Pulmonary stretch receptors activity during thermal polypnea (author's transl)]

1 We have studied the unit activity of 88 pulmonary stretch receptors (RPI) in the vagus nerve of the cat by using the single fibre technique. 2 In spite of a 38% decrease in tidal volume, the discharge frequency of RPI is statistically unchanged during polypnea, However, RPI are recruited earlier, but their discharge overlaps expiration. 3 Individual influences of tidal volume, temperature, and FACO2 on RPI activities are tested. During polypnea, the excitatory influences of hyperthermia and hypocapnia act against the depressing action of tidal volume reduction: RPI are still active. 4 During polypnea, respiratory rhythm and tidal volume are unchanged after bivagotomy. RPI activity seems functionally insignificant. This result suggests that the thermally induced respiratory response is mediated by structures in the upper brain stem (probably the preoptic anterior hypothalamus) and is not dependent on the integrity of the vagus nerve.     

Systemic hemodynamics affecting cardiac output during hypocapnic and hypercapnic hypoxia

Systemic hemodynamic adjustments involved in the control of cardiac output (CO) were examined in chronically instrumented unanesthetized sheep inhaling gas mixtures resulting in hypocapnic hypoxia (H) [arterial pH (pHa) = 7.53, arterial partial pressure of O2 (Pao2) = 30 Torr, arterial partial pressure of CO2 (Paco2) = 29 Torr] or hypercapnic hypoxia (HCH) (pHa = 7.14, Pao2 = 34 Torr, Paco2 = 72 Torr) for 1 h. H (n = 7) and HCH (n = 6) resulted in 26% and 61% increases in CO, respectively, and mean systemic arterial pressure rose to a greater extent during HCH. Both H and HCH resulted in increased blood flow (microsphere method) to the peripheral systemic circulation including the brain, heart, diaphragm, and nonrespiratory skeletal muscle (the latter blood flow increased 120% during H and 380% during HCH). Gastrointestinal and renal blood flow remained unchanged during H and HCH. Transit time of green dye from the pulmonary artery to regional veins in the hindlimb and intestine was 5.0 and 8.2 s, respectively, during base-line conditions and remained unchanged with HCH. During HCH, regional O2 consumption increased 274% for the hindlimb and decreased 39% for the intestine. Total catecholamines rose 250% during H and 3,700% during HCH. During hypocapnic and hypercapnic hypoxia, CO is augmented in part by systemic hemodynamic adjustments that include a redistribution of blood flow and a translocation of blood volume to the fast transit time peripheral systemic circuit. The sympathetic nervous system may play an important role in mediating these systemic hemodynamic adjustments.     

Effect of paced breathing on ventilatory and cardiovascular variability parameters during short-term investigations of autonomic function

Paced breathing (PB) around 0.25 Hz has been advocated as a means to avoid confounding and to standardize measurements in short-term investigations of autonomic cardiovascular regulation. Controversy remains, however, as to whether it causes any alteration in autonomic control. We addressed this issue in 40 supine, middle-aged, healthy volunteers by assessing the changes induced by PB (0.25 Hz for 8 min) on 1) ventilatory parameters, 2) the indexes of autonomic control of cardiovascular function, and 3) the spectral indexes of cardiovascular variability. Subjects were grouped into group 1 (n = 31), if spontaneous breathing was regular and within the high-frequency (HF) band (0.15-0.45 Hz), or group 2 (n = 9), if it was irregular or slow (< 0.15 Hz). In both groups, PB was accompanied by an increase in minute ventilation (both groups, P < 0.01), whereas tidal volume increased only in group 1 (P = 0.0003). End-tidal CO2 decreased by [median (lower quartile, upper quartile)] -0.2 (-0.5, -0.1)% (group 1, P < 0.0001) and -0.6 (-0.8, -0.5)% (group 2, P = 0.008). Mean R-R interval and systolic and diastolic pressure remained remarkably stable (all P > or = 0.13, both groups). No significant changes were observed in spectral indexes of R-R and pressure variability (all P > or = 0.12, measured only in group 1 to avoid confounding), except in the HF power of pressure signals, which significantly increased (all P < 0.05) in association with increased tidal volume. In conclusion, PB at 0.25 Hz causes a slight hyperventilation and does not affect traditional indexes of autonomic control or, in subjects with spontaneous breathing in the HF band, most relevant spectral indexes of cardiovascular variability. These findings support the notion that PB does not alter cardiovascular autonomic regulation compared with spontaneous breathing.     

