Respiratory Center Research Articles

Clinical characteristics of adult asthma patients hospitalized by COVID-19 in Mexico City: a real-world study

Background The COVID-19 pandemic raised concerns about whether individuals with chronic respiratory diseases, such as asthma, were at higher risk of severe outcomes. Although several studies were published on this topic, not all included asthma as a risk factor. Therefore, describing the clinical characteristics of COVID-19-infected asthma patients in a specialized respiratory center is valuable as a real-life study. Objective To investigate the clinical characteristics and disease severity in SARS-CoV-2-infected adults with pre-existing asthma hospitalized at the National Institute of Respiratory Diseases (INER) in Mexico City. Methods We conducted a retrospective, observational study on adults with confirmed COVID-19 hospitalized from March 2020 to June 2021. Out of 2,249 reviewed medical records, we identified asthmatic patients and compared them with a matched non-asthmatic control group to assess asthma’s impact on COVID-19 severity and outcomes. Results Based on the clinical records, asthma prevalence among hospitalized patients was low (1.51%); of these, 73% had allergic and 27% had non-allergic asthma. COVID-19 severity did not vary significantly between asthma phenotypes, although there was higher mortality among patients with non-allergic asthma. Most patients in both groups developed a severe form of the disease and higher mortality rates than non-asthmatics, though the differences were not statistically significant. Conclusion Asthma prevalence among patients with COVID-19 was low, but mortality was higher in asthma patients. Although the small sample size limits the generalizability of these findings, this study in a Mexican population hospitalized in a reference hospital provides insights for improving asthma management in future pandemics.

Clinical and neurological manifestations of COVID-19 and other coronavirus infections: A literature review

As is known, the issues of pathogenesis, diagnosis and treatment of the new coronavirus infection COVID-19 are the most priority areas of scientific research in the modern clinic of internal diseases. The rate of emergence of new scientific data in the leading libraries PubMed, Medline, Cochrane Library and eLibrary, which can potentially be important in the correction of ongoing therapy for infection and its complications, is extremely high. In turn, this dictates the need for a comprehensive discussion of the results of newly published studies. These issues include clinical and neurological manifestations of COVID-19 and other coronavirus infections. The exact mechanism by which the SARS-CoV-2 virus enters the structures of the central nervous system is unknown. Thus, two pathways for the penetration of the COVID-19 pathogen are most actively discussed: the hematogenous pathway (through the systemic circulation into the vessels of the brain with a low linear blood flow velocity, which allows the virus to adhere to the surface of the endothelium and penetrate into the nervous tissue through damage to the latter) and the contact pathway (through the cribriform plate and the olfactory bulb). It should also be noted that a number of experimental works clearly demonstrate the pathogenic effect of other members of the Coronaviridae family on the neurons of the respiratory and vasomotor centers. The review presents an analysis of current literature data on the study of clinical and neurological manifestations of COVID-19 and other coronavirus infections. It is important to emphasize that patients with a severe course of COVID-19 deserve special attention, requiring observation in the intensive care unit in order to prevent the development of fatal neurological complications.

Diaphragm relaxation causes seizure-related apnoeas in chronic and acute seizure models in rats

