SYMPATHETIC NERVOUS SYSTEM/physiology
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Porucha funkce autonomního nervového systému (ANS) způsobená chronickým stresem je velmi pravděpodobně jedním z hlavních patofyziologických mechanizmů vzniku a progrese esenciální hypertenze, zejména u mladších hypertoniků. Závažnost dysfunkce lze hodnotit pomocí jednoduchých testů, jakým je například měření klidové srdeční frekvence. Betablokátory jsou nejúčinnější skupinou pro chronickou léčbu nadměrné aktivity sympatiku.
- MeSH
- fyziologický stres MeSH
- hydrokortison toxicita MeSH
- krysa rodu rattus MeSH
- noradrenalin analýza MeSH
- slezina analýza účinky léků MeSH
- srdce analýza účinky léků MeSH
- sympatický nervový systém patofyziologie růst a vývoj účinky léků MeSH
- thyroxin toxicita MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
[1st ed.] 69 s. : ill.
Acta physiologica Scandinavica, ISSN 0302-2994 vol. 136, suppl. 584, 1989
45 s.
- MeSH
- kardiovaskulární fyziologické jevy MeSH
- sympatický nervový systém MeSH
- Publikační typ
- abstrakty MeSH
- kongresy MeSH
- Konspekt
- Fyziologie člověka a srovnávací fyziologie
- NLK Obory
- fyziologie
- kardiologie
Obstructive sleep apnea (OSA) and hypertension are closely linked conditions. Disordered breathing events in OSA are characterized by increasing efforts against an occluded airway while asleep, resulting in a marked sympathetic response. This is predominantly due to hypoxemia activating the chemoreflexes, resulting in reflex increases in sympathetic neural outflow. In addition, apnea - and the consequent lack of inhibition of the sympathetic system that occurs with lung inflation during normal breathing - potentiates central sympathetic outflow. Sympathetic activation persists into the daytime, and is thought to contribute to hypertension and other adverse cardiovascular outcomes. This review discusses chemoreflex physiology and sympathetic modulation during normal sleep, as well as the sympathetic dysregulation seen in OSA, its extension into wakefulness, and changes after treatment. Evidence supporting the role of the peripheral chemoreflex in the sympathetic dysregulation seen in OSA, including in the context of comorbid obesity, metabolic syndrome, and systemic hypertension, is reviewed. Finally, alterations in cardiovascular variability and other potential mechanisms that may play a role in the autonomic imbalance in OSA are also discussed.
Scandinavian journal of gastroenterology, ISSN 0085-5928 vol. 19, suppl. 89, 1984
144 s. : il., tab., grafy ; 24 cm
- MeSH
- sympatický nervový systém MeSH
- trávicí systém - fyziologické jevy MeSH
- žaludek MeSH
- Publikační typ
- kongresy MeSH
- Konspekt
- Patologie. Klinická medicína
- NLK Obory
- gastroenterologie
- neurovědy
The available studies on cerebrovascular reactivity and cerebral oxygenation in obstructive sleep apnoea (OSA) patients brought conflicting results, yet the overall evidence suggests that resting state cerebral perfusion is diminished in these patients. Interestingly, in a group of healthy professional breath-hold divers who are exercising very long apnoeas - episodes corresponding to the ones observed in patients with OSA - demonstrated that cerebral oxygenation may remain stable at the expense of extreme sympathetic nervous system (SNS) activation. In the present review we address several mechanisms that could potentially explain these discrepancies. We focus in depth on mechanisms of central SNS reinforcement in OSA including dysfunctional baroreflex response, and inflammatory processes within the brain centres controlling the cardiovascular system. Additionally, novel insights into physiology of cerebral blood flow regulation are proposed, including the role of short-term blood pressure changes, heart rate fluctuations and baroreflex alterations. Finally, a potential role of increased blood flow pulsatility in cerebrospinal fluid circulation changes and its influence on SNS drive is highlighted. The presented review provides insights into how sympathetic nervous system reinforcement in OSA promotes maladaptive mechanisms that could alter cerebral perfusion regulation, and result in functional and structural cerebral changes.
- MeSH
- baroreflex fyziologie MeSH
- kardiovaskulární systém MeSH
- krevní tlak fyziologie MeSH
- lidé MeSH
- mozek patofyziologie MeSH
- mozkový krevní oběh fyziologie MeSH
- obstrukční spánková apnoe patofyziologie MeSH
- srdeční frekvence fyziologie MeSH
- sympatický nervový systém patofyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
146 s. : il.