The role of central and peripheral temperature changes in the regulation of thermal polypnea in the chicken

The temperature of free-flowing blood in the aorta, the skin temperature of the comb, and the temperature of the skin under the feathers, of nine male chickens were measured, before, during and after exposure to a hot environment (45°C). Respiratory frequencies were also recorded, and no evidence was obtained that thermal polypnea occured before the deep-body temperature increased. In some birds, the highest respiratory frequency was noted after the air temperature was lowered. It is suggested that, although an increase in skin temperature is not involved in the initiation of thermal polypnea, changes in skin temperature may modify the respiratory pattern once thermal polypnea is established.     

Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.     

Near-maximal voluntary hyperpnea and ventilatory muscle function

Because of its potential relevance to heavy exercise we studied the ventilatory muscle function of five normal subjects before, during, and after shortterm near-maximal voluntary normocapnic hyperpnea. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made at four levels of ventilation: 76, 79, and 86% maximal voluntary ventilation (MVV) and at MVV. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made. The pressure-stimulation frequency relationship of the diaphragm obtained by unilateral transcutaneous phrenic nerve stimulation was studied in two subjects before and after hyperpnea. Decreases in maximal inspiratory (PImax) and transdiaphragmatic (Pdimax) strength were recorded posthyperpnea at 76 and 79% MVV. Decreases in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm EMG occurred in association with decreases in Pdimax. Analysis of the pressure-time product (P X dt) for the inspiratory and expiratory muscles individually indicated the increasing contribution of expiratory muscle force to the attainment of higher levels of ventilation. Demonstrable ventilatory muscle fatigue may limit endurance at high levels of ventilation.     

Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats

Bao, Gang, Preet M. Randhawa, and Eugene C. Fletcher.Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats. J. Appl.Physiol. 82(4): 1071-1078, 1997.Using a ratmodel, we investigated whether episodic eucapnic hypoxia was a morepotent stimulus to acute blood pressure (BP) elevation and bradycardiathan episodic hypocapnic hypoxia. We also investigated therole of sympathetic and parasympathetic nervous system in thiscardiovascular response. Sprague-Dawley (SD) and Wistar Kyoto (WKY)rats were exposed to repetitive 30-s cycles of hypocapnic or eucapnichypoxia before and after intravenous injection of the₁-adrenergic blocker prazosin,₂-adrenergic blocker yohimbine,or atropine. Eucapnic hypoxia caused a threefold elevation in systolicBP from baseline (83.5 ± 3.5 mmHg in WKY, 70.6 ± 4.6 mmHg inSD) and greater bradycardia (178 ± 20 beats/min in WKY,178 ± 21 beats/min in SD) compared with hypocapnic hypoxia (29.8 ± 3.6 mmHg and 43 ± 15 beats/min in WKY,19.0 ± 4.1 mmHg and 45 ± 12 beats/min in SD). Afterprazosin, the BP increase from eucapnic hypoxia was blunted, yohimbineshowed no effect, and atropine blocked the bradycardia. Directmeasurement of sympathetic nerve activity confirmed that addingCO₂ to the hypoxic gas mixture caused a 61% increase in sympathetic nerve activity. WKY rats seemmore vulnerable than SD rats to both hypoxia exposures in terms of theelevation in BP. We conclude that, in the rat, eucapnic hypoxia is amore potent stimulus to acute BP elevation and bradycardia than ishypocapnic hypoxia. An increased sympathetic tone appears to beinvolved in the BP response to acute episodic hypoxia.

     

Physiology of ventilatory regulation during sleep

During light slow-wave sleep, ventilation is principally regulated by automatic metabolic control system. An instability in the respiratory control may be the predominant disturbance leading to very irregular or periodic breathing. During deep sleep, ventilation is progressively more stable. During REM sleep, automatic regulation is abolished and ventilation is particularly dependent on the compartmental control system. The reduction in airways and respiratory muscles tone favors the occurrence of obstructive apneas. The elevation in arousal threshold leads prolongation of the obstructive events.