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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

Glomerular visceral epithelial cells, unlike epithelial cells in other organs or in the more distal segments of the nephron, are highly differentiated, terminal cells that do not undergo cell division under physiological conditions in the postnatal period or during conditions that result in renal hypertrophy. Adjacent cells are connected to each other at the level of complex interdigitations or foot processes by filtration slit diaphragms. This particular arrangement contributes to the extremely high hydraulic conductivity of the normal glomerular capillary. Toxic and metabolic damage to the visceral epithelial cells or conditions of extreme glomerular hypertrophy result, in the short term, in diffuse or focal simplification and flattening of the foot processes. The areas of the capillary wall covered by such a simplified epithelium are likely to have a greatly reduced hydraulic conductivity which results from the greatly diminished surface area available for filtration. The rearrangement of foot processes also leads to focal areas of denudation of the basement membrane. Such denuded areas, however, are likely to result in an increase in local hydraulic flux, especially under conditions of capillary hypertension. Such defects have been shown to be the pathway of increased permeability to macromolecular markers and proteinuria. Large plasma proteins are retained in the subendothelium by the size-restrictive water-filled channels of the lamina densa and accumulate upstream in the form of hyaline which eventually occludes individual loops. More severe epithelial cell injury and denudation may also result in collapse of entire tuft segments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:How does glomerular epithelial cell injury contribute to progressive glomerular damage? 815

Obstructive sleep apnea affects millions of individuals. It usually is due to pharyngeal collapse during sleep, resulting in daytime somnolence. This can have grave consequences on everyday life and in the long term can lead to pulmonary and systemic hypertension, myocardial disease, and stroke. Non-structural obstructive sleep apnea can be relieved by tracheostomy and continuous positive airway pressure, two methods that bypass the overly compliant pharyngeal musculature during inspiration. It may well be desirable to exchange a dynamic and more physiologic approach to obstructive sleep apnea for these purely static solutions. This approach should restore disturbed cyclical stiffening of the upper airway by electronically stimulating the appropriate muscles, timed by information originating during the inspiratory effort. The open-loop systems proposed here are based upon principles pioneered by us for the rehabilitation of the paralyzed larynx that are now well within practical reach of current technologies.
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PMID:The potential for neurostimulation in obstructive sleep apnea. 818 85

This paper describes the history of an 81-year-old female suffering from a giant dissecting aortic aneurysm with concealed perforation within the thorax. The patient had suffered from arterial hypertension for about 10 years and had been treated with thiazide. Nine months prior to admission the patient was in a state of collapse, and ultrasound examination revealed an intra-abdominal aortic aneurysm. At this time thoracic x-ray showed aortic sclerosis and elongation of the aorta but no signs of aneurysm formation. After this episode the patient was symptom-free for the next 9 months. Following a further syncopal attack with severe thoracic pain, the patient was hospitalized at the intensive care unit. Both in thoracic x-ray and computed tomography of the thorax, a pronounced dissecting aortic aneurysm with perforation of the thoracic aorta into the mediastinum could be established. Because of the patient's poor general condition and advanced age, as well as far-reaching pathological findings, surgery was not advised by either the heart and vascular surgeon or the anesthetist. Following 1 week's intensive therapy, the patient's general condition improved greatly, with stabilization of thoracic pain, blood pressure, and respiratory action. On the other hand, thoracic x-ray, computed tomography, and magnetic resonance imaging produced a distinct progression of the aneurysm with consequent mild displacement of mediastinum and left lung. Laboratory examinations for syphilis showed no evidence of that disease. After further improvement the patient was discharged 4 weeks after admission and has been symptom-free for 6 months in spite of the extensive pathological findings described herein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Giant dissecting aortic aneurysm with concealed perforation in an 81-year-old female. 845 18