Ictal central apnoea is a feature of focal temporal seizures. It is implicated as a risk factor for sudden unexpected death in epilepsy (SUDEP). Here we study seizure-related apnoeas in two different models of experimental seizures, one chronic and one acute, in adult genetically-unmodified rats, to determine mechanisms of seizure-related apnoeas. Under general anaesthesia rats receive sensors for nasal temperature, hippocampal and/or neocortical potentials, and ECG or EMG for subsequent tethered video-telemetry. Tetanus neurotoxin (TeNT), injected into hippocampus during surgery, induces a chronic epileptic focus. Other implanted rats receive intraperitoneal pentylenetetrazol (PTZ) to evoke acute seizures. In chronically epileptic rats, convulsive seizures cause apnoeas (9.9 ± 5.3 s; 331 of 730 convulsive seizures in 15 rats), associated with bradyarrhythmias. Absence of EEG and ECG biomarkers exclude obstructive apnoeas. All eight TeNT-rats with diaphragm EMG have apnoeas with no evidence of obstruction, and have apnoea EMGs significantly closer to expiratory relaxation than inspiratory contraction during pre-apnoeic respiration, which we term “atonic diaphragm”. Consistent with atonic diaphragm is that the pre-apnoeic nasal airflow is expiration, as it is in human ictal central apnoea. Two cases of rat sudden death occur. One, with telemetry to the end, reveals a lethal apnoea, the other only has video during the final days, which reveals cessation of breathing shortly after the last clonic epileptic movement. Telemetry following acute systemic PTZ reveals repeated seizures and seizure-related apnoeas, culminating in lethal apnoeas; ictal apnoeas are central – in 8 of 35 cases diaphragms initially contract tonically for 8.5 ± 15.0 s before relaxing, in the 27 remaining cases diaphragms are atonic throughout apnoeas. All terminal apnoeas are atonic. Differences in types of apnoea due to systemic PTZ in rats (mainly atonic) and mice (tonic) are likely species-specific. Certain genetic mouse models have apnoeas caused by tonic contraction, potentially due to expression of epileptogenic mutations throughout the brain, including in respiratory centres, in contrast with acquired focal epilepsies. We conclude that ictal apnoeas in the rat TeNT model result from atonic diaphragms. Relaxed diaphragms could be particularly helpful for therapeutic stimulation of the diaphragm to help restore respiration.

Adherence to long-term non-invasive positive airway pressure therapy.

Studies have shown varying patient adherence to long-term non-invasive positive airway pressure therapy (nPAP). We aimed to investigate adherence to long-term nPAP in a Danish cohort of patients with chronic respiratory insufficiency and/or sleep-disordered breathing (SDB) due to neuromuscular disorders (NMD), obesity-hypoventilation syndrome (OHS) or other reasons. This cohort study included all adult patients with association to the Respiratory Center East treated with long-term nPAP: bilevel (BiPAP), automatic (APAP) and continuous (CPAP) or adaptive servo-ventilation (ASV) with a remote monitoring system in April 2022. The primary outcome was adherence, defined as a median use of nPAP ≥ 4 hrs/day in April 2022. A preplanned extended subgroup analysis was conducted for patients with data on adherence from initiation and six months onwards. The primary analysis included 241 patients, of whom 90% were diagnosed with NMD (54%) or OHS (36%). The nPAP was used ≥ 4 hrs/day by 175 patients (73%), including 22 (100%) with ASV, 129 (72%) with BiPAP and 24 (59%) with APAP/CPAP. Treatment adherence was seen in 75% of patients with NMD, 64% with OHS and 84% with other reasons for SDB. The proportion of adherent subjects in the subgroup analysis of 55 patients was relatively stable throughout the six-month period, ranging from 67% to 75% with slight intraindividual variation. In this retrospective analysis of adults primarily with NMD and OHS, 73% used the prescribed nPAP therapy ≥ 4 hrs/day. None TRIAL REGISTRATION. gov(NCT05379309).

Higher protein intake may benefit in patients with prolonged mechanical ventilation.

