Inhibitory mechanism of slowly adapting pulmonary stretch receptors after release from hyperinflation in anesthetized rabbits

Matsumoto, Shigeji; Ikeda, Mizuho; Nishikawa, Toshimi; Tanimoto, Tsuyoshi; Yoshida, Shinki; Saiki, Chikako

doi:10.1016/s0024-3205(00)00738-4

Cited by 14 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). It is recognized that inhibitory impulses, produced by slowly adapting receptors (SARs) in the lungs during inflation [36], play a role in controlling typically autonomic functions such as breathing pattern, airway smooth muscle tone, systemic vascular resistance, and heart rate [37]. Stretch of connective tissue fibroblasts are capable of effecting the membrane potential of nervous tissue [38].…”

Section: Hypothesismentioning

confidence: 99%

Physiology of Long Pranayamic Breathing: Neural Respiratory Elements may Provide a Mechanism that Explains How Slow Deep Breathing Shifts the Autonomic Nervous System

Jerath¹

2016

J Yoga Phys Ther

View full text Add to dashboard Cite

Summary Pranayamic breathing, defined as a manipulation of breath movement, has been shown to contribute to a physiologic response characterized by the presence of decreased oxygen consumption, decreased heart rate, and decreased blood pressure, as well as increased theta wave amplitude in EEG recordings, increased parasympathetic activity accompanied by the experience of alertness and reinvigoration. The mechanism of how pranayamic breathing interacts with the nervous system affecting metabolism and autonomic functions remains to be clearly understood. It is our hypothesis that voluntary slow deep breathing functionally resets the autonomic nervous system through stretchinduced inhibitory signals and hyperpolarization currents propagated through both neural and non-neural tissue which synchronizes neural elements in the heart, lungs, limbic system and cortex. During inspiration, stretching of lung tissue produces inhibitory signals by action of slowly adapting stretch receptors (SARs) and hyperpolarization current by action of fibroblasts. Both inhibitory impulses and hyperpolarization current are known to synchronize neural elements leading to the modulation of the nervous system and decreased metabolic activity indicative of the parasympathetic state. In this paper we propose pranayama's physiologic mechanism through a cellular and systems level perspective, involving both neural and non-neural elements. This theoretical description describes a common physiological mechanism underlying pranayama and elucidate the role of the respiratory and cardiovascular system on modulating the autonomic nervous system. Along with facilitating the design of clinical breathing techniques for the treatment of autonomic nervous system and other disorders, this model will also validate pranayama as a topic requiring more research.

show abstract

Section: Hypothesismentioning

confidence: 99%

Physiology of Long Pranayamic Breathing: Neural Respiratory Elements may Provide a Mechanism that Explains How Slow Deep Breathing Shifts the Autonomic Nervous System

Jerath¹

2016

J Yoga Phys Ther

View full text Add to dashboard Cite

show abstract

“…This sympathoinhibitory effect is enhanced during slow, deep breathing [26]. SARs hyperpolarize and produce inhibitory impulses posthyperinflation [47] and SARs influence breathing pattern, heart rate, vascular resistance, and smooth muscle tone [48]. The mechanism by which SARs control these functions is not well understood [48].…”

Section: Influence Of Respiratory Rhythm On Olfactory Neuronal Firingmentioning

confidence: 99%

“…Protons from the high-energy bonds of NADH and FADH 2 that are pumped across the mitochondrial membrane [59] lead to membrane hyperpolarization [60], in which the interior matrix voltage of the mitochondria is more negative [61]. At the same time, during inhalation, the inflation of alveoli and the trancheo-bronchial tree may cause SARs to send hyperpolarization impulses to the brain [47]. Protons translocate across the membrane to facilitate establishing a transmembrane potential [62].…”

Section: Influence Of Respiration On the Cellular Levelmentioning

confidence: 99%

Widespread depolarization during expiration: A source of respiratory drive?

