Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to assess whether the cerebrovascular response to hypercapnia is blunted in OSA patients and if this could alter the ventilatory response to hypercapnia before and after CPAP therapy. We measured the cerebrovascular, cardiovascular and ventilatory responses to hypercapnia in 8 patients with OSA (apnoea-hypopnoea index=101+/-10) before and after 4-6 weeks of CPAP therapy and in 10 control subjects who did not undergo CPAP therapy. The cerebrovascular and ventilatory responses to hypercapnia were not different between OSA and controls at baseline or follow-up. The cardiovascular response to hypercapnia was significantly increased in the OSA group by CPAP therapy (mean arterial pressure response: 1.30+/-0.16 vs. 2.04+/-0.36 mmHg Torr(-1); p=0.007). We conclude that in normocapnic, normotensive OSA patients without cardiovascular disease, the ventilatory, cerebrovascular, and cardiovascular responses to hypercapnia are normal, but the cardiovascular response to hypercapnia is heightened following 1 month of CPAP therapy.
 ...
PMID:Ventilatory and cerebrovascular responses to hypercapnia in patients with obstructive sleep apnoea: effect of CPAP therapy. 1899 1

Hypertensive patients with obstructive sleep apnea syndrome (OSAS) constitute a high-risk group for metabolic syndrome. OSAS directly induces negative intrathoracic pressure and decreases pulmonary stretch receptor stimulation, chemoreceptor stimulation, hypoxemia, hypercapnia and microarousal. These changes potentiate various risk factors, including the sympathetic nervous system, renin-angiotensin-aldosterone system and inflammation. Early detection and treatment of OSAS in asymptomatic hypertensive patients is essentially important to prevent hypertensive target organ damage and subsequent cardiovascular events. Continuous positive airway pressure (CPAP) therapy, a first-line treatment in hypertensive patients with moderate to severe OSAS, reduces ambulatory BP level, particularly during the sleep period, and midnight BP surge. However, individual differences in the BP-lowering effect of CPAP have been observed. OSAS hypertensive patients who do not tolerate CPAP remain at a high risk for cardiovascular disease because of negative intrathoracic pressure and need more aggressive antihypertensive treatment to achieve 24-h BP control with nocturnal BP <120/70 mm Hg.
 ...
PMID:Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control. 1946 49

Obstructive sleep apnoea (OSA) is a common disorder characterized by the repetitive complete or partial collapse of the upper airway during sleep. It results in intermittent hypoxaemia and hypercapnia, cortical arousals and surges of sympathetic activity. The occurrence of OSA has also been linked to serious long-term adverse health consequences; such as hypertension, metabolic dysfunction, cardiovascular disease, neurocognitive deficits and motor vehicle accidents. There have been several advances in the field of particular clinical importance: (i) the development of portable monitoring as part of a simplified clinical algorithm for the diagnosis of OSA in selected patients; (ii) growing awareness of the cardio-metabolic health consequences of OSA and (iii) emerging evidence to support a range of non-continuous positive airway pressure (CPAP) treatment modalities, such as oral appliances.
 ...
PMID:Obstructive sleep apnoea--an update. 1981 52

The prevalence of sleep-disordered breathing (SDB) in the advanced chronic kidney disease (CKD) patient population has been estimated to be more than 50 per cent. SDB is associated with episodic upper airway obstruction or cessation of breathing during sleep leading to repetitive episodes of hypoxaemia, hypercapnia, and sleep fragmentation, activation of the sympathetic nervous system, endothelial dysfunction, oxidative stress, and inflammation. Clinical consequences of this disorder may include excessive daytime sleepiness, depressed mood, cognitive impairment, hypertension, as well as increased risk for cardiovascular disease and metabolic dysregulation. SDB may also contribute substantially to the daytime sleepiness, poor quality of life, and high rate of cardiovascular disease in CKD patients. Although the causal links between CKD and SDB remain speculative, there are multiple factors related to fluid overload and azotaemia that may contribute to the increased propensity to SDB. Renal transplantation, nocturnal automated peritoneal dialysis and nocturnal haemodialysis have been found to be associated with a reduction in the severity of SDB when compared to conventional forms of dialysis. Nocturnal dialysis modalities may facilitate further understanding of the pathophysiology of SDB as well as provide therapeutic alternatives for patients with both kidney failure and SDB. SDB is an important but often overlooked public health problem in the CKD patient population. Early diagnosis and treatment of SDB may provide better quality of life and attenuate the cardiovascular risk of morbidity and mortality in these patients.
 ...
PMID:Sleep disordered breathing in patients with chronic kidney disease. 2030 53

Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. Increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality, but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhythmias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes, and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intrathoracic pressure, micro-arousal, sympathetic hyperactivity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulability, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders. In this article we discuss the different aspects of the relationship between OSAS and pathogenically different conditions such as systemic hypertension, coronary artery disease, stroke, metabolic abnormalities, arrhythmias, and heart failure, and we also discuss the kaleidoscope of phenomena implicated in the pathogenesis of this challenging disease.
 ...
PMID:Obstructive sleep apnea syndrome and cardiovascular diseases. 2145 62