Patients with prolonged mechanical ventilation (PMV) is usually associated with muscle wasting and diaphragm weakness, resulting in high medical costs and mortality. Adequate energy and protein intake were beneficial in sarcopenia patients. We aimed to investigate the impact of protein intake in weaning parameters in patients with PMV. We enrolled patients with PMV (mechanical ventilation ≥6 h/day for ≥21 days) from a respiratory care center (RCC) of a tertiary medical center from December 2020 to October 2022, and classified them into weaning success and weaning failure groups. The patients' characteristics, nutrition records, weaning parameters and outcomes were analyzed. A total of 289 patients were included (mean age 73.5 years). Of the 289 patients, 149 were weaned successfully and 140 were not. The average protein intake was higher in the weaning success group than in the weaning failure group (1.22 ± 0.320 versus 0.99 ± 0.332 g/kg/day, p < 0.001). No significant differences were noted in the average calorie intake and whey protein intake between the two groups. RSBI <90 breaths/min/L (OR = 2.38, p = 0.045), serum albumin at 4th week ≥3 g/dL (OR = 2.89, p = 0.027), daily protein intake ≥1.01 g/kg/day (OR = 8.10, p < 0.001), PaO2/FiO2 (PF) ratio ≥ 300 (OR = 2.56, p = 0.027) were independent predictors for weaning from ventilator. Weak positive correlations were found between average protein intake with PF ratio (r = 0.1576, p = 0.0227) and PaO2 (r = 0.13359, p = 0.0497). Daily protein intake had positively correlated with PF ratio and had independently benefit for weaning in patients with PMV.

Brainstem opioid peptidergic neurons regulate cough reflexes in mice

Cough is a vital defensive reflex for expelling harmful substances from the airway. The sensory afferents for the cough reflex have been intensively studied. However, the brain mechanisms underlying the cough reflex remain poorly understood. Here, we developed a paradigm to quantitatively measure cough-like reflexes in mice. Using this paradigm, we found that prodynorphin-expressing (Pdyn+) neurons in the nucleus of the solitary tract (NTS) are critical for capsaicin-induced cough-like reflexes. These neurons receive cough-related neural signals from Trpv1+ vagal sensory neurons. The activation of Pdyn+ NTS neurons triggered respiratory responses resembling cough-like reflexes. Among the divergent projections of Pdyn+ NTS neurons, a glutamatergic pathway projecting to the caudal ventral respiratory group (cVRG), the canonical cough center, was necessary and sufficient for capsaicin-induced cough-like reflexes. These results reveal that Pdyn+ NTS neurons, as a key neuronal population at the entry point of the vagus nerve to the brainstem, initiate cough-like reflexes in mice.

Prevalence and Clinico-sociodemographic Factors of Asthmatic Children Aged 1 to 14 Years: A Prospective Descriptive Cross-sectional Study in Gandaki Province, Nepal

Introduction Pediatric asthma poses a significant public health challenge, impacting children’s health and quality of life. As asthma prevalence continues to rise globally, understanding its epidemiology is crucial for developing effective management strategies. This study aims to investigate the prevalence and associated demographic, socioeconomic, and clinical characteristics of pediatric asthma among children aged 1 to 14 years. Methods This study employed a prospective descriptive cross-sectional design. Data were collected from a diagnosed asthmatic children attending pediatric department of the GP Koirala National Respiratory Centre and Hospital, Tanahun, Ganaki, Nepal over three months from April 20, 2023 by assessing demographic factors (age, gender, residence), socioeconomic status, clinical history (family history and comorbid conditions), and asthma severity. Data were analyzed with SPSS version 23 using descriptive statistics. Results Prevalence rate of pediatric asthma was 3.08%. The demographic analysis revealed that most participants were aged 1-5 years (53%), predominantly male (64.9%), and resided in urban areas (59.6%). Socioeconomic data indicated that 59.6% came from low-income households, suggesting a potential link between socioeconomic status and asthma prevalence. Clinically, 53% had a family history of asthma, with 26.3% presenting with comorbid allergic rhinitis. Asthma severity assessments showed that 50% had mild asthma, 33.33% had moderate asthma, and 16.67% had severe asthma. Conclusion This study highlights a low prevalence of asthma in the pediatric population at GP Koirala National Respiratory Centre and Hospital, yet emphasizes the burden faced by younger children, especially those from low-income backgrounds. The correlations between asthma prevalence, socioeconomic status, and comorbid conditions underscore the need for targeted public health interventions and comprehensive management strategies. Further research is warranted to deepen understanding and enhance healthcare services for affected children.