The effect of angiotensin II-induced hypertension on tumor interstitial fluid pressure (TIFP) and tumor blood flow (TBF) was investigated to examine blood flow and pressure regulation in solid tumors. TIFP measurements were made before and after administration of angiotensin II using the wick-in-needle method in s.c. tumor implants. Relative TBF was continuously monitored by laser doppler velocimetry. The effect of host strain on TIFP was evaluated in MCA-IV mammary carcinoma, transplanted in C3H and SCID mice, and showed no significant difference. The effects of tumor types were evaluated by comparing two murine tumors, MCA-IV mammary carcinoma and FSaII fibrosarcoma, and a human tumor xenograft, LS174T adenocarcinoma, transplanted in SCID mice. Baseline TIFP was elevated in all three tumor lines to significantly different pressures. AII-induced hypertension (approximately 150 mm Hg) had a variable but tumor line-specific effect on TIFP and TBF. The increase in TIFP was correlated with the baseline TIFP (r2 = 0.853) (increasing from 6.9 to 8.7 mm Hg, 10.5 to 15.8 mm Hg, and 21.7 to 29.4 mm Hg in FSaII, MCA-IV, and LS174T, respectively). These data suggest that in addition to blood flow redistribution due to the steal phenomenon, arterial control of TBF and TIFP exists within these solid tumors; however, the extent of control is tumor line dependent and less than that in normal tissues. Moreover, parallel increases in TIFP and TBF do not support the hypothesis that elevated TIFP causes vascular collapse and thus decreases TBF.
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PMID:Effect of angiotensin II induced hypertension on tumor blood flow and interstitial fluid pressure. 849 5

In this clinico-pathologic study, post-mortem kidney material from 30 cases with malignant hypertension (MHT) defined as severe hypertension with bilateral retinal haemorrhages and exudates (grade III retinopathy) with (grade IV retinopathy) or without papilloedema, were studied. Mucoid intimal proliferation (MIP) in interlobular artery and ischaemic collapse of the glomerular tufts occurred in all cases, whereas fibrinoid necrosis (FN) was seen in only 24 (80%) of the cases. FN was not correlated nor associated with sex, age, blood pressure, retinopathy or serum creatinine. Tubular atrophy and interstitial fibrosis occurred in 24 (80%) and correlated best (rS = 0.8, p < 0.05) with serum creatinine in comparison to glomerular sclerosis (rS = 0.6, p = n.s), fibrinoid necrosis (rS = 0.49, p = n.s) and epithelial crescents (rS = 0.43, p = n.s). This study provides histologic evidence of lack of difference between grades III and IV retinopathy, shows MIP as the more characteristic vascular lesion in MHT and also, good correlation between renal function and tubulointerstitial involvement.
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PMID:Kidney histology and clinical correlates in malignant hypertension. 851 38

Obstructive sleep apnea is a breathing disorder characterized by repeated collapse of the upper airway during sleep, with cessation of breathing. Four percent of middle-aged men and 2 percent of middle-aged women meet minimal criteria for the sleep apnea syndrome. Risk factors include loud, chronic snoring, obesity (especially nuchal), hypertension, excessive daytime sleepiness, and an increased tendency for automobile and work-related accidents. Cardiovascular comorbidity and complications include systemic hypertension, arrhythmias and possibly myocardial ischemia and myocardial infarction in patients with coronary artery disease. Diagnosis is confirmed by a sleep study; currently, polysomnography is the optimum test. Treatment options range from behavioral therapy alone for mild cases to a combination of behavioral approaches and continuous positive airway pressure and/or surgery for moderate and severe cases. Continuous positive airway pressure is the most effective noninvasive treatment. Primary care physicians play a key role in the identification, management and follow-up of patients with sleep apnea.
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PMID:Sleep apnea: is your patient at risk? National Heart, Lung, and Blood Institute Working Group on Sleep Apnea. 854 58

Chronic nitric oxide (NO) blockade promotes progressive hypertension, marked renal vasoconstriction, and glomerular and renal interstitial injury. Inhibition of the renin/angiotensin system prevents only partially the functional and structural abnormalities associated with this model. Because endothelin (ET) is a powerful endogenous vasoconstrictor and promitogen, we examined the hypothesis that it might also mediate the hemodynamic and renal structural effects of chronic NO blockade. Four groups of 16 adult male Munich-Wistar rats were studied. Group C received daily i.p. saline injections and no drug treatment. Group C+FR received daily i.p. injections of the ETA inhibitor FR139317, 32 mg/kg. Group NAME received the NO inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), 65 mg/kg/day in the drinking water, and group NAME+FR received both L-NAME and FR139317. At 2 weeks of treatment, renal and systemic hemodynamic parameters assessed under anesthesia were similar in Groups C and C+FR. Rats of Group NAME exhibited systemic hypertension and renal vasoconstriction characteristic of this model. FR139317 was ineffective in preventing these abnormalities in Group NAME+FR. In eight additional rats of each group observed at 30 days, FR139317 treatment was equally inactive in the prevention of glomerular collapse and interstitial expansion, the two chief modalities of renal injury in this model. These results suggest that ET does not participate, at least via the ETA receptor, in the pathogenesis of hypertension, renal dysfunction, or renal injury associated with the chronic NO inhibition model.
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PMID:Do ETA receptors participate in the hemodynamic and renal effects of chronic nitric oxide blockade? 858 46

