Skip to main content
Clinical Cardiology logoLink to Clinical Cardiology
. 2006 Dec 5;28(11):519–522. doi: 10.1002/clc.4960281106

Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24‐hour urinary catecholamines

Mayo Sukegawa 1, Akiko Noda 1,, Tatsuki Sugiura 2, Senchi Nakata 3, Shigehito Yoshizaki 2, Taro Soga 2, Yoshinari Yasuda 2, Norihisa Iwayama 2, Shigeru Nakai 2, Yasuo Koike 1
PMCID: PMC6653944  PMID: 16450795

Abstract

Background: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease.

Hypothesis: The study investigated whether 24‐h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity.

Methods: Standard poly somnography was performed in 17 patients with OSAS (age 53.7 ± 13.5 years, mean ± standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1, 2, 3/4, and rapid eye movement sleep (% stage 1, −2, and ‐ 3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty‐four‐hour urinary adrenaline and noradrenaline were also examined.

Results: During the CPAP treatment, both 24‐h urinary adrenaline and noradrenaline were significantly lower compared with natural sleep. Continuous positive airway pressure significantly decreased the AHI, DSI, % stage 1, and arousal index and significantly increased the lowest SpO2. There were no significant differences in % stage 2, % stage 3/4, and % REM between before and during CPAP treatment. Multiple analysis of covariance tests revealed that lowest SpO2 was the most important factor for increasing 24‐h urinary noradrenaline levels (F = 4.75, p = 0.048).

Conclusions: One night CPAP treatment could improve autonomic dysfunction. The assessment of 24‐h urinary noradrenaline would provide important information for evaluating the effect of CPAP treatment.

Keywords: catecholamine, adrenaline, noradrenaline, obstructive sleep apnea syndrome, autonomic activity, continuous positive airway pressure, lowest oxygen saturation

Full Text

The Full Text of this article is available as a PDF (34.1 KB).