Bronchoscopic Interventional Treatment of Mixed Squamous Cell and Glandular Papilloma of Diffuse Trachea: A Case Report and Literature Review

Pulmonary mixed squamous cell and glandular papilloma (MSCGP) is a subtype of pulmonary papilloma, which can be classified as central type and peripheral type based on its site of development. The central type is the most common. The clinical manifestations of pulmonary MSCGP are mainly related to the location of the tumor. Surgery is the main treatment for this disease. Bronchoscopic interventional treatment for the MSCGP in the central trachea could receive satisfactory effect. We reported a patient suffered from diffuse tracheal MSCGP who was treated by bronchoscopic interventional treatment in Respiratory Disease Center, Dongzhimen Hospital of Beijing University of Chinese Medicine, aiming to enhance the recognition of the clinical features and provide clinical references for the diagnosis and treatment of such disease. .

Identification of a histone deacetylase inhibitor as a therapeutic candidate for congenital central hypoventilation syndrome

Congenital central hypoventilation syndrome (CCHS), a rare genetic disease caused by heterozygous PHOX2B mutations, ischaracterized by life-threatening breathing deficiencies. PHOX2B is a transcription factor required for the specification of the autonomic nervous system, which contains, in particular, brainstem respiratory centers. In CCHS, PHOX2B mutations lead to cytoplasmic PHOX2B protein aggregations, thus compromising its transcriptional capability. Currently, the only available treatment for CCHS is assisted mechanical ventilation. Therefore, identifying molecules with alleviating effects on CCHS-related breathing impairments is of primary importance. A transcriptomic analysis of cells transfected with different PHOX2B constructs was used to identify compounds of interest with the CMap tool. Using fluorescence microscopy and luciferase assay, the selected molecules were further tested invitro for their ability to restore the nuclear location and function of PHOX2B. Finally, an electrophysiological approach was used to investigate exvivo the effects ofthe most promising molecule on respiratory activities of PHOX2B-mutant mouse isolated brainstem. The histone deacetylase inhibitor SAHA was found to have low toxicity invitro, to restore the proper location and function of PHOX2B protein, and to improve respiratory rhythm-relatedparameters exvivo. Thus, our results identify SAHA as a promising agent to treat CCHS-associated breathing deficiencies.

Impact Of Inhalational Anesthetics On Respiratory System

Inhalational anaesthetics, commonly used in general anaesthesia, profoundly impact respiratory function and lung mechanics. These agents depress the central nervous system, including the respiratory centres in the brainstem, leading to reduced breathing rate and depth. This suppression results in diminished tidal volume, reduced inspiratory and expiratory reserve volumes, and potentially decreased functional residual capacity. The central nervous system depression also weakens airway reflexes such as coughing, gagging, and swallowing, increasing the risk of airway obstruction and aspiration. Additionally, inhalational anaesthetics can impair gas exchange, causing lower oxygen levels (hypoxemia) and elevated carbon dioxide levels (hypercapnia). Respiratory complications during surgery may include hypoxia, bronchospasm, and impaired ventilation, especially in patients with pre-existing respiratory conditions. To manage these risks, continuous monitoring of respiratory parameters, preoperative assessment, and effective airway management are crucial. This paper reviews the effects of inhalational anaesthetics on respiratory function and outlines strategies for minimising associated risks during surgical procedures

Correlation of sputum inflammatory markers with severity and blood inflammatory markers in bronchiectasis.