Long-term nitric oxide blockade by N omega -nitro-L-arginine methyl ester (L-NAME) leads to severe and progressive hypertension. The role of salt intake in this model is unclear. To verify whether salt dependence in this model is related to the extent of nitric oxide inhibition, we gave adult male Munich-Wistar rats a low salt, standard salt, or high salt diet and oral L-NAME treatment at either 3 or 25 mg/kg per day. At 10 to 15 days of treatment, the slope of the pressure-natriuresis line was decreased in rats receiving low-dose L-NAME compared with untreated controls. In rats treated with the higher dose, the line was shifted to the right but remained parallel to that obtained in untreated controls. Renal vascular resistance was moderately increased in rats receiving low-dose L-NAME, whereas high-dose L-NAME induced a marked vasoconstriction that was aggravated by salt overload. Low-dose L-NAME treatment induced hypertension only when associated with sodium overload. In rats receiving high-dose L-NAME, hypertension was aggravated by sodium excess but was not ameliorated by sodium restriction. Long-term (6 weeks) L-NAME treatment was associated with progressive hypertension, which was aggravated by salt overload, and with the development of albuminuria, focal glomerular collapse, glomerulosclerosis, and renal interstitial expansion. These abnormalities were worsened by salt overload and largely prevented by salt restriction. In the model of chronic nitric oxide blockade, salt dependence is a function of the inhibitor dose, and renal injury varies directly with the level of salt intake.
Hypertension 1996 May
PMID:Effect of salt intake and inhibitor dose on arterial hypertension and renal injury induced by chronic nitric oxide blockade. 862 Dec 12

A case of thrombotic microangiopathy presenting as a hemolytic uremic syndrome complicated by untreatable hypertension and ultimately requiring bilateral nephrectomy is discussed. Severe hypertension and renal failure may complicate the course of vascular diseases of the kidney, including thrombotic microangiopathy, chronic hypertension, and scleroderma. Toxins, pressure stress, and immune material may trigger the initial injury to vascular endothelium. The malignant course of these renal vascular diseases seems linked to the severity of vascular injury. Endothelial injury manifests with swelling and detachment of endothelial cells from the basement membrane, expansion of the subendothelial space, and newly formed basement membrane-like material. In arterioles, endothelial injury precedes myointimal swelling and proliferation, leading to vascular lumina narrowing or obliteration and secondary glomerular ischemia, with glomerular tuft collapse and garland-like wrinkling and thickening of the capillary wall. Endothelial cell injury is very likely the common determinant of a cascade of events that lead to irreversible renal failure. When the initial insult (toxins, mechanical stress, antibodies) is promptly removed, lesions are self-limiting and the patient usually recovers. However, a severe insult persisting for some time can lead to chronic and irreversible vascular lesions that, through renal ischemia, trigger maximal activation of the renin angiotensin system with a brisk elevation in arterial blood pressure that may combine to further vascular injury and renal ischemia. Moreover, enhanced shear stress in the severely narrowed microcirculation, through abnormal von Willebrand factor processing, can also favor endothelial injury and platelet aggregation, which may further worsen the vascular lesions and sustain the microangiopathic process. Plasma manipulation, arteriolar vasodilators, and angiotensin-converting enzyme inhibitors normally control the vicious circle, but in few severe cases bilateral nephrectomy remains the last chance to save the patient's life.
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PMID:Malignant vascular disease of the kidney: nature of the lesions, mediators of disease progression, and the case for bilateral nephrectomy. 867 55


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