An induced blood pressure rise does not alter upper airway resistance in sleeping humans

Wilson, Charles Morrow; Manchanda, Shalini; Crabtree, David C.; Skatrud, James B.; Dempsey, Jerome A.

doi:10.1152/jappl.1998.84.1.269

Cited by 17 publications

(10 citation statements)

References 32 publications

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“…Further experiments are needed to clarify the role of blood pressure and blood volume status on lung ventilation in anurans. In mammals, the link between lung ventilation and blood pressure is better defined, with hypotension causing a stimulation of lung ventilation and hypertension resulting in hypoventilation (Saupe et al, 1995;Wilson et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Lung ventilation contributes to vertical lymph movement in anurans

Hedrick

Drewes

Hillman

et al. 2007

Journal of Experimental Biology

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SUMMARY Anurans (frogs and toads) generate lymphatic fluid at 10 times the rate in mammals, largely as a consequence of their very `leaky' vasculature and high interstitial compliance. Lymph is ultimately pumped into the venous system by paired, dorsally located lymph hearts. At present, it is unclear how lymphatic fluid that accumulates in central body subcutaneous lymph sacs is moved to the anterior and posterior lymph hearts in the axillary regions and how lymph is moved, against gravity, to the dorsally located lymph hearts. In this study,we tested the hypothesis that lung ventilation, through its consequent effects on lymph sac pressure, contributes to the vertical movement of lymphatic fluid in the cane toad (Chaunus marinus) and the North American bullfrog(Lithobates catesbeiana). We measured pressure in the dorsal, lateral and subvertebral lymph sacs of anesthetized cane toads and bullfrogs during artificial lung inflation and deflation. We also measured pressure in the subvertebral lymph sac, which adheres to the dorsal surface of the lungs,simultaneously with brachial (forelimb) and pubic (posterior) sac pressure during ventilation in freely behaving animals. There were highly significant(P<0.001) relationships between lung pressure and lymph sac pressures (r2=0.19–0.72), indicating that pulmonary pressure is transmitted to the highly compliant lymph sacs that surround the lungs. Subvertebral sac pressure of resting animals was not significantly different between L. catesbeiana (518±282 Pa) and C. marinus (459±111 Pa). Brachial sac compliance (ml kPa–1 kg–1) also did not differ between the two species (33.6±5.0 in L. catesbeiana and 37.0±9.4 in C. marinus). During expiration (lung deflation), reductions in expanding subvertebral sac pressure are communicated to the brachial lymph sac. Changes in brachial and pubic lymph sac pressures were correlated almost entirely during expiration rather than inspiration. The change in brachial sac pressure during expiration was 235±43 Pa for C. marinus and 215±50 Pa for L. catesbeiana, which is of sufficient magnitude to move lymph the estimated 0.5–1.0 cm vertical distance from the forelimb to the vicinity of the anterior lymph hearts. We suggest that lymph is moved during expiration to the subvertebral sac from anterior and posterior lymph sacs. During lung inflation, increased lymph sac pressure moves lymph to axillary regions, where lymph hearts can return lymph to the vascular space. Consequently, pulmonary ventilation has an important role for lymph movement and, hence, blood volume regulation in anurans.

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Section: Discussionmentioning

confidence: 99%

Lung ventilation contributes to vertical lymph movement in anurans

Hedrick

Drewes

Hillman

et al. 2007

Journal of Experimental Biology

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“…Subjects breathed through a mouthpiece with the nose occluded. Airflow rates, tidal volume (VT), mouth pressure (PM), and end-tidal PCO2 were measured using equipment and techniques described previously (24,33). Inspiratory muscle force development was calculated as the product of the time integral of PM (͐PM) and breathing frequency ( fb).…”

Section: Methodsmentioning

confidence: 99%

Threshold effects of respiratory muscle work on limb vascular resistance

Sheel

Derchak

Pegelow

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Threshold effects of respiratory muscle work onlimb vascular resistance. Am J Physiol Heart Circ Physiol 282: H1732-H1738, 2002; 10.1152/ajpheart.00798.2001.-The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (Q L) and utilized the changes in mouth twitch pressure (⌬P MT) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 Ϯ 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1-3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and Q L, limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control (P Ͼ 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 Ϯ 12% reduction in P MT with bilateral phrenic nerve stimulation. During the fatigue trial, Q L and LVR were unchanged from baseline at minute 1, but LVR rose 36% and Q L fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and Q L returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and Q L, whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q L. We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions. diaphragm fatigue; leg blood flow; metaboreflex threshold; Doppler ultrasound; bilateral phrenic nerve stimulation IT IS WELL ESTABLISHED THAT thinly myelinated group III and unmyelinated IV afferent nerve fibers innervate limb skeletal muscle. These afferents are stimulated by metabolic byproducts (23), mechanical deformation (29), temperature (18), and vascular distension during muscular contraction (4). Stimulation of these afferents during muscular contraction elicits a powerful pressor response where sympathetic vasoconstrictor outflow is augmented to both resting and exercising skeletal muscle. A threshold exists for activation of this metaboreflex as numerous human studies have demonstrated a link between the metabolic events occurring within a contracting muscle (forearm) and the cardiovascular adjustments to handgrip exercise (3, 21). The current concept is that inadequate blood flow (or O 2 delivery) to the contracting muscle leads to an increase in the concentration of metabolites and the stimulation of chemosensitive afferents (type IV). The resulting ...

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“…Airflow rates, VT, mask pressure (P m ), and end-tidal partial pressure of CO 2 (P ET CO 2 ) were measured using equipment and techniques described previously. 6 A single-lead ECG was continuously recorded. Diaphragmatic electromyogram (EMG di ) was obtained from surface electrodes placed over the sixth and seventh intercostal spaces in the anterior axillary line.…”

Section: General Proceduresmentioning

confidence: 99%

Role of Respiratory Motor Output in Within-Breath Modulation of Muscle Sympathetic Nerve Activity in Humans

Croix

Satoh

Morgan

et al. 1999

Circulation Research

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126

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Abstract-We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO 2 , but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H 2 O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human. (Circ Res. 1999;85:457-469.)Key Words: autonomic nervous system Ⅲ cardiorespiratory interaction Ⅲ positive pressure ventilation T he independent influence of the respiratory rhythm generator on the timing of sympathetic outflow has been studied using reduced preparations in which peripheral reflex mechanisms were eliminated by vagotomy and/or sinoaortic denervation. In these deafferented animal preparations, sympathetic neurons fire mainly during inspiration (ie, in synchrony with phrenic discharge), with their minimum activity occurring during expiration. 1,2 The close temporal relationship between phrenic discharge and sympathetic activity recorded in anesthetized, paralyzed, and vagotomized animals has led to the hypothesis that the 2 neural outputs either arise from the same brain stem neurons or are driven by a common oscillator. 1,3 However, in the intact human, sympathetic outflow to skeletal muscle (muscle sympathetic nerve activity; MSNA) declines during inspiration, reaching its nadir at end inspiration/early expiration, and then rises, reaching its peak at end expiration. 4,5 The influence of central respiratory motor output on the within-breath modulation of MSNA has not been studied in humans.The purpose of the present study was to ex...

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An induced blood pressure rise does not alter upper airway resistance in sleeping humans

Cited by 17 publications

References 32 publications

Lung ventilation contributes to vertical lymph movement in anurans

Lung ventilation contributes to vertical lymph movement in anurans

Threshold effects of respiratory muscle work on limb vascular resistance

Role of Respiratory Motor Output in Within-Breath Modulation of Muscle Sympathetic Nerve Activity in Humans

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