As a disease characterized by chronic neutrophilic inflammation, various sputum biomarkers have been investigated in the association with the severity and prognosis of bronchiectasis. However, there is lack of data on the association between sputum interleukin-1beta (IL-1β), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) levels at clinical stable state and the clinical, spirometric and blood inflammatory parameters, as well as prognostic scores. The purpose of the study is to assess the association between sputum IL-1β, IL-8 and TNF-α levels at clinical stable state and various clinical and laboratory parameters in bronchiectasis. A prospective study was conducted in a major regional hospital and tertiary respiratory referral centre in Hong Kong, including 44 Chinese patients with bronchiectasis. The correlation between stable state sputum IL-1β, IL-8 and TNF-α levels with various clinical, laboratory and spirometric parameters in bronchiectasis, as well as FACED [forced expiratory volume in one second (FEV1), age, chronic colonisation by Pseudomonas aeruginosa, radiological extension and dyspnoea]/E-FACED (FACED plus exacerbations) scores were assessed. Baseline sputum IL-1β level was found to have significant moderate positive correlation with baseline blood high sensitivity C-reactive protein (hs-CRP) level with Pearson correlation coefficient (r) of 0.529 (P=0.001). Baseline sputum IL-8 level was found to have significant moderate positive correlation with baseline FACED and E-FACED score with r of 0.574 (P<0.001) and 0.539 (P<0.001) respectively. Baseline sputum TNF-α level was found to have significant moderate positive correlation with baseline FACED score with r of 0.520 (P<0.001). Sputum IL-1β and, IL-8 and TNF-α levels were shown to have significant correlation with various clinical, laboratory and spirometry parameters in bronchiectasis, as well as more severe disease as measured by FACED and E-FACED scores.

Role of the pontine respiratory group in the suppression of cough by codeine in cats

Codeine was microinjected into the area of the Kölliker-Fuse nucleus and the adjacent lateral parabrachial nucleus, within the pontine respiratory group in 8 anesthetized cats. Electromyograms (EMGs) of the diaphragm (DIA) and abdominal muscles (ABD), esophageal pressures (EP), and blood pressure were recorded and analyzed during mechanically induced tracheobronchial cough. Unilateral microinjections of 3.3 mM codeine (3 injections, each 37 ± 1.2 nl) had no significant effect on the cough number. However, the amplitudes of the cough ABD EMG, expiratory EP and, to a lesser extent, DIA EMG were significantly reduced. There were no significant changes in the temporal parameters of the cough. Control microinjections of artificial cerebrospinal fluid in 6 cats did not show a significant effect on cough data compared to those after codeine microinjections. Codeine-sensitive neurons in the rostral dorsolateral pons contribute to controlling cough motor output, likely through the central pattern generator of cough.

Severe bronchiectasis is associated with increased carotid intima-media thickness

BackgroundAlthough bronchiectasis has been shown to be associated with cardiovascular disease, there is limited evidence of an association with subclinical atherosclerosis, especially carotid intima-media thickness (CIMT).MethodsThis prospective study compared CIMT among patients with and without bronchiectasis, and among bronchiectatic patients classified according to disease severity using the FACED score. The study was carried out at a major regional hospital and tertiary respiratory referral centre in Hong Kong.ResultsTotal 155 Chinese patients with non-cystic fibrosis (CF) bronchiectasis and 512 controls were recruited. The mean CIMT was 0.58 ± 0.10 mm, 0.63 ± 0.11 mm and 0.66 ± 0.08 mm respectively among controls, patients with mild-to-moderate bronchiectasis and patients with severe bronchiectasis. There was no statistically significant difference in CIMT between patients with mild-to-moderate bronchiectasis and controls. Multivariate linear regression revealed that CIMT was significantly increased in patients with severe bronchiectasis relative to controls. The same phenomenon was observed among patients without a history of cardiovascular disease or cardiovascular risk factors.ConclusionsCIMT was significantly increased in patients with severe bronchiectasis compared with controls without bronchiectasis, but not among patients with mild-to-moderate bronchiectasis, which suggested the subclinical atherosclerosis to be more prevalent among patients with severe bronchiectasis.

Amygdalar involvement in respiratory dysfunction.

The brainstem has long been recognized as the major respiratory control center, but it has become increasingly appreciated that areas upstream of the brainstem modulate respiration and airway defensive behaviors. This review aims to define the role of the amygdala, a key temporal brain region essential for limbic function, in respiration and airway defenses. We summarize literature describing roles for the amygdala in control of respiration, swallow, cough, airway smooth muscle contraction, and mucus secretion. We emphasize the need to understand how the amygdala regulates these functions both at a local scale and network scale and identify knowledge gaps for current and future investigations. Lastly, we highlight literature suggesting that amygdala dysfunction may contribute to respiratory dysfunction.

