scholarly journals Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

2021 ◽  
Vol 12 ◽  
Author(s):  
Michał Proczka ◽  
Jacek Przybylski ◽  
Agnieszka Cudnoch-Jędrzejewska ◽  
Ewa Szczepańska-Sadowska ◽  
Tymoteusz Żera
Keyword(s):  
Antidiuretic Hormone ◽  
Pulmonary Ventilation ◽  
Surrogate Marker ◽  
Fine Tuning ◽  
Type I ◽  
Posterior Lobe ◽  
Arterial Blood ◽  
Obstructive Sleep ◽  
Brainstem Nuclei ◽  
Vasopressinergic Neurons

Vasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blood pressure, sympathetic activity, baroreflex sensitivity, glucose homeostasis, release of glucocorticoids and catecholamines, stress response, anxiety, memory, and behavior. Vasopressin is synthesized in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the circulation from the posterior lobe of the pituitary gland together with a C-terminal fragment of pro-vasopressin, known as copeptin. Additionally, vasopressinergic neurons project from the hypothalamus to the brainstem nuclei. Increased release of AVP into the circulation and elevated levels of its surrogate marker copeptin are found in pulmonary diseases, arterial hypertension, heart failure, obstructive sleep apnoea, severe infections, COVID-19 due to SARS-CoV-2 infection, and brain injuries. All these conditions are usually accompanied by respiratory disturbances. The main stimuli that trigger AVP release include hyperosmolality, hypovolemia, hypotension, hypoxia, hypoglycemia, strenuous exercise, and angiotensin II (Ang II) and the same stimuli are known to affect pulmonary ventilation. In this light, we hypothesize that increased AVP release and changes in ventilation are not coincidental, but that the neurohormone contributes to the regulation of the respiratory system by fine-tuning of breathing in order to restore homeostasis. We discuss evidence in support of this presumption. Specifically, vasopressinergic neurons innervate the brainstem nuclei involved in the control of respiration. Moreover, vasopressin V1a receptors (V1aRs) are expressed on neurons in the respiratory centers of the brainstem, in the circumventricular organs (CVOs) that lack a blood-brain barrier, and on the chemosensitive type I cells in the carotid bodies. Finally, peripheral and central administrations of AVP or antagonists of V1aRs increase/decrease phrenic nerve activity and pulmonary ventilation in a site-specific manner. Altogether, the findings discussed in this review strongly argue for the hypothesis that vasopressin affects ventilation both as a blood-borne neurohormone and as a neurotransmitter within the central nervous system.

Effect of enlarged adenoids on arterial blood gases in children

1991 ◽  
Vol 105 (6) ◽  
pp. 436-438 ◽  
Author(s):  
Mohammed S. Khalifa ◽  
Reda H. Kamel ◽  
Mona Abu Zikry ◽  
Tarek M. Kandil
Keyword(s):  
Statistical Evaluation ◽  
Pulmonary Ventilation ◽  
Blood Gases ◽  
Sleep Apnoea ◽  
Nasal Resistance ◽  
Arterial Blood Gases ◽  
Normal Children ◽  
Arterial Blood ◽  
Obstructive Sleep ◽  
Resistance To Respiration

AbstractThe enlarged adenoid is a common disorder in children resulting in nasopharyngeal obstruction. Many authors suggest that increased nasal resistance to respiration may cause disturbances in the pulmonary ventilation and carry the risk of obstructive sleep apnoea and/or cardiopulmonary syndrome.This study comprised 30 children complaining of long-standing nasal obstruction due to enlarged adenoids. Adenoidectomy was performed and the arterial blood gases were measured before and one month after surgery. Twelve normal children were also included as controls. Statistical evaluation of the results showed that O2 saturation and arterial O2 tension (PaO2) were significantly low before the operation, and increased significantly after surgery. Arterial CO2 tension (PaCO2) was insignificantly low before operation, but decreased significantly after adenoidectomy. It was concluded that enlarged adenoid may be associated with ventilatory impairment which is reversible after adenoidectomy.

