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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We postulated that three extremely obese Yucatan miniature pigs would have more sleep apnea than three nonobese Yucatan miniature pigs. Pigs were studied with the use of electroencephalograms, inductance plethysmography, oximetry, expired nasal CO2, or thermistors. All of the obese pigs, but none of the nonobese pigs, had both sleep apnea (8.5, 10.3, and 97.0 in obese pigs vs. O apnea + hypopnea/h in all nonobese pigs; P < 0.05) and oxyhemoglobin desaturation episodes during sleep [9.4 +/- 3.0 vs. 0 + 0.53 (SD) mean desaturation episodes/h in obese pigs vs. nonobese pigs, respectively; P < 0.05]. Two of the extremely obese pigs had obstructive sleep apnea, whereas the third obese pig had central sleep apnea. We conclude that sleep apnea occurs in extremely obese Yucatan minipigs and suggest that this animal can be used as a model for sleep apnea in obesity.
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PMID:Sleep apnea in obese miniature pigs. 947 62

Noninvasive positive pressure ventilation (NPPV) can improve ventilation in obese subjects during the postoperative period after abdominal surgery. Compared to nasal continuous positive airway pressure (nCPAP), NPPV was superior in correcting blood gas abnormalities both during the night-time and during the daytime in a subgroup of patients with the obesity hypoventilation syndrome (OHS). However, as it is unknown, if and to what extent NPPV can unload the respiratory muscles in the face of the increased impedance of the respiratory system in obesity, this is what was investigated. Eighteen obese subjects with a body mass index > or = 40 kg x m(-2) were investigated during the daytime, which included five healthy controls (simple obesity (SO)), seven patients with obstructive sleep apnoea (OSA) and six patients with the obesity hypoventilation syndrome (OHS). Assisted PPV was performed with bi-level positive airway pressure (BiPAP), applied via a face mask. Inspiratory positive airway pressure (IPAP) was set to 1.2 or 1.6 kPa and expiratory positive airway pressure (EPAP) was set to 0.5 kPa. Inspiratory muscle activity was measured as diaphragmatic pressure time product (PTPdi). Comparison of spontaneous breathing with BiPAP ventilation showed no significant difference in breathing pattern, although there was a tendency towards an increase in tidal volume (VT) in all three groups and a decrease in respiratory frequency (fR) in patients with OSA and OHS. End-tidal carbon dioxide (PET,CO2) with BiPAP was unchanged in SO and OSA, but was decreased in OHS. In contrast, inspiratory muscle activity was reduced by at least 40% in each group. This was indicated by a decrease in PTPdi with BiPAP 1.2/0.5 kPa from mean+/-SD 39+/-5 to 20+/-9 kPa x s (p<0.05) in SO, from 42+/-7 to 21+/-8 kPa x s (p<0.05) in OSA, and from 64+/-20 to 38+/-17 kPa x s (p<0.05) in OHS. With BiPAP 1.6/0.5 kPa, PTPdi was further reduced to 17+/-6 kPa x s in SO, and to 17+/-6 kPa x s in OSA, but not in OHS (40+/-22 kPa x s). We conclude that noninvasive assisted ventilation unloads the inspiratory muscles in patients with gross obesity.
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PMID:Influence of noninvasive positive pressure ventilation on inspiratory muscle activity in obese subjects. 949 72

The pulmonary complications remain the prime cause of morbidity and mortality in sickle cell disease. The pathogenetic mechanisms consists both of an alteration of the rheological properties of the blood, the existence of a hypercoagulability state and above all specific interactions between the abnormal sickle cells and the vascular endothelium and a dysregulation of the vascular reactivity in which nitrous oxide intervenes. The acute chest syndrome (ACS) is characterised by chest pain with dyspnoea and recent radiological abnormalities and it is an acute lung complication whose problem is one of aetiology. The infectious pneumonias are rarely documented. On the other hand, alveolar hypoventilation linked to infarcts of the thoracic ribs, thoracoabdominal trauma, subdiaphragmatic pain, the administration of analgesics causing respiratory depression, obesity or sleep disturbance are frequent causes of ACS. Bronchoalveolar lavage has revealed a frequency of fat emboli following infarcts in the long bones. Pulmonary emboli is rarely a cause. Pulmonary thrombosis is a serious complication, the diagnosis is difficult and is seen in a predisposed clinical setting. The treatment of ACS rests on controlled hydration and antibiotic therapy, oxygen therapy and controlled analgesic therapy. The indications for blood transfusion and for exchange transfusion merits a better evaluation. In the long term patients with sickle cell disease present with a failure of normal thoracopulmonary growth with a restrictive ventilatory defect and progressive diminution in the transfer factor of carbon monoxide with age. A history of ACS favours chronic lung disease. Pulmonary arterial hypertension is less frequent.
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PMID:[The sickle cell anemia lung from childhood to adulthood]. 960 86

