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Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms. We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean ± sd MSNA increased across the exposure (17.2 ± 5.1 versus 21.7 ± 7.3 bursts·min⁻¹; p < 0.01) and baroreflex control of sympathetic outflow declined from -965.3 ± 375.1 to -598.4 ± 162.6 AIU·min⁻¹ ·mmHg⁻¹ (p < 0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.

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Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17-24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr (n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 +/- 1.3 vs. 74 +/- 1.7 mmHg, P < 0.01), MSNA [9.94 +/- 2.0 to 14.63 +/- 1.5 bursts/min (P < 0.05); 16.89 +/- 3.2 to 26.97 +/- 3.3 bursts/100 heartbeats (hb) (P = 0.01)], and forearm vascular resistance (FVR) (35.3 +/- 5.8 vs. 55.3 +/- 6.5 mmHg x ml(-1) x min x 100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

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Obstructive sleep apnea is characterized by repetitive nocturnal upper airway obstructions that are associated with sleep disruption and cyclic intermittent hypoxia (CIH) The cyclic oscillations in O(2) saturation are thought to contribute to cardiovascular and other morbidity, but animal and patient studies of the pathogenic link between CIH and these diseases have been complicated by species differences and by the effects of confounding factors such as obesity, hypertension, and impaired glucose metabolism. To minimize these limitations, we set up a model of nocturnal CIH in healthy humans. We delivered O(2) for 15 s every 2 min during sleep while subjects breathed 13% O(2) in a hypoxic tent to create 30 cycles/h of cyclic desaturation-reoxygenation [saturation of peripheral O(2) (Sp(O(2))) range: 95-85%]. We exposed subjects overnight for 8-9 h/day for 2 wk (10 subjects) and 4 wk (8 subjects). CIH exposure induced respiratory disturbances (central apnea hypopnea index: 3.0 +/- 1.9 to 31.1 +/- 9.6 events/h of sleep at 2 wk). Exposure to CIH for 14 days induced an increase in slopes of hypoxic and hypercapnic ventilatory responses (1.5 +/- 0.6 to 3.1 +/- 1.2 l.min(-1).% drop in Sp(O(2)) and 2.2 +/- 1.0 to 3.3 +/- 0.9 l.min(-1).mmHg CO(2)(-1), respectively), consistent with hypoxic acclimatization. Waking normoxic arterial pressure increased significantly at 2 wk at systolic (114 +/- 2 to 122 +/- 2 mmHg) and for diastolic at 4 wk (71 +/- 1.3 to 74 +/- 1.7 mmHg). We propose this model as a new technique to study the cardiovascular and metabolic consequences of CIH in human volunteers.

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Cassini images of Saturn's small inner satellites (radii of less than approximately 100 kilometers) have yielded their sizes, shapes, and in some cases, topographies and mean densities. This information and numerical N-body simulations of accretionary growth have provided clues to their internal structures and origins. The innermost ring-region satellites have likely grown to the maximum sizes possible by accreting material around a dense core about one-third to one-half the present size of the moon. The other small satellites outside the ring region either may be close to monolithic collisional shards, modified to varying degrees by accretion, or may have grown by accretion without the aid of a core. We derived viscosity values of 87 and 20 square centimeters per second, respectively, for the ring material surrounding ring-embedded Pan and Daphnis. These moons almost certainly opened their respective gaps and then grew to their present size early on, when the local ring environment was thicker than it is today.

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The mechanisms by which obstructive apneas produce intermittent surges in arterial pressure remain poorly defined. To determine whether termination of obstructive apneas produce peripheral vasoconstriction, we assessed forearm blood flow during and after obstructive events in sleeping patients experiencing spontaneous upper airway obstructions. In all subjects, heart rate was monitored with an electrocardiogram and blood pressure was monitored continuously with digital plethysmography. In 10 patients (protocol 1), we used forearm plethysmography to assess forearm blood flow, from which we calculated forearm vascular resistance by performing venous occlusions during and after obstructive episodes. In an additional four subjects, we used simultaneous Doppler and B-mode images of the brachial artery to measure blood velocity and arterial diameter, from which we calculated brachial flow continuously during spontaneous apneas (protocol 2). In protocol 1, forearm vascular resistance increased 71% after apnea termination (29.3 +/- 15.4 to 49.8 +/- 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In protocol 2, brachial resistance increased at apnea termination in all subjects (219.8 +/- 22.2 to 358.3 +/- 46.1 mmHg x l(-1) x min; P = 0.01). We conclude that termination of obstructive apneas is associated with peripheral vasoconstriction.