scholarly journals Pathogenesis of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea: A Hypothesis with Emphasis on the Nucleus Tractus Solitarius

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Mak Adam Daulatzai
Keyword(s):  
Cognitive Decline ◽  
Cognitive Dysfunction ◽  
Nucleus Tractus Solitarius ◽  
Negative Impact ◽  
Upper Airway ◽  
Brain Regions ◽  
It Projects ◽  
Obstructive Sleep ◽  
Brainstem Nuclei ◽  
And Oxidative Stress

OSA is characterized by the quintessential triad of intermittent apnea, hypoxia, and hypoxemia due to pharyngeal collapse. This paper highlights the upstream mechanisms that may trigger cognitive decline in OSA. Three interrelated steps underpin cognitive dysfunction in OSA patients. First, several risk factors upregulate peripheral inflammation; these crucial factors promote neuroinflammation, cerebrovascular endothelial dysfunction, and oxidative stress in OSA. Secondly, the neuroinflammation exerts negative impact globally on the CNS, and thirdly, important foci in the neocortex and brainstem are rendered inflamed and dysfunctional. A strong link is known to exist between neuroinflammation and neurodegeneration. A unique perspective delineated here underscores the importance of dysfunctional brainstem nuclei in etiopathogenesis of cognitive decline in OSA patients. Nucleus tractus solitarius (NTS) is the central integration hub for afferents from upper airway (somatosensory/gustatory), respiratory, gastrointestinal, cardiovascular (baroreceptor and chemoreceptor) and other systems. The NTS has an essential role in sympathetic and parasympathetic systems also; it projects to most key brain regions and modulates numerous physiological functions. Inflamed and dysfunctional NTS and other key brainstem nuclei may play a pivotal role in triggering memory and cognitive dysfunction in OSA. Attenuation of upstream factors and amelioration of the NTS dysfunction remain important challenges.

Anterior Palatoplasty for the Treatment of OSA

2009 ◽  
Vol 141 (2) ◽  
pp. 253-256 ◽  
Author(s):  
Kenny P. Pang ◽  
Raymond Tan ◽  
Puravi Puraviappan ◽  
David J. Terris
Keyword(s):  
Body Mass Index ◽  
Clinical Stage ◽  
Long Term Results ◽  
Apnea Hypopnea Index ◽  
Type I ◽  
Obstructive Sleep ◽  
The Mean ◽  
Anterior Palatoplasty

OBJECTIVE: Review long-term results of the modified cautery-assisted palatoplasty (mod CAPSO)/anterior palatoplasty for the treatment of mild-moderate obstructive sleep apnea (OSA). STUDY DESIGN: Prospective series of 77 patients. All patients were >18 years old, type I Fujita, body mass index (BMI) < 33, Friedman clinical stage II, with apnea-hypopnea index (AHI) from 1.0 to 30.0. The mean follow-up time was 33.5 months. The procedure involved an anterior soft palatal advancement technique with or without removal of the tonsils. The procedure was done under general or local anesthesia. RESULTS: There were 69 men and eight women; the mean age was 39.3 years old; and mean BMI was 24.9 (range 20.7–26.8). There were 38 snorers and 39 OSA patients. The AHI improved in patients with OSA, 25.3 ± 12.6 to 11.0 ± 9.9 ( P < 0.05). The overall success rate for this OSA group was 71.8 percent (at mean 33.5 months). The mean snore scores (visual analog score) improved from 8.4 to 2.5 (for all 77 patients). Lowest oxygen saturation also improved in all OSA patients. Subjectively, all patients felt less tired. CONCLUSION: This technique has been shown to be effective in the management of patients with snoring and mild-moderate OSA.

scholarly journals Energy Conversion Monitoring in Skin Tissue: A More Sensitive Measure of Hypoxia Occurring With Sleep Disordered Breathing Than Pulse Oximetry

2019 ◽  
Author(s):  
Guy M. Hatch ◽  
Liza Ashbrook ◽  
Aric A. Prather ◽  
Andrew D. Krystal
Keyword(s):  
Pulse Oximetry ◽  
Energy Conversion ◽  
Sleep Disordered Breathing ◽  
Skin Tissue ◽  
Current Standard ◽  
Blood Oxygen Saturation ◽  
Primary Snoring ◽  
Arterial Blood ◽  
Obstructive Sleep ◽  
Disordered Breathing

