ventilation response
Recently Published Documents


TOTAL DOCUMENTS

39
(FIVE YEARS 6)

H-INDEX

9
(FIVE YEARS 0)

2021 ◽  
Vol 29 (3) ◽  
pp. 36-40
Author(s):  
E. O. Asanov ◽  
Yu. I. Golubova ◽  
I. A. Dyba ◽  
S. O. Asanova

FEATURES OF RESISTANCE TO HYPOXIA IN ELDERLY PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE E. O. Asanov, Yu. I. Golubova, I. A. Dyba, S. O. Asanova Abstract Aim: to study the features of resistance to hypoxia in elderly patients with COPD. Material and methods. We examined 46 elderly patients with COPD and 18 apparently healthy elderly people. Hypoxia resistance was determined by performing a hypoxic test with inhalation of 12 % O2 for 20 minutes. The state of ventilation and blood saturation were assessed. Results. Hypoxia caused the reduction of SpO2 and the development of arterial hypoxemia in elderly patients with COPD, which were more significant than in healthy elderly people. It was found that among elderly patients with COPD and healthy elderly subjects there were people with preserved and reduced resistance to hypoxia. However, reduced resistance to hypoxia was much more common in elderly patients with COPD. Decreased resistance to hypoxia in elderly patients with COPD was associated with the degree of bronchial obstruction: deterioration of bronchial passability led to reduced resistance to hypoxia. Elderly patients with COPD with reduced resistance to hypoxia had a decrease in the ΔVE/ ΔSpO2 ratio and a slow ventilation response to hypoxic exposure. Conclusions. Among healthy elderly people and elderly patients with COPD there were subjects with reduced and preserved resistance to hypoxia. Decreased resistance to hypoxia was much more common in elderly patients with COPD. Decreased resistance to hypoxia was more common in patients with moderate than mild bronchial obstruction. Elderly patients with COPD with reduced resistance to hypoxia had reduced ventilation response to hypoxia and chemoreflex sensitivity. Key words: COPD, older age, resistance to hypoxia, ventilation, saturation. Ukr. Pulmonol. J. 2021;29(3):36–40:


2020 ◽  
Vol 124 (6) ◽  
pp. e224-e225
Author(s):  
Jakob Wittenstein ◽  
Martin Scharffenberg ◽  
Anja Braune ◽  
Robert Huhle ◽  
Thomas Bluth ◽  
...  

Author(s):  
A.A. Klinnikova ◽  
G.A. Danilova ◽  
N.P. Aleksandrova

The purpose of the study is to identify the role of nitrergic mechanisms in the ability of the pro-inflammatory cytokine IL-1β to influence the respiration pattern and hypoxic ventilation response. Materials and Methods. The experiments were performed on 42 anesthetized rats. To conduct an inhibitory analysis of the nitric oxide role in the manifestation of IL-1β respiratory effects, the authors used a non-selective inhibitor of NO-synthases of Nitro-L-arginine-methyl ether (L-NAME), and a highly specific inhibitor of inducible nitric oxide synthase, aminoguanidine bicarbonate. The hypoxic ventilation response was evaluated by a rebreathing method with a hypoxic gas mixture before and after intravenous administration of human recombinant IL-1β. Pneumatic tachometry was used to register the parameters of external respiration. Results. Intravenous administration of IL-1β has an activating effect on respiration and causes an increase in tidal volume by 36±5.2 %, minute respiration volume by 23±3.8 % and average inspiratory flow rate by 20±3.0 %. However, an increase in IL-1β systemic level decreases the ventilation response to hypoxia. Inhibition of NO-synthase activity with both L-NAME and aminoguanidine reduces IL-1β respiratory effects. Conclusion. One of the mechanisms to implement the respiratory effects of the key pro-inflammatory cytokine IL-1β in case of increase in its circulating level is an increase in the synthesis of nitric oxide with vascular endothelium cells. Keywords: cytokines, interleukin-1β, ventilation, ventilation response to hypoxia, hypoxic chemoreflex, nitric oxide. Цель исследования. Выявление роли нитрергических механизмов в способности провоспалительного цитокина ИЛ-1β оказывать влияние на паттерн дыхания и гипоксический вентиляционный ответ. Материалы и методы. Эксперименты выполнены на 42 наркотизированных крысах. Для проведения ингибиторного анализа роли оксида азота в проявлении респираторных эффектов ИЛ-1β использовались неселективный ингибитор NO-синтаз L-нитро-аргинин-метилэфира (L-NAME), а также высокоспецифичный ингибитор индуцибельной синтазы оксида азота аминогуанидина бикарбоната. Гипоксический вентиляционный ответ оценивался методом возвратного дыхания гипоксической газовой смесью до и после внутривенного введения человеческого рекомбинантного ИЛ-1β. Для регистрации параметров внешнего дыхания использовался метод пневмотахометрии. Результаты. Показано, что внутривенное введение ИЛ-1β оказывает активирующее влияние на дыхание, вызывая увеличение дыхательного объема на 36,0±5,2 %, минутного объема дыхания – на 23,0±3,8 % и средней скорости инспираторного потока – на 20,0±3,0 %. Вместе с тем повышение системного уровня ИЛ-1β вызывает ослабление вентиляционного ответа на гипоксию. Ингибирование NO-синтазной активности с помощью как L-NAME, так и аминогуанидина ослабляет респираторные эффекты ИЛ-1β. Выводы. Одним из механизмов реализации респираторных эффектов ключевого провоспалительного цитокина ИЛ-1β при повышении его циркулирующего уровня является усиление синтеза оксида азота клетками сосудистого эндотелия. Ключевые слова: цитокины, интерлейкин-1β, вентиляция, вентиляционный ответ на гипоксию, гипоксический хеморефлекс, оксид азота.