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Spontaneous and provoked nonrespiratory arousals can be accompanied by a patterned hemodynamic response. To investigate whether a patterned response is also elicited by respiratory arousals, we compared nonrespiratory arousals (NRA) to respiratory arousals (RA) induced by airway occlusion during non-rapid eye movement sleep. We monitored mean arterial blood pressure (MAP), heart rate, iliac and renal blood flow, and sleep stage in 7 pigs during natural sleep. Iliac and renal vascular resistance were calculated. Airway occlusions were obtained by manually inflating a chronically implanted tracheal balloon during sleep. The balloon was quickly deflated as soon as electroencephalogram arousal occurred. As previously reported, NRA generally elicited iliac vasodilation, renal vasoconstriction, little change in MAP, and tachycardia. In contrast, RA generally elicited iliac and renal vasoconstriction, an increase in MAP and tachycardia. The frequent occurrence of iliac vasoconstriction and arterial pressure elevation following RA but not NRA suggests that sleep state change alone does not account for the hemodynamic response to airway occlusion during sleep.

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BACKGROUND: Optimization of the culture environment for the ex vivo expansion of T cells is crucial for obtaining the large doses of cells needed for cellular immunotherapy. O2 tension is a key parameter that impacts the proliferation and quality of the expanded T cells. METHODS: Peripheral blood mononuclear cells were stimulated with either PHA or an anti-CD3 monoclonal antibody under 5% (low) or 20% (high) O2 atmospheres. After stimulation, cells were cultured in the presence of IL-2 under either low or high O2 conditions. RESULTS: T cells stimulated and grown under 5% O2 exhibited higher proliferation rates and a mean (n = 11) of 5.8-fold greater total expansion over T cells grown under 20% O2. Stimulation under 5% O2 produced a lasting proliferative effect even after a switch to 20% O2. Examination of apoptosis by the flow cytometry-based TUNEL assay showed a mean (n = 9) of 2.9-fold greater percentage of apoptotic cells under 20% O(2). Flow-cytometric analysis of the IL-2 receptor (CD25) showed that the normal downregulation kinetics - following stimulation-induced CD25 upregulation - were slowed under 5% O(2), such that the 5% O2 cultures had a greater number of CD25+ cells, and those CD25+ cells expressed an average (n = 6) of 41% higher levels of CD25 receptor per cell. No significant O2 tension effects were observed on other surface antigens (CD3, CD28, and CD62L) examined. The key metabolic parameters, specific glucose uptake rate, q(glu), and specific lactate production rate, q(lac), were both increased by a mean (n = 5) of 47% under 5% O2. DISCUSSION: Beyond the physiological significance, improved T-cell proliferation under 5% O2 would allow for decreased culture times in expanding T cells for cellular immunotherapies. Evidence of increased IL-2R expression and reduced apoptosis levels under 5% O2 may help explain this phenomenon.

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Abrupt changes in arterial pressure produce arousal in sleeping animals. To determine whether arterial pressure elevations can cause arousal from sleep in humans, we studied five healthy individuals without sleep complaints or cardiac abnormalities. Monitoring included electroencephalogram, electrooculogram, and electromyogram to determine stage sleep; finger cuff to measure arterial pressure; and electrocardiogram to measure heart rate. We administered intravenous bolus doses of either phenylephrine or saline after performing a dose-response curve to establish the amount of phenylephrine that produced a 20-mmHg increase in mean arterial pressure. Ten boluses of phenylephrine and ten boluses of saline were then administered in random order during stable non-rapid-eye-movement sleep. An observer blinded to the order of drug administration identified arousals using a standard definition. Arousals were five times more likely to occur after phenylephrine than after saline (58 vs. 12%; P = 0.0071). Phenylephrine administration produced heart rate slowing, indicative of baroreflex stimulation. We conclude that pharmacologically induced arterial pressure elevation is associated with arousal from sleep in normal volunteers.