Pulse oximetry is the current standard for detecting drops in arterial blood oxygen saturation (SpO2) associated with obstructive sleep apnea and hypopnea events in polysomnographic (PSG) testing. In cases of hypoxic challenge, such as occurs during apneic events, regulatory mechanisms restrict blood flow to the skin to preferentially maintain SpO2 for more vital organs. As a result, a measure related to skin tissue oxygenation is likely to be more sensitive to inadequate breathing during sleep than pulse oximetry. Energy Conversion Monitoring (ECM) provides a method for measuring skin tissue oxygen-dependent energy conversion and, as such, is promising for more sensitively detecting sleep disordered breathing (SDB) events compared to pulse oximetry. We hypothesized that ECM would detect hypoxia occurring with SDB events associated with drops in SpO2 but also would detect hypoxic challenge occurring with SDB events not associated with drops in SpO2 (hypopneas defined by a drop in nasal pressure occurring in conjunction with an arousal, respiratory-related arousals, and primary snoring). Primary snoring is of particular interest with respect to the potential of ECM because it is statistically associated with co-morbidities of SDB, such as hypertension, but is not considered pathological because of the lack of a proximal measure of pathology occurring with PSG. In this article we review ECM technology and methodology, present preliminary data indicating that it detects hypoxia occurring in the skin during SDB events that is not detected as blood desaturation by pulse oximetry, and make the case that it is a promising tool for identifying pathology occurring at the mild end of the SDB spectrum.

Methylation of the nuclear poly(A)-binding protein by type I protein arginine methyltransferases – how and why

2013 ◽  
Vol 394 (8) ◽  
pp. 1029-1043 ◽  
Author(s):  
Elmar Wahle ◽  
Bodo Moritz
Keyword(s):  
Active Sites ◽  
Binding Protein ◽  
Arginine Methylation ◽  
Fine Tuning ◽  
General Mechanism ◽  
Type I ◽  
Protein Arginine Methyltransferases ◽  
Low Protein ◽  
Backbone Conformation ◽  
Arginine Residues

Abstract Asymmetric dimethylation of arginine side chains in proteins is a frequent posttranslational modification, catalyzed by type I protein arginine methyltransferases (PRMTs). This article summarizes what is known about this modification in the nuclear poly(A)-binding protein (PABPN1). PABPN1 contains 13 dimethylated arginine residues in its C-terminal domain. Three enzymes, PRMT1, 3, and 6, can methylate PABPN1. Although 26 methyl groups are transferred to one PABPN1 molecule, the PRMTs do so in a distributive reaction, i.e., only a single methyl group is transferred per binding event. As PRMTs form dimers, with the active sites accessible from a small central cavity, backbone conformation around the methyl-accepting arginine is an important determinant of substrate specificity. Neither the association of PABPN1 with poly(A) nor its role in poly(A) tail synthesis is affected by arginine methylation. At least at low protein concentration, methylation does not affect the protein’s tendency to oligomerize. The dimethylarginine residues of PABPN1 are located in the binding site for its nuclear import receptor, transportin. Arginine methylation weakens this interaction about 10-fold. Very recent evidence suggests that arginine methylation as a way of fine-tuning the interactions between transportin and its cargo may be a general mechanism.

scholarly journals Pilot study of intracranial venous physiology in craniosynostosis

2018 ◽  
Vol 21 (6) ◽  
pp. 626-631 ◽  
Author(s):  
Martijn J. Cornelissen ◽  
Robbin de Goederen ◽  
Priya Doerga ◽  
Iris Cuperus ◽  
Marie-Lise van Veelen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pilot Study ◽  
Flow Velocity ◽  
Outpatient Clinic ◽  
Early Stage ◽  
Cerebral Vein ◽  
Type I ◽  
Venous Blood Flow ◽  
Flow Waveform ◽  
Obstructive Sleep