2018 ◽  
Vol 86 (5) ◽  
pp. 240-244 ◽  
Author(s):  
Aysun Isiklar ◽  
Sibel Ocak Serin ◽  
Antonio M. Esquinas

2016 ◽  
Vol 310 (8) ◽  
pp. R766-R775 ◽  
Author(s):  
Tushar S. Sirsat ◽  
Edward M. Dzialowski

Precocial birds begin embryonic life with an ectothermic metabolic phenotype and rapidly develop an endothermic phenotype after hatching. Switching to a high-energy, endothermic phenotype requires high-functioning respiratory and cardiovascular systems to deliver sufficient environmental oxygen to the tissues. We measured tidal volume (VT), breathing frequency (ƒ), minute ventilation (V̇e), and whole-animal oxygen consumption (V̇o2) in response to gradual cooling from 37.5°C (externally pipped paranates, EP) or 35°C (hatchlings) to 20°C along with response to hypercapnia during developmental transition from an ectothermic, EP paranate to endothermic hatchling. To examine potential eggshell constraints on EP ventilation, we repeated these experiments in artificially hatched early and late EP paranates. Hatchlings and artificially hatched late EP paranates were able to increase V̇o2 significantly in response to cooling. EP paranates had high ƒ that decreased with cooling, coupled with an unchanging low VT and did not respond to hypercapnia. Hatchlings had significantly lower ƒ and higher VT and V̇e that increased with cooling and hypercapnia. In response to artificial hatching, all ventilation values quickly reached those of hatchlings and responded to hypercapnia. The timing of artificial hatching influenced the temperature response, with only artificially hatched late EP animals, exhibiting the hatchling ventilation response to cooling. We suggest one potential constraint on ventilatory responses of EP paranates is the rigid eggshell, limiting air sac expansion during inhalation and constraining VT. Upon natural or artificial hatching, the VT limitation is removed and the animal is able to increase VT, V̇e, and thus V̇o2, and exhibit an endothermic phenotype.


2016 ◽  
Vol 55 (02) ◽  
pp. 200-201 ◽  
Author(s):  
S. Fletcher ◽  
A. Esquinas ◽  
G. Glover

SummaryPredicting the outcome from NIV is important and the study by Martin-Gonzalez and colleagues applies data mining techniques to improve our understanding of the field. Nevertheless, the predictor variables must be robust and reliably available before NIV is applied. A predictive model must be generalisable in other clinical settings. Until models such as this are extremely robust in their predictive ability and have been shown to positively influence patient centered outcomes, they may be able to assist decision making but cannot replace clinical judgement by an experienced bedside clinician.


Sign in / Sign up

Export Citation Format

Share Document