Obstructive sleep apnea (OSA) is associated with hypertension (HTN) and cardiovascular disease. Transient episodes of hypoxia, hypercapnia, and blood pressure elevation during OSA may lead to neural damage and subsequently white matter disease (WMD). As WMD is usually the result of chronic small vessel ischemia, a relationship between OSA and cerebrovascular disease may exist. This case series aimed to establish a relationship between OSA and WMD. Sixty-two patients without cerebrovascular disease who had both a polysomnogram and brain magnetic resonance imaging were identified. All patients carried the diagnosis of HTN. WMD was evaluated using the age-related white matter changes scale. Although half of the study population had WMD on magnetic resonance imaging, no association was found between WMD with severity of OSA (P=0.9). Our results are limited by the small sample size and by coexistent HTN in all patients. Further studies are needed to elucidate the relationship between OSA and WMD, especially among nonhypertensive patients. Future research should also address if OSA treatment has any effect on WMD.
 ...
PMID:Sleep apnea and white matter disease in hypertensive patients: a case series. 2188 75

Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction, resulting in hypoxemia, hypercapnia and sleep fragmentation. Pathophysiological sequelae include sympathetic activation, increased oxidative stress and a generalized inflammatory response, culminating in endothelial dysfunction. These are the proposed mechanisms that mediate the increased risk of hypertension and cardiovascular disease among patients with OSA outside of pregnancy. It is intriguing to consider the consequences of these events on pregnancy outcomes. There is a growing literature on the impact of maternal OSA on hypertensive disorders of pregnancy, gestational diabetes and impaired fetal growth. The data, while promising, require confirmation with larger numbers to verify the findings. OSA may be an important mediator of the poor perinatal outcomes associated with maternal obesity; moreover, one which may be amenable to treatment. This review discusses OSA and summarizes the current literature linking OSA with adverse perinatal outcomes.
 ...
PMID:Obstructive sleep apnea and pregnancy: the effect on perinatal outcomes. 2236 75

Obstructive sleep apnea (OSA)-induced biological changes include intermittent hypoxia, intermittent hypercapnia, intrathoracic pressure changes, sympathetic activation and sleep fragmentation. OSA can cause metabolic dysregulation, endothelial dysfunction, systemic inflammation, oxidative stress and hypercoagulation, and neurohumoral changes. There is evidence suggesting that OSA is independently associated with metabolic syndrome. OSA has been shown to increase the risk for systemic hypertension, pulmonary vascular disease, ischemic heart disease, cerebral vascular disease, congestive heart failure and arrhythmias. Although there are evidences accumulating that there may be a causal relationship between OSA and cardiovascular disorders, there is a need for more data from randomized controlled intervention trials to confirm this relationship. Many risk factors of OSA (age, male gender and obesity) are also known risk factors for cardiovascular disease. Severe OSA-hypopnea significantly increases the risk of fatal and nonfatal cardiovascular events in both men and women, and continuous positive airway pressure treatment reduces this risk in both. Neurocognitive consequences of OSA include daytime sleepiness, loss of alertness, memory deficit, reduced vigilance, impaired executive function, increased risk for automobile and occupational accidents, and decreased quality of life.
 ...
PMID:Morbidities associated with obstructive sleep apnea. 2313 49

A wide range of clinical consequences may be associated with obstructive sleep apnea (OSA) including systemic hypertension, cardiovascular disease, pulmonary hypertension, congestive heart failure, cerebrovascular disease, glucose intolerance, impotence, gastroesophageal reflux, and obesity, to name a few. Despite this, 82 % of men and 93 % of women with OSA remain undiagnosed. OSA affects many body systems, and induces major alterations in metabolic, autonomic, and cerebral functions. Typically, OSA is characterized by recurrent chronic intermittent hypoxia (CIH), hypercapnia, hypoventilation, sleep fragmentation, peripheral and central inflammation, cerebral hypoperfusion, and cerebral glucose hypometabolism. Upregulation of oxidative stress in OSA plays an important pathogenic role in the milieu of hypoxia-induced cerebral and cardiovascular dysfunctions. Strong evidence underscores that cerebral amyloidogenesis and tau phosphorylation--two cardinal features of Alzheimer's disease (AD), are triggered by hypoxia. Mice subjected to hypoxic conditions unambiguously demonstrated upregulation in cerebral amyloid plaque formation and tau phosphorylation, as well as memory deficit. Hypoxia triggers neuronal degeneration and axonal dysfunction in both cortex and brainstem. Consequently, neurocognitive impairment in apneic/hypoxic patients is attributable to a complex interplay between CIH and stimulation of several pathological trajectories. The framework presented here helps delineate the emergence and progression of cognitive decline, and may yield insight into AD neuropathogenesis. The global impact of CIH should provide a strong rationale for treating OSA and snoring clinically, in order to ameliorate neurocognitive impairment in aged/AD patients.
 ...
PMID:Death by a thousand cuts in Alzheimer's disease: hypoxia--the prodrome. 2340 Jun 34

This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.
...
PMID:Hyperventilation, cerebral perfusion, and syncope. 2426 79


<< Previous 1 2 3 Next >>