Abstract-Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO 2 (CO 2 -et) were monitored in 20 subjects with essential hypertension (56.4Ϯ1.9 years) and in 26 controls (52.3Ϯ1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Key Words: baroreceptors Ⅲ blood pressure Ⅲ heart rate Ⅲ hypertension Ⅲ nervous system, autonomic Ⅲ respiration A utonomic imbalance has a major role in the etiology of hypertension. 1-4 Such imbalance, characterized by an increase in sympathetic activity (with a possible reduction in parasympathetic activity), is present not only in early and borderline hypertension but also contributes to the maintenance of sustained hypertension. 2 Moreover, several cardiovascular risk factors frequently associated with hypertension are etiologically linked to sympathetic activation. 2,5 At least one of the mechanisms associated with this autonomic imbalance is the reduced baroreflex sensitivity. The baroreflex is reduced or reset toward elevated blood pressure values in hypertension, blunting its ability to suppress the increased sympathetic activity. 6 An impairment of the baroreflex has a direct relation to increased 24-hour blood pressure variability, which in turn correlates with the increase in target-organ damage. 7 Furthermore, there are reports indicating a chemoreflex activation in essential hypertension, which can be an additional mechanism responsible for the increase in sympathetic activity. 8 Given the clinical and prognostic value of reducing sympathetic activation and increasing baroreflex sensitivity in hypertension, it is interesting to note that slow breathing at 6 cycles/min increases baroreflex sensitivity in normal subjects and patients with chronic heart failure 9,10 and also reduces muscle nerve sympathetic activity 11 and chemoreflex activation, 12 thus suggesting a potentially beneficial effect in hypertension. However, there is little evidence about the effect of slow breathing on arterial baroreflex in hypertensive patients, although a few recent studies have shown that device-guided breathing exercise may reduce blood pressure in hypertensive patients. 13 This study aims to test whether slow breathing at 6 cycles/min reduces blood pressure in hypertensive and normal subjects, and if this effect is linked to a...
To determine whether nocturnal hypoxaemia contributes to the excessive erythrocytosis (EE) in Andean natives, standard polysomnographies were performed in 10 patients with EE and in 10 controls (mean haematocrit 76.6 ¡ 1.3% and 54.4 ¡ 0.8%, respectively) living at an altitude of 4,380 m. In addition, the effect of O 2 administration for 1 h prior to sleep, and the relationship between the hypoxic/ hypercapnic ventilatory response and the apnoea/hypopnoea index (AHI) during sleep were studied.Awake arterial oxygen saturation (Sa,O 2 ) was significantly lower in patients with EE than in controls (83.7¡0.3% versus 85.6¡0.4%). In both groups, the mean Sa,O 2 significantly decreased during sleep (to 80.0¡0.8% in EE and to 82.8¡0.5% in controls). The mean Sa,O 2 values remained significantly lower in patients with EE than in controls at all times of the night, and patients with EE spent significantly more time than the controls with an Sa,O 2 of v80%. There were no differences between the two groups in the number and duration of the apnoeas/hypopnoeas. None of these variables were affected by O 2 administration. In both groups the AHI positively correlated with the hypercapnic ventilatory response.Andean natives undergo minor respiratory disorders during sleep. The reduction in oxygen saturation found in subjects with excessive erythrocytosis was small, yet consistent and potentially important, as it remained below the threshold known for the increase in erythropoietin stimulation. This may be an important factor promoting erythropoiesis, but its relevance needs to be further explored.
We evaluated autonomic cardiovascular regulation in subjects with polycythemia and chronic mountain sickness (CMS) and tested the hypothesis that an increase in arterial oxygen saturation has a beneficial effect on arterial baroreflex sensitivity in these subjects. Ten Andean natives with a Hct >65% and 10 natives with a Hct <60%, all living permanently at an altitude of 4,300 m, were included in the study. Cardiovascular autonomic regulation was evaluated by spectral analysis of hemodynamic parameters, while subjects breathed spontaneously or frequency controlled at 0.1 and 0.25 Hz, respectively. The recordings were repeated after a 1-h administration of supplemental oxygen and after frequency-controlled breathing at 6 breaths/min for 1 h, respectively. Subjects with Hct >65% showed an increased incidence of CMS compared with subjects with Hct <60%. Spontaneous baroreflex sensitivity was significantly lower in subjects with high Hct compared with the control group. The effects of supplemental oxygen or modification of the breathing pattern on autonomic function were as follows: 1) heart rate decreased significantly after both maneuvers in both groups, and 2) spontaneous baroreflex sensitivity increased significantly in subjects with high Hct and did not differ from subjects with low Hct. Temporary slow-frequency breathing may provide a beneficial effect on the autonomic cardiovascular function in high-altitude natives with CMS.
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