Jerath¹,

Crawford²,

Barnes

et al. 2015

Medical Hypotheses

View full text Add to dashboard Cite

a b s t r a c tRespiration influences various pacemakers and rhythms of the body during inspiration and expiration but the underlying mechanisms are relatively unknown. Understanding this phenomenon is important, as breathing disorders, breath holding, and hyperventilation can lead to significant medical conditions. We discuss the physiological modulation of heart rhythm, blood pressure, sympathetic nerve activity, EEG, and other changes observed during inspiration and expiration. We also correlate the intracellular mitochondrial respiratory metabolic processes with real-time breathing and correlate membrane potential changes with inspiration and expiration. We propose that widespread minor hyperpolarization occurs during inspiration and widespread minor depolarization occurs during expiration. This depolarization is likely a source of respiratory drive. Further knowledge of intracellular and extracellular ionic changes associated with respiration will enhance our understanding of respiration and its role as a modulator of cellular membrane potential. This could expand treatment options for a wide range of health conditions, such as breathing disorders, stress-related disorders, and further our understanding of the Hering-Breuer reflex and respiratory sinus arrhythmia.Ó 2014 Elsevier Ltd. All rights reserved. IntroductionIn addition to gas exchange and oxygenation of the blood, respiration in the lungs can regulate multiple physiological processes throughout the body. Studies of the cardiovascular system, the peripheral nervous system, and the central nervous system provide evidence that respiratory patterns can exert a significant and immediate influence on a wide range of bodily functions, including changes in blood pressure and sympathovagal balance. Patterned respiration can regulate blood pressure and heart rate [1], as well as regulate rhythmic centers of the brain that control cardiovascular output [2,3]. While the majority of these findings have demonstrated the impact of respiration on cardiac output and other processes in isolated preparations, little work has focused on respiration's direct influence on membrane potential.This article reviews the current understanding of respiration as a regulator of cardiovascular physiology and nervous system function. More specifically, we discuss the role of respiratory rhythm and rate on both systemic and local control of these systems. We describe the role of pulmonary stretch receptors (with a focus on slowly adapting receptors) in converting breathing patterns into a functional, multi-faceted, mechanism that allows respiration to communicate with, and direct various aspects of cardiovascular and nervous system physiology. We propose a hypothesis in which inspiration and expiration are associated with transient increases and decreases in membrane potential that may underlie these widespread changes and how these membrane potential changes may underlie the chaotic dynamics of rhythmic breathing.Many studies focus on the brainstem as the primary modulator of resp...

show abstract

“…Air hunger intensity was rated at the end of each breath on a visual analog scale. The increase in EEV was the same in the seated and supine positions; however, air hunger was reduced to a greater extent in the seated position (13,30,31, and 44% seated vs. 3,9,23, and 27% supine at 2, 4, 6, and 8 cmH 2O PEEP, respectively, P Ͻ 0.05). Removing PEEP produced a slight increase in air hunger that was greater than pre-PEEP levels (P Ͻ 0.05).…”

mentioning

confidence: 79%

Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults

Vovk

Binks²

2007

Journal of Applied Physiology

View full text Add to dashboard Cite

Air hunger is an unpleasant urge to breathe and a distressing respiratory symptom of cardiopulmonary patients. An increase in tidal volume relieves air hunger, possibly by increasing pulmonary stretch receptor cycle amplitude. The purpose of this study was to determine whether increasing end-expiratory volume (EEV) also relieves air hunger. Six healthy volunteers (3 women, 31 +/- 4 yr old) were mechanically ventilated via a mouthpiece (12 breaths/min, constant end-tidal Pco(2)) at high minute ventilation (Ve; 12 +/- 2 l/min, control) and low Ve (6 +/- 1 l/min, air hunger). EEV was raised to approximately 150, 400, 725, and 1,000 ml by increasing positive end-expiratory pressure (PEEP) to 2, 4, 6, and 8 cmH(2)O, respectively, for 1 min during high and low Ve. The protocol was repeated with the subjects in the seated and supine positions to test for the effect of shifting baseline EEV. Air hunger intensity was rated at the end of each breath on a visual analog scale. The increase in EEV was the same in the seated and supine positions; however, air hunger was reduced to a greater extent in the seated position (13, 30, 31, and 44% seated vs. 3, 9, 23, and 27% supine at 2, 4, 6, and 8 cmH(2)O PEEP, respectively, P < 0.05). Removing PEEP produced a slight increase in air hunger that was greater than pre-PEEP levels (P < 0.05). Air hunger is relieved by increases in EEV and tidal volume (presumably via an increase in mean pulmonary stretch receptor activity and cycle amplitude, respectively).

show abstract

Inhibitory mechanism of slowly adapting pulmonary stretch receptors after release from hyperinflation in anesthetized rabbits

Cited by 14 publications

References 0 publications

Physiology of Long Pranayamic Breathing: Neural Respiratory Elements may Provide a Mechanism that Explains How Slow Deep Breathing Shifts the Autonomic Nervous System

Physiology of Long Pranayamic Breathing: Neural Respiratory Elements may Provide a Mechanism that Explains How Slow Deep Breathing Shifts the Autonomic Nervous System

Widespread depolarization during expiration: A source of respiratory drive?

Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults

Contact Info

Product

Resources

About