Hematocrit Levels in Sleep Apnea

Hoffstein, V.; Herridge, Margaret S.; Mateika, Susan; Redline, Susan

doi:10.1378/chest.106.3.787

Cited by 89 publications

(51 citation statements)

References 23 publications

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“…Polycythemia is not consistently observed in SA animal models, with or without CO 2 supplementation, and SA patients (2,9,12,16,23,30,35,42,43,56). In the present study, H-IH did not induce significant polycythemia in mice.…”

Section: Discussioncontrasting

confidence: 60%

NFATc3 is required for intermittent hypoxia-induced hypertension

Garcı́a¹,

Duling²,

Alò³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Sleep apnea, defined as intermittent respiratory arrest during sleep, is associated with increased incidence of hypertension and peripheral vascular disease. Exposure of rodents to brief periods of intermittent hypercarbia/hypoxia (H-IH) during sleep mimics the cyclical hypoxia-normoxia of sleep apnea. Endothelin-1, an upstream activator of nuclear factor of activated T cells (NFAT), is increased during H-IH. Therefore, we hypothesized that NFATc3 is activated by H-IH and is required for H-IH-induced hypertension. Consistent with this hypothesis, we found that H-IH (20 brief exposures per hour to 5% O2-5% CO2 for 7 h/day) induces systemic hypertension in mice [mean arterial pressure (MAP) ϭ 97 Ϯ 2 vs. 124 Ϯ 2 mmHg, P Ͻ 0.05, n ϭ 5] and increases NFATc3 transcriptional activity in aorta and mesenteric arteries. Cyclosporin A, an NFAT inhibitor, and genetic ablation of NFATc3 [NFATc3 knockout (KO)] prevented NFAT activation. More importantly, H-IHinduced hypertension was attenuated in cyclosporin A-treated mice and prevented in NFATc3 KO mice. MAP was significantly elevated in wild-type mice (⌬ ϭ 23.5 Ϯ 6.1 mmHg), but not in KO mice (⌬ ϭ Ϫ3.9 Ϯ 5.7). These results indicate that H-IH-induced increases in MAP require NFATc3 and that NFATc3 may contribute to the vascular changes associated with H-IH-induced hypertension.nuclear factor of activated T cells; hypercarbic; mouse; endothelin-1; sleep apnea SLEEP APNEA (SA), defined as intermittent respiratory arrest during sleep, affects up to 20% of the adult population. Among the major consequences of SA are decreased O 2 saturation (hypoxia) and increased CO 2 saturation (hypercapnia). In SA patients, incidence of hypertension, peripheral vascular disease, stroke, and sudden cardiac death is increased (for review see Refs. 21 and 44). Thus SA appears to directly initiate vascular changes that predispose individuals to cardiovascular disease.Recently, it was demonstrated that exposure of rodents to periods of intermittent hypoxia with CO 2 supplementation [intermittent hypercarbia/hypoxia (H-IH)] during sleep mimics the cyclical hypoxia-normoxia of SA. In rats exposed to H-IH, blood pressure (34, 35) and circulating endothelin-1 (ET-1) are elevated (35), vasoconstrictor sensitivity to ET-1 is increased (2), and blood pressure is normalized with ET antagonists (35). These studies, together with clinical studies showing increased circulating ET-1 in SA (10, 55), suggest that augmented ET-1 vasoconstriction contributes to SA hypertension. The sustained increased blood pressure observed in SA patients and animal models also appears to involve activation of the sympathetic nervous and renin-angiotensin systems and diminished activity of nitric oxide synthase (for review see Refs. 44 and 52).ET-1 acts through G␣ q -coupled receptors as a Ca 2ϩ -mobilizing agent and as a potent activator of the nuclear factor of activated T cells (NFAT) (1, 25, 57). ANG II, glucose through UTP release, and ␣ 1 -adrenergic agonists are also potent stimuli of NFAT activation (1,25,27,46,57).NFAT...

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Section: Discussioncontrasting

confidence: 60%

NFATc3 is required for intermittent hypoxia-induced hypertension

Garcı́a¹,

Duling²,

Alò³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…HOFFSTEIN et al [14] suggested that the intermittent nocturnal hypoxaemia of OSA patients did not lead to polycythaemia, although they did report slight elevations in their haematocrit values. BRADLEY et al [3] showed raised haematocrit and pulmonary hypertension in OSA patients, but these also presented daytime hypoxaemia.…”

Section: Discussionmentioning

confidence: 98%

“…It has been suggested that an increased haematocrit only occurs in the presence of daytime hypoxaemia [4]. HOFFSTEIN et al [14] reported no change or slight elevations in haematocrit in a large group of sleep apnoea patients without daytime hypoxaemia, whereas LAKS et al [5] did observe an elevated haematocrit in the absence of daytime hypoxaemia. Therefore, in the present investigation, the effects of chronic intermittent hypercapnic hypoxia on haematocrit, right ventricular weight and pulmonary arterial pressure are examined using a rat model which mimics the nocturnal pattern of hypercapnic hypoxia of sleepdisordered breathing in humans.…”

