi ve teta dalgasına olumsuz etkisinin daha fazla olduğu gösterilmiştir. 19 Diğer yandan, eroin yoksunluğu-nun uyku bozuklukları ilişkili olduğu bilinmektedir.…”
Section: Discussionunclassified
“…7 Endojen opiyatların peptid yapılı nörohormon vasopressin ile birlikte uykunun başlatılması ve sürdürülmesinde, suprakiyazmatik nükleus tarafından düzenlenen sirkadiyen ritm üzerinden etkili oldukları var sayılmıştır. 8 Ağrı ve opiyatlar hipofiz bezinden vasopressin salınımını uyarır-lar, vasopressin de beyin omurilik sıvısına endorfinlerin salınımına neden olur. 9 Suprakiyazmatik ve paraventriküler nükleuslarda vazopressin, kan düzeyi sirkadiyen olarak değişkenlik gösteren dinorfinle birlikte depolanır.…”
Section: Introductionunclassified
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“…The International Diabetes Federation (IDF) Taskforce on Epidemiology and Prevention [Shaw, 2008] stated that the pathophysiological consequences of hypoxemia and sleep fragmentation might be involved in the development of insulin resistance and pancreatic -cell dysfunction through various biological mechanisms, such as direct effects of 1) intermittent hypoxia/desaturation and hypoxemia, 2) sympathetic nervous system activation (catecholamine) [Prabhakar & Kumar, 2010;Esleradrenal dysfunction (cortisol) [Follenius, 1992;Henley, 2009;Vgontzas & Chrousos, 2002], 5) dysregulation of adipocytokines (plasminogen activator inhibitor-1 [PAI-1], adiponectin) [Lam, 2008], 6) sleep architecture [Wang & Teichtahl, 2007] and 7) other factors. Both SDB/SA and T2DM are strongly associated with ACVD [Bradley & Floras, 2009] (Figure 1).…”
Section: Type 2 Diabetes and Sleep Apneamentioning
confidence: 99%