OBJECTIVEIn addition to craniocerebral disproportion, other factors, such as Chiari malformation type I, obstructive sleep apnea, and venous outflow obstruction, are considered to have a role in the occurrence of intracranial hypertension in craniosynostosis. This pilot study examined cerebral venous flow velocity to better characterize the complex intracranial venous physiology of craniosynostosis.METHODSThe authors performed a prospective cohort study of craniosynostosis patients (n = 34) referred to a single national (tertiary) craniofacial unit. Controls (n = 28) consisted of children who were referred to the unit’s outpatient clinic and did not have craniosynostosis. Transfontanelle ultrasound scans with venous Doppler flow velocity assessment were performed at the first outpatient clinic visit and after each surgery, if applicable. Mean venous blood flow velocities of the internal cerebral vein (ICVv) and the superior sagittal sinus (SSSv) were recorded and blood flow waveform was scored.RESULTSPreoperatively, SSSv was decreased in craniosynostosis patients compared with controls (7.57 vs 11.31 cm/sec, p = 0.009). ICVv did not differ significantly between patients and controls. Postoperatively, SSSv increased significantly (7.99 vs 10.66 cm/sec, p = 0.023). Blood flow waveform analyses did not differ significantly between patients and controls.CONCLUSIONSPremature closure of cranial sutures was associated with decreased SSSv but not ICVv; indicating an effect on the superficial rather than deep venous drainage. Further Doppler ultrasound studies are needed to test the hypothesis that at an early stage of craniosynostosis pathology SSSv, but not pulsatility, is abnormal, and that abnormality in both SSSv and the superficial venous waveform reflect a more advanced stage of evolution in suture closure.

Carotid Body Chemoreceptors: Physiology, Pathology, and Implications for Health and Disease

2021 ◽  
Author(s):  
Rodrigo Iturriaga ◽  
Julio Alcayaga ◽  
Mark W. Chapleau ◽  
Virend K Somers
Keyword(s):  
Carotid Body ◽  
Metabolic Diseases ◽  
Ionic Channels ◽  
Type I ◽  
Peripheral Chemoreceptor ◽  
Type I Cells ◽  
Obstructive Sleep ◽  
Carotid Body Chemoreceptors ◽  
Respiratory Gases ◽  
I Cells

The carotid body (CB) is the main peripheral chemoreceptor for arterial respiratory gases O2 and CO2, and pH, eliciting reflex ventilatory, cardiovascular and humoral responses to maintain homeostasis. This review examines the fundamental biology underlying CB chemoreceptor function, its contribution to integrated physiologic responses, and its role in maintaining health and potentiating disease. Emphasis will be placed on: i) Transduction mechanisms in chemoreceptor (type I) cells, highlighting the role played by the hypoxic inhibition of O2-dependent K+ channels and mitochondrial oxidative metabolism, and their modification by intracellular molecules and other ionic channels; ii) Synaptic mechanisms linking type I cells and petrosal nerve terminals, focusing on the role played by the main proposed transmitters and modulatory gases, and the participation of glial cells in regulation of the chemosensory process; iii) Integrated reflex responses to CB activation, emphasizing that the responses differ dramatically depending on the nature of the physiological, pathological or environmental challenges, and the interactions of the chemoreceptor reflex with other reflexes in optimizing oxygen delivery to the tissues; and iv) The contribution of enhanced CB chemosensory discharge to autonomic and cardiorespiratory pathophysiology in obstructive sleep apnea, congestive heart failure, resistant hypertension and metabolic diseases, and how modulation of enhanced CB reactivity in disease conditions may attenuate pathophysiology.