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confidence: 99%

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

McGuire

Bradford

2001

Eur Respir J

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Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats. M. McGuire, A. Bradford. #ERS Journals Ltd 2001. ABSTRACT: Sleep-disordered breathing is associated with pulmonary hypertension and raised haematocrit. The multiple episodes of apnoea in this condition cause chronic intermittent hypoxia and hypercapnia but the effects of such blood gas changes on pulmonary pressure or haematocrit are unknown. The present investigation tests the hypothesis that chronic intermittent hypercapnic hypoxia causes increased pulmonary arterial pressure and erythropoiesis.Rats were treated with alternating periods of normoxia and hypercapnic hypoxia every 30 s for 8 h per day for 5 days per week for 5 weeks, as a model of the intermittent blood gas changes which occur in sleep-disordered breathing in humans. Haematocrit, red blood cell count and haemoglobin concentration were measured each week and systemic and pulmonary arterial blood pressure and heart weight were measured after 5 weeks.In relation to control, chronic intermittent hypercapnic hypoxia caused a significant increase in systemic (104.3¡4.7 mmHg versus 121.0¡10.4 mmHg) and pulmonary arterial pressure (20.7¡6.8 mmHg versus 31.3¡7.2 mmHg), right ventricular weight (expressed as ratios) and haematocrit (45.2¡1.0% versus 51.5¡1.5%).It is concluded that the pulmonary hypertension and elevated haematocrit associated with sleep-disordered breathing is caused by chronic intermittent hypercapnic hypoxia. Sleep disordered breathing affects 1-4% of adults [1]. It is associated with multiple episodes of hypoxia and hypercapnia due to hypopnoea or apnoea, which are either caused by intermittent collapse of the upper airway (UA), termed obstructive sleep apnoea (OSA; the most common form of sleep disordered breathing), or a reduced drive to breath, termed central apnoea [2]. The condition is associated with a number of cardiovascular changes, including increased pulmonary and systemic arterial blood pressure, right ventricular hypertrophy, cardiac arrhythmias and increased haematocrit. Diurnal pulmonary hypertension is present in 17-42% of OSA patients [3][4][5][6][7] and represents a serious threat to long-term outcome in these patients [8]. The cause of pulmonary hypertension in these patients is unknown. During an apnoeic event, pulmonary arterial pressure is acutely increased [9], presumably due to hypoxic pulmonary vasoconstriction, so that repetitive episodes of increased pressure may ultimately give rise to daytime pulmonary hypertension [10]. In support of this, it has recently been shown that chronic intermittent hypocapnic hypoxia in rats causes right ventricular hypertrophy, suggesting that pulmonary arterial pressure is increased [11]. However, apnoeas are accompanied by hypercapnia as well as hypoxia [12], but the effects of this combination of chronic intermittent blood gas changes on pulmonary arterial pressure are unknown. It is known that chronic continuous hypercapnia protects against the effects of continuous hypoxia...

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“…In uncomplicated OSA polycythemia is rare. A relationship between nocturnal hypoxaemia and haematocrit may be demonstrated only on very large samples of OSA patients and its clin-ical significance is uncertain [12,13]. Furthermore, treatment of OSA with continuous positive pressure ventilation (CPAP) prevented the acute increase in morning haematocrit secondary to nocturnal haemoconcentration, but did not otherwise affect it in the long term [14].…”

Section: Introductionmentioning

confidence: 99%

Reticulocytes in untreated Obstructive Sleep Apnoea

Marrone

Salvaggio

Gioia

et al. 2016

Monaldi Arch Chest Dis

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Background and Aim. The short, repetitive hypoxaemic episodes observed in obstructive sleep apnoea (OSA) may determine small augmentations in mature red blood cells. It is unknown whether they affect reticulocyte release. This study explored whether the number and degree of maturation of circulating reticulocytes may be altered in OSA, possibly through the effect of erythropoietin. Methods. Fifty male adult patients with suspected OSA, normoxic during wakefulness, were studied. After nocturnal polysomnography, a blood sample was withdrawn for blood cells count, erythropoietin, iron and transferrin determination. Reticulocyte concentration and degree of immaturity [high (H), medium (M), or low (L)] were also determined. Immature reticulocyte fraction (IRF) was calculated as (M+H) percentage of reticulocytes. Results. A wide range of OSA severity was found [apnoea/ hypopnoea index (AHI): 44.3±30.4, range 0.3-105; sleep time spent at oxyhaemoglobin saturation 2% had higher EPO levels (p<0.05), but not worse nocturnal desaturations, than those with values <2%. By contrast, subjects with IRF <15% showed worse desaturations (p<0.05), but similar EPO concentrations, when compared to subjects whose IRF was <10%. At univariate analysis, reticulocyte count correlated to erythropoietin, while IRF to transferrin saturation, BMI and OSA severity. At multiple regression, only lowest nocturnal oxygen saturation remained a significant contributor to IRF (r2 0.223, p<0.05). Conclusions. This data suggests that hypoxaemia due to OSA could influence the release of immature reticulocytes, but this effect is not mediated by erythropoietin.

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Hematocrit Levels in Sleep Apnea

Cited by 89 publications

References 23 publications

NFATc3 is required for intermittent hypoxia-induced hypertension

NFATc3 is required for intermittent hypoxia-induced hypertension

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

Reticulocytes in untreated Obstructive Sleep Apnoea

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