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Patients with obstructive sleep apnea (OSA) have been reported to have an augmented pressor response to hypoxic rebreathing. To assess the contribution of the peripheral vasculature to this hemodynamic response, we measured heart rate, mean arterial pressure (MAP), and forearm blood flow by venous occlusion plethysmography in 13 patients with OSA and in 6 nonapneic control subjects at arterial oxygen saturations (Sa(O(2))) of 90, 85, and 80% during progressive isocapnic hypoxia. Measurements were also performed during recovery from 5 min of forearm ischemia induced with cuff occlusion. MAP increased similarly in both groups during hypoxia (mean increase at 80% Sa(O(2)): OSA patients, 9 +/- 11 mmHg; controls, 12 +/- 7 mmHg). Forearm vascular resistance, calculated from forearm blood flow and MAP, decreased in controls (mean change -37 +/- 19% at Sa(O(2)) 80%) but not in patients (mean change -4 +/- 16% at 80% Sa(O(2))). Both groups decreased forearm vascular resistance similarly after forearm ischemia (maximum change from baseline -85%). We conclude that OSA patients have an abnormal peripheral vascular response to isocapnic hypoxia.

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The repetitive respiratory events that characterize obstructive sleep apnea (OSA) are each followed by abrupt increases in heart rate and in pulmonary and systemic artery pressure and by sudden decreases in right and left ventricular stroke volume. The changes in systemic pressure may be profound, with patients who are normotensive while awake having systolic pressures approaching 300 mm Hg after apnea termination. Because of these dramatic hemodynamic oscillations during sleep, many clinicians and investigators have postulated a connection between sleep-disordered breathing and cardiovascular morbidity and even mortality. This review critically examines the evidence for such a causal relationship. We begin, however, by reviewing the normal hemodynamic changes that occur during sleep. We then describe the acute hemodynamic events associated with OSA. Finally, we summarize the evidence for and against a causal connection between sleep apnea and cardiovascular morbidity.

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Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by -29.6 +/- 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 +/- 4.0%), tachycardia (heart rate increase: +23.8 +/- 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

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The levator veli palatini (LVP) and the superior pharyngeal constrictor (SPC) influence velopharyngeal patency and soft palate position, but their behavior during respiration is incompletely characterized. To further clarify their respiratory function, we recorded electromyographic activity (EMG) in the LVP and the SPC in awake normal subjects breathing orally. EMG data were obtained in six subjects for the LVP and in nine subjects for the SPC. EMG activity and timing and ventilation were measured during isocapnic hypoxia and hyperoxic hypercapnia. Phasic EMG activity was inconsistently present during unstimulated oral breathing. Timing of EMG phasic activity was variable for both muscles. Peak LVP activity was mainly or exclusively expiratory in three of six subjects. Peak SPC activity was mainly or exclusively expiratory in five of nine subjects. With chemostimulation, recruitment of phasic activity was observed in the LVP and in four of six subjects and in the SPC in five of nine subjects. Tonic activity increased in four of six subjects for the LVP and in three of nine subjects for the SPC. However, the response was alinear, and intersubject as well as breath-to-breath variability was substantial. In conclusion, LVP and SPC are characterized by the higher inter- and intrasubject variability of EMG activity, timing of activation, and response to chemostimulation.