Successful Treatment of Experimental Neonatal Respiratory Failure Using Extracorporeal Membrane Lung Assist

1986 ◽  
Vol 9 (6) ◽  
pp. 427-432 ◽  
Author(s):  
R. Fumagalli ◽  
T. Kolobow ◽  
P. Arosio ◽  
V. Chen ◽  
D.K. Buckhold ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Pulmonary Ventilation ◽  
Blood Gases ◽  
Blood Gas ◽  
Arterial Blood Gases ◽  
Arterial Blood Gas ◽  
Membrane Lung ◽  
Arterial Blood ◽  
Long Term Survivors

A total of 44 preterm fetal lambs at great risk of developing respiratory failure were delivered by Cesarean section, and were then managed on conventional mechanical pulmonary ventilation. Fifteen animals initially fared well, and 14 of these were long term survivors. Twenty-nine other lambs showed a progressive deterioration in arterial blood gases within 30 minutes of delivery, of which 10 lambs were continued on mechanical pulmonary ventilation (20% survival), while the remaining 19 lambs were placed on an extracorporeal membrane lung respiratory assist (79% survival). Extracorporeal membrane lung bypass rapidly corrected arterial blood gas values, and permitted the use of high levels of CPAP instead of the continuation of mechanical pulmonary ventilation at high peak airway pressures. Improvement in lung function was gradual, and predictable. Early institution of extracorporeal respiratory assist using a membrane artificial lung rapidly corrected arterial blood gas values and significantly improved on neonate survival.

Hypoxic ventilatory response and arterial desaturation during heavy work

1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Ideal Gas ◽  
Respiratory Drive ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Arterial Desaturation ◽  
Exercise Ventilation ◽  
Arterial O2 Saturation

Arterial desaturation in athletes during intense exercise has been reported by several authors, yet the etiology of this phenomenon remains obscure. Inadequate pulmonary ventilation, due to a blunted respiratory drive, has been implicated as a factor. To investigate the relationship between the ventilatory response to hypoxia, exercise ventilation, and arterial desaturation, 12 healthy male subjects [age, 23.8 +/- 3.6 yr; height, 181.6 +/- 5.6 cm; weight, 73.7 +/- 6.2 kg; and maximal O2 uptake (VO2max), 63.0 +/- 2.2 ml.kg-1 min-1] performed a 5-min treadmill test at 100% of VO2max, during which arterial blood samples and ventilatory data were collected every 15 s. Alveolar PO2 (PAO2) was determined using the ideal gas equation. On a separate occasion the ventilatory response to isocapnic hypoxia was measured. Arterial PO2 decreased by an average of 29 Torr during the test, associated with arterial desaturation [arterial O2 saturation (SaO2) 92.0%]. PAO2 was maintained; however, alveolar-arterial gas pressure difference increased progressively to greater than 40 Torr. Minimal hypocapnia was observed, despite marked metabolic acidosis. There was no significant correlation observed between hypoxic drives and ventilation-to-O2 uptake ratio or SaO2 (r = 0.1 and 0.06, respectively, P = NS). These data support the conclusions that hypoxic drives are not related to maximal exercise ventilation or to the development of arterial desaturation during maximal exercise.

Acclimatization to high altitude in goats with ablated carotid bodies

1983 ◽  
Vol 55 (1) ◽  
pp. 16-21 ◽  
Author(s):  
R. A. Steinbrook ◽  
J. C. Donovan ◽  
R. A. Gabel ◽  
D. E. Leith ◽  
V. Fencl
Keyword(s):  
High Altitude ◽  
Pulmonary Ventilation ◽  
Base Deficit ◽  
Co2 Production ◽  
Regulation Of Respiration ◽  
Response Curves ◽  
Co2 Response ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Simulated High Altitude

In awake goats with ablated carotid bodies, we studied resting pulmonary ventilation, CO2 production, composition of arterial blood and cerebrospinal fluid (CSF), and ventilatory responsiveness to hyperoxic CO2 rebreathing at sea level (SL) and after 3 days at simulated high altitude (HA) (PB 446 +/- 5 Torr, equivalent to 4,300 m). At HA, resting pulmonary ventilation was increased, resulting in marked hypocapnia with appropriate base deficit in blood plasma; CSF became more alkaline; CO2-response curves were shifted to lower PCO2 levels, and their slopes were steeper than at SL. Although these changes in regulation of respiration were not demonstrably different from those seen after normal acclimatization to HA with carotid bodies intact, the mechanisms of their initiation and development are probably different.

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