Relationship between sympathetic and phrenic nerve responses to peripheral chemoreflex in the cat

Huang, W.-X.; Lahiri, S.; Mokashi, A.; Sherpa, A. K.

doi:10.1016/0165-1838(88)90014-8

Cited by 30 publications

(14 citation statements)

References 20 publications

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“…This could be the reason for the powerful bradycardic effect we observed here and reported previously in conscious, freely moving rats 16 as opposed to the modest bradycardia usually observed during general anaesthesia. We did not observe the pressor component of the chemoreflex normally present in conscious animals 17–19 . In our arterially perfused preparation, the most likely explanation for this is the absence of most vascular beds where vasoconstriction occurs, because in other experiments (in the same preparation) we have consistently seen increases in sympathetic activity destined for vascular beds following chemoreflex stimulation 20 …”

Section: Discussionmentioning

confidence: 52%

Activation of Peripheral Chemoreceptors Causes Positive Inotropic Effects in a Working Heart–brainstem Preparation of the Rat

Braga

Zoccal

Soriano

et al. 2007

Clin Exp Pharma Physio

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1. The aim of the present study was to evaluate the effects of peripheral chemoreceptor activation on myocardial contractility in an anaesthetic-free decerebrated rat preparation. 2. In the decerebrated and retrogradely perfused working heart-brainstem preparation, we recorded phrenic nerve activity, left ventricular (LV) pressure (microtip Millar catheter), LV dP/dT, heart rate and aortic perfusion pressure before and after activating peripheral chemoreceptors with bolus intra-arterial injections of KCN. 3. Without cardiac pacing, chemoreflex activation caused falls in heart rate (-108 +/- 21 b.p.m.) and complex polyphasic changes in LV pressure and LV dP/dT. If the heart was paced, chemoreflex activation caused significant rises in LP pressure (+16 +/- 3 mmHg) and LV dP/dt (+778 +/- 93 mmHg/s). These positive inotropic effects were significantly and substantially attenuated by beta-adrenoceptor blockade with atenolol. In all instances, chemoreflex activation elicited potent tachypnoeic responses. 4. In conclusion, activation of peripheral chemoreceptors in non-anaesthetized rats evokes a positive inotropic response that is sympathetically mediated. This observation may be relevant for the evaluation of neurally induced effects of acute hypoxia on the ventricular myocardium.

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Section: Discussionmentioning

confidence: 52%

Activation of Peripheral Chemoreceptors Causes Positive Inotropic Effects in a Working Heart–brainstem Preparation of the Rat

Braga

Zoccal

Soriano

et al. 2007

Clin Exp Pharma Physio

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“…For example, chemoreceptor stimulation in humans via hypoxia and/or CO 2 markedly increases MSNA in a dose-dependent manner, even in the face of increased VT and minute ventilation (13). However, other studies (8,25,27) during apnea in humans and in anesthetized cats show that sympathetic responses to carotid body stimulation occur via pathways, which are independent of the central respiratory pattern generator and of respiratory motor output. In our present studies, we used cortically driven voluntary efforts to increase inspiratory motor output and this volitional increase in the drive to breathe, unlike chemoreceptor stimulation, had no effect on sympathetic outflow in the face of increased ventilation.…”

Section: Discussionmentioning

confidence: 92%

“…There are instances in the intact animal or human where an increased "drive" to breathe does indeed coincide with increased MSNA (8). For example, chemoreceptor stimulation in humans via hypoxia and/or CO 2 markedly increases MSNA in a dose-dependent manner, even in the face of increased VT and minute ventilation (13).…”

Section: Discussionmentioning

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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“…This concept is consistent with 2 sets of findings in anesthetized cats. Huang et al 14 showed that transient carotid chemoreceptor stimulation (via sodium cyanide) during hypocapnia-induced apnea stimulated cervical sympathetic outflow in the absence of phrenic nerve activity. Trzebski and Kubin 15 demonstrated that the PaCO 2 threshold for sympathetic activation during posthyperventilation apnea was 36 mm Hg, whereas the threshold for resumption of phrenic activity was 44 mm Hg.…”

Section: Influence Of Central Respiratory Motor Output On Msnamentioning

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

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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Relationship between sympathetic and phrenic nerve responses to peripheral chemoreflex in the cat

Cited by 30 publications

References 20 publications

Activation of Peripheral Chemoreceptors Causes Positive Inotropic Effects in a Working Heart–brainstem Preparation of the Rat

Activation of Peripheral Chemoreceptors Causes Positive Inotropic Effects in a Working Heart–brainstem Preparation of the Rat

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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