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

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

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

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.
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PMID:Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats. 1131 30

High pressure CO2-peritoneum for laparoscopic surgery is not indicated in patients with impairment of cardiorespiratory and renal function and in high risk patients and in obesity. On the other site the uncontrolled abdominal insufflation and the blind insertion of the first trocar in patients with extended intraperitoneal adhesions, often cause bleeding and the intestinal loops dislocation, and can determine visceral lesions. In these patients gasless technique with an abdominal laparolifter can be employed. We report an experience of 36 patients undergoing laparoscopic cholecystectomy by a subcutaneous planar retractor. It was observed a good operative exposure in 83.3%; the surgery was safely performed in 88.8%. Two suprafascial hematoma related to the insertion of the needles of the Laparo Tenser occurred. A regular post-operative discharge was observed in 84.4%. These good results supports the extension of the laparoscopic approach for the cholecystectomy to complicated or to high risk patients.
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PMID:[Use of abdominal wall retractor Laparo Tenser in gasless laparoscopic cholecystectomy]. 1219 87

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

A 59-year-old man without a history of ischemic heart disease underwent elective laparoscopic cholecystectomy under general anesthesia with epidural anesthesia. About 15 min after pneumoperitoneum had been achieved, the patient developed ST elevation and hypotension. Vagal stimulation resulting from stretching peritoneum, the procedure and epidural anesthesia are thought to have induced vasospasm. The ST segment became normal after interruption of CO2 insufflation. A postoperative coronary artery angiogram showed normal coronary arteries, but diffuse coronary artery spasm was seen after intracoronary injection of acetylcholine. The patient was discharged on nitrates. Patients with gall bladder stones sometimes have coronary risk factors of obesity, hyperlipidemia and hyperglycemia. Careful attention should also be given to patients who do not have a history of coronary disease.
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PMID:[Coronary artery spasm during cholecystectomy with pneumoperitoneum--a case report]. 1496 4


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