Neural mechanism of the pressor response  to obstructive and nonobstructive apnea

Katragadda, Srinivas; Xie, Ailiang; Puleo, Dominic S.; Skatrud, James B.; Morgan, Barbara J.

doi:10.1152/jappl.1997.83.6.2048

Cited by 74 publications

(68 citation statements)

References 19 publications

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“…Treatment with a bronchodilator for mild to moderate COPD improves respiratory function and exercise tolerance, but does not improve gas exchange abnormalities in the absence of oxygen therapy. 14 Nonetheless, in the present case tiotropium inhalation improved the airway obstruction and also suppressed activation of the sympathetic nerve system via an improvement in both the negative intrathoracic pressure 15,16 and the continuous fatigue of the respiratory muscles. Indeed, the plasma norepinephrine level was decreased significantly.…”

Section: Circulation Journal Vol70 December 2006mentioning

confidence: 54%

Tiotropium, a Novel Muscarinic M3 Receptor Antagonist, Improved Symptoms of Chronic Obstructive Pulmonary Disease Complicated by Chronic Heart Failure

Kato

Komamura

Kitakaze

2006

Circ J

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n the elderly population unrecognized heart failure is very common in patients with stable chronic obstructive pulmonary disease (COPD), 1 and the high prevalence of COPD, chronic heart failure (CHF) and their combination in this group [2][3][4] suggests that customized treatment may be required for such complicated disease status. We report using tiotropium, a non--adrenergic bronchodilator and novel M3 muscarinic receptor antagonist, for COPD complicated with CHF. Case ReportA 77-year-old man was referred to hospital because of dyspnea on exertion. He was a heavy smoker of 60 cigarettes/day for 34 years and had CHF with history of hypertension and mild aortic regurgitation (AR) for 7 years, for which he was being treated with an angiotensin-converting enzyme inhibitor (temocapril, 2 mg) and loop diuretics (furosemide, 20 mg). His weight, blood pressure and heart rate were 56.8 kg, 124/64 mmHg and 80 beats/min, respectively. The breath sounds were decreased with fine rales in both of the posterior lung bases. Physical examination revealed no overt signs of right-sided heart failure, such as dilated jugular vein, hepatomegaly or peripheral edema.Chest X-ray showed increased fibro-linear infiltration in both lung bases ( Fig 1A) and ECG revealed sinus rhythm with complete right bundle branch block and high voltage in the chest leads ( Fig 1B). Laboratory investigations were normal except for a high concentration of brain natriuretic peptide (BNP: 222 pg/ml), which had been chronically elevated at approximately 200-300 pg/ml at least for 2 years.Echocardiography revealed left ventricular (LV) hypertrophy with an enlarged LV cavity and diffuse hypokinesis of the LV wall, with an ejection fraction (EF) of 27%. Right ventricular (RV) dimensions and wall motion were normal. The inferior vena cava showed respiratory movement and was not enlarged. Doppler echocardiography showed early diastolic transmitral flow velocity (E) of 1.2 m/s and the peak diastolic velocity during early filling of the longitudinal mitral annular motion (Ea) was 9.9 cm/s (Fig 2). The E/Ea ratio was 12.2, indicating high LV end-diastolic pressure (LVEDP). 5 The E/A ratio was 0.67, which indicated an abnormal relaxation pattern. Doppler echocardiographic estimated pressure gradient between right atrial (RA) and RV was 22 mmHg (Table 2) and systolic pulmonary artery (PA) pressure was 32 mmHg, indicating hemodynamic load on the right side of the heart. Right-heart catheterization, coronary angiography (CAG) and left ventriculography (LVG) were performed. Pulmonary capillary wedge pressure was 16 mmHg, PA pressure was 30/12 mmHg (mean PA pressure =22 mmHg), RA pressure was 4 mmHg and cardiac output was 5.6 L/min. Pulmonary vascular resistance was 86 dyne· s -1 ·cm -5 . CAG showed normal coronary arteries. LVG revealed diffuse hypokinesis with EF of 30% and mild AR. LVEDP was 14 mmHg. Therefore, we diagnosed left-sided heart failure and hemodynamic load on the right heart with neither pulmonary hypertension nor right-sided heart failure.Pulmonary func...

