Cardiorespiratory function is altered by picomole injections of 5′-N-ethylcarboxamidoadenosine into the nucleus tractus solitarius of rats

Barraco, Robin A.; Janusz, Cynthia A.; Schoener, Eugene P.; Simpson, Lori

doi:10.1016/0006-8993(90)90277-i

Cited by 41 publications

(19 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Brain adenosine levels increase during seizures and inhibit neuronal activity (During and Spencer, 1992). Injection of an adenosine analog into the brainstem depresses respiratory function (Barraco et al, 1990). Adenosine may thus be involved in postictal hypoxemia however direct evidence for such a mechanism is lacking.…”

Section: Neural Mechanisms Generating and Modulating Respiratory Rhytmentioning

confidence: 99%

Respiratory Pathophysiology With Seizures and Implications for Sudden Unexpected Death in Epilepsy

Kennedy

Seyal

2015

Journal of Clinical Neurophysiology

View full text Add to dashboard Cite

There is increasing evidence that periictal respiratory disturbances are an important contributor to the pathophysiological changes leading to sudden unexpected death in epilepsy (SUDEP). In patients with SUDEP occurring in epilepsy monitoring units, respiratory disturbances occurred early in the postictal period and frequently preceded terminal bradycardia and asystole. Periictal hypoxemia and hypercapnia are observed in about one-third of patients undergoing video-EEG telemetry. Pulmonary edema is frequently observed at autopsy in cases of SUDEP and may be relevant as a contributing cause in a subset of SUDEP. Animal studies support the notion that periictal respiratory disturbances are crucial to the pathophysiology of SUDEP. Serotonergic neurons modulate the excitability of the neuronal network generating the respiratory rhythm. Ictal and periictal impairment of serotonergic and glutaminergic neurons involved in the arousal system may also predispose to SUDEP by impeding the patient's ability to reposition the head and facilitate ventilation after a seizure. Periictal functional impairment of serotonergic neurons seems to be important in the pathophysiology of SUDEP and a potential target for pharmacotherapy aimed at SUDEP risk reduction.

show abstract

Section: Neural Mechanisms Generating and Modulating Respiratory Rhytmentioning

confidence: 99%

Respiratory Pathophysiology With Seizures and Implications for Sudden Unexpected Death in Epilepsy

Kennedy

Seyal

2015

Journal of Clinical Neurophysiology

View full text Add to dashboard Cite

show abstract

“…During seizures, adenosine levels increase in the brain and suppress seizure activity 93 . However, activation of adenosine receptors in the brainstem also induces severe respiratory depression 94 . It is possible that the increase in extracellular adenosine causes hypoventilation, apnea, and arrhythmias in the postictal period.…”

Section: Cellular Mechanismsmentioning

confidence: 99%

Mechanisms of sudden unexpected death in epilepsy: the pathway to prevention

et al. 2014

View full text Add to dashboard Cite

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy, and yet many physicians do not know about this high risk of sudden death. It has been widely believed that SUDEP is due to cardiac abnormalities during the post-ictal period. However, recent studies have demonstrated that respiratory depression is common following a seizure, and can be severe enough to cause a substantial decrease in oxygen saturation. In this review we summarize evidence for cardiac, respiratory, and arousal abnormalities during the ictal and post-ictal period and potential mechanisms for these abnormalities. We discuss mouse models of seizure-induced death and how these models are useful for understanding the mechanisms that underlie SUDEP. Some of these are due to genetic mutations that have counterparts in human syndromes. Controversy remains regarding the relative importance of cardiac failure versus respiratory arrest as the primary cause of death. Resolving this controversy will require simultaneous monitoring of cardiac and respiratory parameters during cases of near SUDEP in humans and detailed pathophysiological data from animal models during seizure-induced death. Effective preventive strategies in high-risk patients will rely on defining the mechanisms that initiate the sequence of events that lead from seizures to death.

show abstract

“…gene approach in association studies as applied in this Adenosine analogues have depressant effects on respirstudy will provide for numerous false positive results atory function in the brainstem, 3 an impairment of by chance with the commonly accepted significance level of P Ͻ 0.05 given the numerous possible candidepressant brainstem respiratory mechanisms being …”

mentioning

confidence: 99%

Systematic mutation screening and association study of the A1 and A2a adenosine receptor genes in panic disorder suggest a contribution of the A2a gene to the development of disease

et al. 1998

View full text Add to dashboard Cite

Cardiorespiratory function is altered by picomole injections of 5′-N-ethylcarboxamidoadenosine into the nucleus tractus solitarius of rats

Cited by 41 publications

References 39 publications

Respiratory Pathophysiology With Seizures and Implications for Sudden Unexpected Death in Epilepsy

Respiratory Pathophysiology With Seizures and Implications for Sudden Unexpected Death in Epilepsy

Mechanisms of sudden unexpected death in epilepsy: the pathway to prevention

Systematic mutation screening and association study of the A1 and A2a adenosine receptor genes in panic disorder suggest a contribution of the A2a gene to the development of disease

Contact Info

Product

Resources

About