References

  • 1. Fletcher EC: Obstructive sleep apnea and cardiovascular morbidity. Monaldi Arch Chest Dis 1996; 51: 77–80 [PubMed] [Google Scholar]
  • 2. Brooks D, Horner RL, Kozar LF, Render‐Teixeira CL, Phillipson EA: Obstructive sleep apnea as a cause of systemic hypertension: Evidence from a canine model. J Clin Invest 1997; 99: 106–109 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3. Somers VK, Dyken ME, Mark AL: Parasympathetic hyperresponsiveness and bradyarrhythmias during apnea in hypertension. Clin Auton Res 1992; 2: 171–176 [DOI] [PubMed] [Google Scholar]
  • 4. Somers VK, Dyken ME, Clary MP, Abboud FM: Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995; 96: 1897–1904 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Levinson PD, Millman RP: Causes and consequences of blood pressure alterations in obstructive sleep apnea. Arch Intern Med 1991; 151: 455–462 [PubMed] [Google Scholar]
  • 6. Noda A, Yasuma F, Okada T, Yokota M: Circadian rhythm of autonomic activity in patients with obstructive sleep apnea syndrome. Clin Cardiol 1998; 21: 271–276 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Kansanen M, Vanninen E, Tuunainen A, Pesonen P, Tuononen V, Hartikainen J, Mussalo H, Uusitupa M: The effect of a very low‐calorie diet‐induced weight loss on the severity of obstructive sleep apnea and autonomic nervous function in obese patients with obstructive sleep apnea syndrome. Clin Physiol 1998; 18: 377–385 [DOI] [PubMed] [Google Scholar]
  • 8. Khoo MCK, Kim TS, Berry RB: Spectral indices of cardiac autonomic function in obstructive sleep apnea. Sleep 1999; 22: 443–451 [DOI] [PubMed] [Google Scholar]
  • 9. Svanborg E, Carlsson‐Nordlander B, Larsson H: Autonomic nervous system function in patients with primary obstructive sleep apnea syndrome. Clin Auton Res 1991; 1: 125–130 [DOI] [PubMed] [Google Scholar]
  • 10. He J, Kryger MH, Zorick FJ, Conway W, Roth T: Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988; 94: 9–14 [PubMed] [Google Scholar]
  • 11. Noda A, Okada T, Hayashi H, Yasuma F, Yokota M: 24‐hour ambulatory blood pressure variability in obstructive sleep apnea syndrome. Chest 1993; 103: 1343–1347 [DOI] [PubMed] [Google Scholar]
  • 12. Noda A, Okada T, Yasuma F, Sobue T, Nakashima N, Yokota M: Cardiac hypertrophy in obstructive sleep apnea syndrome. Chest 1995; 107: 1538–1544 [DOI] [PubMed] [Google Scholar]
  • 13. Noda A, Okada T, Yasuma F: Prognosis of the middle‐aged and aged patients with obstructive sleep apnea syndrome. Psychiat Clin Neurosci 1998; 52: 79–85 [DOI] [PubMed] [Google Scholar]
  • 14. Narkiewicz K, Montano N, Cogliati C, Borne PJH, Dyken ME, Somers VK: Altered cardiovascular variability in obstructive sleep apnea. Circulation 1998; 98: 1071–1077 [DOI] [PubMed] [Google Scholar]
  • 15. Luft R, Ulf S, Von Euler US: Two cases of postural hypotension showing a deficiency in release of norepinephrine and epinephrine. J Clin Invest 1953; 32: 1065–1069 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Rechtschaffen A, Kales A: A Manual of Standardized Techniques and Scoring System for Sleep Stages of Human Subjects. Washington, D. C.: US Government Printing Office, 1968. [Google Scholar]
  • 17. The Report of an American Academy of Sleep Medicine Task Force : American Academy of Sleep Medicine: Sleep‐related breathing disorders in adults. Recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999; 22: 667–689 [PubMed] [Google Scholar]
  • 18. Macdonald IA, Lake DM: An improved technique for extracting catecholamines from body fluids. J Neurosci Meth 1985; 13: 239–248 [DOI] [PubMed] [Google Scholar]
  • 19. Laederach K, Weidmann P: Plasma and urinary catecholamines as related to renal function in man. Kidney Inc 1987; 31: 107–111 [DOI] [PubMed] [Google Scholar]
  • 20. Phillipson EA: Sleep apnea. A major public health problem. N Engl J Med 1993; 328: 1271–1273 [DOI] [PubMed] [Google Scholar]
  • 21. Marrone O, Ricobono L, Salvaggio A, Mirabella A, Bonaao A, Bonsignore MR: Catecholamines and blood pressure in obstructive sleep apnea syndrome. Chest 1993; 103: 722–727 [DOI] [PubMed] [Google Scholar]
  • 22. Fletcher EC, Miller J, Schaaf JW, Fletcher JG: Urinary catecholamines before and after tracheostomy in patients with obstructive sleep apnea and hypertension. Sleep 1987; 10: 35–44 [DOI] [PubMed] [Google Scholar]
  • 23. Eisensehr I, Ehrenberg BL, Noachtar S, Korbett K, Byrne A, McAuley A, Palabrica T: Platelet activation, epinephrine, and blood pressure in obstructive sleep apnea syndrome. Neurology 1998; 51: 188–195 [DOI] [PubMed] [Google Scholar]
  • 24. Waravdekar NV, Sinoway LI, Zwillich CW, Leuenberger UA: Influence of treatment on sympathetic nerve activity in sleep apnea. Am J Respir Crit Care Med 1996; 153: 1333–1338 [DOI] [PubMed] [Google Scholar]
  • 25. Minemura H, Akashiba T, Yamamoto H, Akahoshi T, Kosaka N, Horie T: Acute effects of nasal continuous positive airway pressure on 24‐hour blood pressure and catecholamines in patients with obstructive sleep apnea. Intern Med 1998; 37: 1009–1013 [DOI] [PubMed] [Google Scholar]
  • 26. Davidson L, Baum A: Chronic stress and posttraumatic stress disorders. J Consult Clin Psychol 1986; 54: 303–308 [DOI] [PubMed] [Google Scholar]
  • 27. Dimsdale J, Moss J: Short‐term catecholamine response to psychologic stress. Psychosom Med 1980; 42: 493–497 [DOI] [PubMed] [Google Scholar]
  • 28. Esler M, Jennings G, Korner P: Assessment of human sympathetic nervous system activity from measurements of norepinephrine turnover. Hypertension 1988; 11: 3–20 [DOI] [PubMed] [Google Scholar]

Articles from Clinical Cardiology are provided here courtesy of Wiley

RESOURCES