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Section: Circulation Journal Vol70 December 2006mentioning

confidence: 54%

Tiotropium, a Novel Muscarinic M3 Receptor Antagonist, Improved Symptoms of Chronic Obstructive Pulmonary Disease Complicated by Chronic Heart Failure

Kato

Komamura

Kitakaze

2006

Circ J

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“…RR duration is influenced by the baroreflex loop, reflects phasic sympathetic activity and interacts with power oscillations during apnoea or hyperventilation [5]. The increase in LFn power demonstrates central tonic sympathetic activation [5,19]. This is associated with an increase in respiratory effort due to the inspiratory attempts against the occluded/narrowed airways and the gradual elevation of negative intrathoracic pressure towards the end of apnoeas/hypopnoeas.…”

Section: Discussionmentioning

confidence: 99%

Spectral oscillations of RR intervals in sleep apnoea/hypopnoea syndrome patients

Dingli¹,

Assimakopoulos²,

Wraith³

et al. 2003

European Respiratory Journal

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A recent study has shown that daytime heart rate variability is reduced in obstructive sleep apnoea/hypopnoea syndrome (OSAHS) patients. In the present study, the hypothesis was that sympathovagal balance around apnoeas/hypopnoeas and nocturnal autonomic activity are altered in OSAHS patients.Frequency-and time-domain analyses of RR intervals were performed to monitor sympathovagal activity noninvasively. Fourteen untreated OSAHS patients and seven healthy subjects underwent overnight polysomnography.Low (LF) and total (TF) frequency power increased 2 min around the end of apnoeas/ hypopnoeas (LF 229¡38 ms 2 , TF 345¡45 ms 2 ) compared with undisturbed sleep (LF 106¡18 ms 2 , TF 203¡23 ms 2 ). The increase in high frequency (HF) power was not significant. LF increase was proportionally higher than the HF increase (normalised LF (LFn) 67¡1 units, normalised HF (HFn) 33¡1 units) compared with undisturbed sleep (LFn 52¡2 units, HFn 48¡2 units). RR duration did not change around apnoeas/ hypopnoeas (RR 904¡28 ms). The LF and TF power increase was greater around arousal-inducing (LF 260¡45 ms ) apnoeas/hypopnoeas; the LF and LFn increases were significant in both groups compared with undisturbed sleep and HF power differences were nonsignificant. RR intervals were longer around self-terminating apnoeas/hypopnoeas (RR 914¡29 ms); the differences were not significant compared with undisturbed sleep. RR interval spectral power was not influenced by the event type. RR duration decreased (912 ¡ 28 ms) and LF, HF and TF power increased ( ). LFn and HFn did not change significantly.Sympathetic activity increases around apnoeas/hypopnoeas. The recurrent nocturnal fluctuations of sympathovagal balance and the overall increase of nocturnal autonomic activity may be of importance in the development of cardiovascular disease in sleep apnoea patients. Eur Respir J 2003; 22: 943-950.

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“…[4][5][6][7] Their underlying pathological mechanisms include recurrent intermittent hypoxemia and increased sympathetic activity, primarily at the termination of the apneic events. 8,9 In a previous study, 10 our group showed that OSAS is also associated with ED in a dose-related fashion. This association is very strong in patients with severe OSAS and weaker in patients with mild or moderate OSAS.…”

Section: Introductionmentioning

confidence: 89%

Predictors of erectile function improvement in obstructive sleep apnea patients with long-term CPAP treatment

et al. 2004

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The long-term effect of treatment with continuous positive airway pressure (CPAP) on erectile function was assessed in 60 patients with obstructive sleep apnea syndrome (OSAS). Severity of OSAS was evaluated by respiratory disturbance index (RDI) and minimal oxygen saturation (OxiMin). Severity of erectile dysfunction (ED) was assessed with the five question International Index of Erectile Function (IIEF-5) before and after CPAP treatment. Subjects were categorized into three groups on the basis of the change in IIEF-5 score: Group 1, no change (n ¼ 37); Group 2, improvement from 1075.65 to 19.175.7, Po0.01 (n ¼ 12); Group 3, worsening from 19.974.7 to 9.577.8, Po0.01 (n ¼ 11). Group 2 had significantly higher RDI and lower OxiMin than the other groups, and was also more compliant and satisfied with CPAP. Change in IIEF-5 with CPAP treatment was negatively correlated (Pearson coefficient) with OxiMin (r ¼ À0.374), and positively correlated with adherence to CPAP treatment (r ¼ 0.689). In conclusion, in selected patients, CPAP treatment for OSAS may by itself have a positive effect on erectile function by improving respiration during sleep. Predictors of erectile improvement include high RDI, low OxiMin, and CPAP compliance.

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Neural mechanism of the pressor response to obstructive and nonobstructive apnea

Cited by 74 publications

References 19 publications

Tiotropium, a Novel Muscarinic M3 Receptor Antagonist, Improved Symptoms of Chronic Obstructive Pulmonary Disease Complicated by Chronic Heart Failure

Tiotropium, a Novel Muscarinic M3 Receptor Antagonist, Improved Symptoms of Chronic Obstructive Pulmonary Disease Complicated by Chronic Heart Failure

Spectral oscillations of RR intervals in sleep apnoea/hypopnoea syndrome patients

Predictors of erectile function improvement in obstructive sleep apnea patients with long-term CPAP treatment

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