We measured body temperature (Tb) and ventilatory and metabolic variables in lean (n = 8) and obese (n = 8) Zucker rats. Measurements were made while rats breathed air, 4% CO2, and 10% O2. Under control conditions, Tb in obese rats was always less than that of their lean counterparts. Obese rats adopted a more rapid, shallow breathing pattern than lean rats in air and had a lower ventilation rate in 4% CO2. Respiration in 10% O2 was similar for the two groups. Metabolic variables did not differ between lean and obese rats whatever the gas breathed. When lean rats were cooled to match Tb in control obese rats with an implanted abdominal heat exchanger, they increased ventilation and metabolism in air; there was no effect of cooling on responses to 4% CO2; and ventilation increased while metabolism decreased in 10% O2. When obese rats were warmed to match Tb in control lean rats, trends in ventilation and metabolism resulted in a tendency toward hyperventilation in air and 4% CO2, but not in 10% O2. Taken overall, matching Tb in lean and obese rats accentuated differences in respiratory and metabolic variables between the two groups. We conclude that differences in respiration between lean and obese Zucker rats are not due to the difference in Tb.
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PMID:Effect of changing body temperature on the ventilatory and metabolic responses of lean and obese Zucker rats. 968 90

The presence of abnormalities of the respiratory center in obstructive sleep apnea (OSA) patients and their correlation with polysomnographic data are still a matter of controversy. Moderately obese, sleep-deprived OSA patients presenting daytime hypersomnolence, with normocapnia and no clinical or spirometric evidence of pulmonary disease, were selected. We assessed the ventilatory control and correlated it with polysomnographic data. Ventilatory neuromuscular drive was evaluated in these patients by measuring the ventilatory response (VE), the inspiratory occlusion pressure (P.1) and the ventilatory pattern (VT/TI, TI/TTOT) at rest and during submaximal exercise, breathing room air. These analyses were also performed after inhalation of a hypercapnic mixture of CO2 (delta P.1/delta PETCO2, delta VE/delta PETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.6 l/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 l/s; TI/TTOT: 0.47 and 0.46 l/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (delta VE/delta PETCO2: 1.51 l min-1 mmHg-1) and inspiratory occlusion pressure (delta P.1/delta PETCO2: 0.22 cmH2O) were normal or slightly reduced in the normocapnic OSA patients. No association or correlation between ventilatory neuromuscular drive and ventilatory pattern, hypersomnolence score and polysomnographic data was found; however a significant positive correlation was observed between P.1 and weight. Our results indicate the existence of a group of normocapnic OSA patients who have a normal awake neuromuscular ventilatory drive at rest or during exercise that is partially influenced by obesity.
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PMID:Assessment of ventilatory neuromuscular drive in patients with obstructive sleep apnea. 969 1

Because of the oscillatory pattern of upper airway resistance and breathing during sleep in patients with obstructive sleep apnea (OSA), we hypothesized that OSA patients have an underlying instability of ventilatory drive to inspiratory muscles. To assess the stability of ventilatory drive in OSA patients and controls, we used the pseudorandom binary stimulation (PRBS) test and examined the closed- and open-loop responses to hyperoxic hypercapnia. The closed-loop response is produced by interactions of dynamic gain in controller, plant, and ventilatory feedback. The open-loop response reflects controller dynamic gain or frequency-dependent chemosensitivity. As compared with 16 nonapneic, nonobese control subjects, a group of nine obese OSA patients had a higher peak response and a more rapid and irregular recovery phase of the closed-loop CO2 response in the PRBS test. The two groups had similar open-loop responses in the PRBS test, suggesting that central dynamic CO2 chemosensitivity was not abnormal in OSA. We conclude that the differences between OSA patients and controls in the closed-loop response in the PRBS test are not due to differences in dynamic controller gain, but are related to differences in dynamic plant gain and/or negative ventilatory feedback. In addition to OSA, obesity may affect these variables and may have been responsible for our findings.
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PMID:Instability of ventilatory control in patients with obstructive sleep apnea. 976 73