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BACKGROUND AND OBJECTIVE: Laser-assisted uvulopalatoplasty (LAUP) is being used increasingly as a surgical treatment for snoring and obstructive sleep apnea (OSA). There is limited evidence for the success of LAUP in eliminating OSA. This study assesses the efficacy of LAUP in eliminating snoring and OSA and addresses which patients may be the best candidates for LAUP treatment. STUDY DESIGN/MATERIALS AND METHODS: From January 1994 to January 1996, 297 patients were evaluated for snoring, with 190 (64%) exhibiting some degree of OSA documented by a PSG: 41/ 190 (22%) mild OSA; 33/190 (17%) moderate OSA; 85/190 (45%) severe OSA; 31/190 (16%) severity unknown. Ninety patients (90/ 297) have undergone LAUP treatment: 58/90 (64%) with OSA and 32/90 (36%) with snoring only. RESULTS: Our results indicate a significant reduction of snoring in patients without OSA, but diminishing success in patients with increasing degrees of OSA. Additionally, LAUP was not efficacious in treating OSA: pre-op respiratory disturbance index (RDI) of 10.8 vs. post-op RDI of 19.5 for mild OSA (P = 0.14); pre-op RDI of 22.9 vs. post-op RDI of 25.4 for moderate OSA (P = 0.43); pre-op RDI of 56.8 vs. post-op RDI of 46.3 (P < 0.05), which is statistically but not clinically significant (i.e., RDI remained in the severe range). CONCLUSION: We conclude that LAUP is an effective treatment for nonapneic snoring, but does not provide sufficient resolution of OSA, and based on our results, LAUP should be considered as an adjunctive therapy rather than a sole treatment for OSA in most cases.

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RATIONALE AND OBJECTIVES: We assessed whether intestinal ischemia would result in transudation of orally administered gadopentetate dimeglumine into the peritoneal cavity. METHODS: Twenty-eight rats were anesthetized and midline laparotomy was performed. Animals were divided into four groups: control, ligation of a single mesenteric arcade, ligation of six consecutive arcades, and ligation of the anterior mesenteric artery (analogous to the superior mesenteric artery in humans). A 1.0-ml enteric bolus of gadopentetate dimeglumine diluted with sterile water (1:1) was given via gavage. Magnetic resonance imaging was performed 2 hr after laparotomy and reviewed for the presence of intraperitoneal gadopentetate dimeglumine by two experienced observers. Animals were sacrificed 24 hr after surgery for pathologic examination. RESULTS: Four animals died prior to sacrifice. The bladder had a grossly high signal in all cases, implying some degree of intravascular absorption of the contrast material. A correlation was found between increasing mean radiology scores and increasing numbers of ligated vessels. The intraperitoneal signal tended to be higher in experimental animals than in control animals. Histologic damage was more severe in experimental animals (ischemic changes extending deeper into the intestinal wall) than in control animals. CONCLUSION: Direct visualization of spilled gastrointestinal gadopentetate dimeglumine helped discriminate ischemic from control rats in this model.

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Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.

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To examine the contribution of specific palatal muscles to velopharyngeal dimensions, we recorded electromyographic (EMG) activity in the levator veli palatini, the tensor veli palatini, and the palatoglossus while examining the velopharynx (VP) with videoendoscopy in eight awake normal adults. Simultaneous display of VP images and airflow provided precise timing of events. Video images and EMG signals were recorded during progressive hypercapnia. Every tenth breath was analyzed. For each selected breath, VP area, anteroposterior and lateral diameters, and EMG activity were determined at five points: beginning, middle, and end of inspiration and middle and end of expiration. VP measurements changed significantly during the respiratory cycle. Although maximum area was measured at end inspiration or middle expiration and minimum area at the beginning or end of the breath, respiratory-related changes in VP measurements and EMG activity were characterized by substantial inter- and intrasubject variability. This variability is similar to velopharyngeal behavior during nonrespiratory tasks and suggests that upper airway patency is determined by multiple factors.

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To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP) and heart rate (HR), pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified balloon catheter was placed in the trachea to obstruct the upper airway during sleep. Following control studies, the role of beta adrenergic receptors in hemodynamic responses to AWO was assessed by administering propranolol, a beta adrenoreceptor blocking agent. In control studies, during nonrapid eye movement sleep (NREM), MAP was 85 +/- 2 mmHg before AWO and increased by 8 +/- 2 mmHg upon arousal. Mean arterial pressure was lower during rapid eye movement (REM) sleep (64 +/- 2 mmHg) and the increase upon arousal was threefold greater (22 +/- 2 mmHg). Heart rate was similar in both sleep stages (NREM 123 +/- 5 bpm; REM 125 +/- 6 bpm) and increased significantly upon arousal (NREM, 11 +/- 2 bpm; REM, 18 +/- 3 bpm increase). Coronary blood flow was similar during both stages (NREM 44 +/- 5 ml/min; REM 44 +/- 6 ml/min) and increased by 13% (NREM) and 22% (REM) during arousal. Coronary vascular resistance increased significantly by 17% during arousal from AWO during REM sleep. All changes were significant at p < 0.05. Following beta adrenergic receptor blockade studies using propranolol, baseline HR was reduced in NREM sleep and HR and coronary blood flow increases during arousal from apnea were eliminated. Adrenoreceptor blockade studies suggest that these effects were mediated by the beta adrenergic component of the sympathetic nervous system.

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Blood pressure (BP) rises at the termination of obstructive episodes in patients with sleep apnea. Although the relationship of these BP elevations to oxygen saturation (SaO2) and arousal has been explored, the influence of sleep stage is undefined. To examine the effects of sleep stage on the postapnea BP elevation, we enrolled 12 patients with obstructive sleep apnea (OSA), and successfully collected data from seven of these (all male). Subjects slept overnight in the sleep laboratory, with full sleep and respiratory monitoring. Arterial pressure was assessed continuously with a radial artery catheter (six patients) or with digital photoplethysmography (one patient). Apneas occurring in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep were matched for duration and degree of desaturation. When mean arterial pressure (MAP) at termination of apneas during NREM sleep associated with SaO2 nadirs 78 to 82% (NREM 80%) was compared with MAP following apneas in REM with the same SaO2 nadir (REM 80%), there was a significant difference (NREM 80% 122 +/- 15.3 mm Hg, REM 80% 132 +/- 11.0; p = 0.0109). We also analyzed the effect of oxygen desaturation on MAP during REM sleep, by comparing events with SaO2 nadirs of 78 to 82% with events with nadirs of < 75% (REM < 75%). In REM, further desaturation was associated with significant lengthening of the obstructive episodes and significantly higher postapnea BP increases (REM 75% 143 +/- 19.9 mm Hg, p = 0.0392). We conclude that sleep stage alters the hemodynamic response to obstructive apneas during sleep.

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OBJECTIVE: The purpose of our study was to evaluate the color Doppler findings of acute cholecystitis in a controlled canine model. MATERIALS AND METHODS: Fourteen animals had a laparotomy: cystic duct ligation was done in eight, and incision with closure was performed in six control subjects. Animals were scanned in a blinded fashion preoperatively, immediately postoperatively, and on postoperative days 1-5. On postoperative day 5, a hepatobiliary scan was done with 2 mCi (74 MBq) 99mTc-mebrofenin. Blinded histopathology was performed and correlated with imaging. RESULTS: Flow was seen in the wall of each gallbladder at some point during the postoperative course, demonstrating vascular patency. Hepatobiliary scintigraphy confirmed cystic duct status in 12 cases; two animals died before radionuclide imaging was complete. Color Doppler signal decreased in the gallbladder wall in ligated dogs from postoperative day 1 to postoperative day 3 (p = .03 versus controls at postoperative day 2) and increasingly returned by postoperative day 5. Hyperemia was seen in only two cases (both with severe necrotizing cholecystitis) and only at postoperative day 5. Although not statistically significant, a weak trend of increasing flow with more severe pathologic grades of cholecystitis was observed (p = .20). CONCLUSIONS: In this animal model, loss of vascular signal (not hyperemia) at postoperative day 2 was the finding to diagnose early acute cholecystitis, although lack of flow can also be seen in some normal subjects. Flow tended to return by postoperative day 5, and it increased in some of the more severe cases of cholecystitis. Hyperemia was a somewhat useful sign of acute necrotizing cholecystitis.

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