The paper concerns surgical treatment of rhonchus. 41 patients with rhonchus and sleep apnea were examined and treated. The patients were characterized by obesity, short fat neck, diseases of the upper respiratory tracts (chronic tonsillitis, adenoids, distortion of the nasal septum, deformity of the external nose, weakness of the palatine curtain). After cleansing of the upper respiratory tracts and recovery of nasal breathing all the patients underwent CO2 laser surgery on the soft palate with good effect.
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PMID:[On aspects of surgical treatment of pathological snoring]. 979 29

Work capacity and cardiopulmonary performance were studied in a group of 11 young obese subjects (BMI 39.9 kg/m2) and a group of 10 young normal subjects (BMI 22 kg/m2). First of all they underwent an incremental cycle ergometer test up to exhaustion. Subsequently, every subject of the two groups performed a constant work rate test at different work loads to estimate cardiac output (Q) below anaerobic threshold (AT) by a 20-second CO2 rebreathing method. Obese subjects had a significantly lower AT (79 vs. 109 W). The ratio between oxygen uptake and heart rate (VO2/HR) (O2 pulse) was higher in the obese group; nevertheless, this variable became significantly lower if we took into consideration the ratio between O2 pulse and kilogram fat-free body mass or kilogram body weight. Both these observations suggest that their reduced work tolerance is linked with a reduced oxygen supply to the muscles in activity. Q increased in similar ways in obese and normal subjects at the preset work rates. The ratio Q/body surface (cardiac index; CI) that we considered in order to try to minimize the differences in body sizes between the two groups, increased less in response to increasing work rates in our obese subjects than in normal subjects. As a whole, these data appear to be in line with a relatively less efficient cardiac performance during progressive work rates in obese subjects.
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PMID:Oxygen uptake and cardiac performance in obese and normal subjects during exercise. 997 87

In this overview general risk factors for postoperative complications are discussed with special reference to pulmonary complications, which frequently occur in patients with chronic obstructive pulmonary disease (COPD). In a second part the functional evaluation of lung resection candidates is presented. Pulmonary complications are the most frequent cause of postoperative morbidity and mortality. Risk factors include: underlying respiratory disease, especially COPD, current smoking, duration of anaesthesia, type of surgical procedure (upper abdominal or thoracic surgery), age and obesity. The preoperative evaluation of patients at risk is discussed. For non-thoracic surgery preoperative pulmonary function testing and a preoperative chest radiograph are indicated for high-risk patients only, whereas they are mandatory for all lung resection candidates. There are no cut-off values in pulmonary function testing which would preclude non-thoracic surgical procedures. In patients with COPD, laparascopic procedures are recommended; and regional or epidural anaesthesia have less adverse effects on pulmonary function than general anaesthesia. Prevention of postoperative pulmonary complications includes smoking cessation at least eight weeks before surgery, and, if indicated preoperative treatment with antibiotics, beta2-agonists, steroids (steroid-trial) and intensive perioperative chest physiotherapy (incentive spirometry). The functional reserves of lung resection candidates is assessed with an algorithm based on the forced expiratory volume in one second (FEV1), the transfer factor of the lung for carbon monoxide (DLCO), and the maximal oxygen uptake on exercise (VO2max). In critical patients additional split function studies are necessary to estimate the remaining pulmonary function depending on the extent of resection.
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PMID:[Evaluation of surgical risk in patients with COPD]. 1021 38

Human obesity leads to an increase in respiratory demands. As obesity becomes more pronounced some individuals are unable to compensate, leading to elevated arterial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidity and mortality (Pickwickian syndrome). The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depression of central respiratory control mechanisms. Here we report that obese C57BL/6J-Lepob mice, which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p < 0. 0001). A role for leptin in restoring ventilation in these obese, mutant mice was investigated. Three days of leptin infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, but particularly during rapid eye movement (REM) sleep when respiration was otherwise profoundly depressed. The effect of leptin was independent of food intake, weight, and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory control centers. Furthermore, leptin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4.0 +/- 0.5 to 5.6 +/- 0.4 ml/min/%CO2; p < 0.01) and REM (-0.1 +/- 0.5 to 3.0 +/- 0.8 ml/min/%CO2; p < 0.01) sleep. We also demonstrate in wild-type mice that ventilation is appropriately compensated when obesity is diet-induced and endogenous leptin levels are raised more than tenfold. These results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects. O'Donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR, Smith PL. Leptin prevents respiratory depression in obesity.
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PMID:Leptin prevents respiratory depression in obesity. 1022 14


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