Respiratory pathology in the TDP-43 transgenic mouse model of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that results in death within 2-5years of diagnosis. Respiratory failure is the most common cause of death in ALS. Mutations in the transactive response DNA binding protein 43 (TDP-43) encoded by the TARDBP gene are associated with abnormal cellular aggregates in neurons of patients with both familial and sporadic ALS. The role of these abnormal aggregates on breathing is unclear. Since respiratory failure is a major cause of death in ALS, we sought to determine the role of TDP-43 mutations on the respiratory motor unit in the Prp-hTDP-43A315T mouse model - a model that expresses human TDP-43 containing the A315T mutation. We assessed breathing using whole-body plethysmography, and investigated neuropathology in hypoglossal and phrenic respiratory motor units. Postmortem studies included quantification of hypoglossal and putative phrenic motor neurons, activated microglia and astrocytes in respiratory control centers, and assessment of hypoglossal and phrenic nerves of TDP43A315T mice. The male TDP43A315T mice display an early onset of rapid progression of disease, and premature death (less than 15weeks) compared to control mice and compared to female TDP43A315T mice who die between 20 and 35weeks of age. The TDP43A315T mice have progressive and profound breathing deficits at baseline and during a respiratory challenge. Histologically, hypoglossal and putative phrenic motor neurons of TDP43A315T mice are decreased and have increased microglial and astrocyte activation, indicating pronounced neurodegeneration and neuroinflammation. Further, there is axonopathy and demyelination in the hypoglossal and phrenic nerve of TDP43A315T mice. Thus, the TDP-43A315T mice have significant respiratory pathology and neuropathology, which makes them a useful translatable model for the study of novel therapies on breathing in ALS.

Imitating the respiratory activity of the brain stem by using artificial neural networks: exploratory study on an animal model of lactic acidosis and proof of concept

Artificial neural networks (ANNs) are versatile tools capable of learning without prior knowledge. This study aims to evaluate whether ANN can calculate minute volume during spontaneous breathing after being trained using data from an animal model of metabolic acidosis. Data was collected from ten anesthetized, spontaneously breathing pigs divided randomly into two groups, one without dead space and the other with dead space at the beginning of the experiment. Each group underwent two equal sequences of pH lowering with pre-defined targets by continuous infusion of lactic acid. The inputs to ANNs were pH, ΔPaCO2 (variation of the arterial partial pressure of CO2), PaO2, and blood temperature which were sampled from the animal model. The output was the delta minute volume (ΔVM), (the change of minute volume as compared to the minute volume the animal had at the beginning of the experiment). The ANN performance was analyzed using mean squared error (MSE), linear regression, and the Bland-Altman (B-A) method. The animal experiment provided the necessary data to train the ANN. The best architecture of ANN had 17 intermediate neurons; the best performance of the finally trained ANN had a linear regression with R2 of 0.99, an MSE of 0.001 [L/min], a B-A analysis with bias ± standard deviation of 0.006 ± 0.039 [L/min]. ANNs can accurately estimate ΔVM using the same information that arrives at the respiratory centers. This performance makes them a promising component for the future development of closed-loop artificial ventilators.

A Neural Basis for Mutant ATAXIN-1 Induced Respiratory Dysfunction in Mouse Models of Spinocerebellar Ataxia Type 1.

Spinocerebellar ataxia type 1 (SCA1), a dominantly inherited neurodegenerative disorder caused by an expanded trinucleotide repeat in the ATAXIN-1 (ATXN1) gene, is characterized by motor dysfunction, cognitive impairment, and death from compromised swallowing and respiration. To delineate specific cell types that contribute to respiratory dysfunction, we utilized the floxed conditional knock-in f-ATXN1 146Q/2Q mouse. Whole body plethysmography during spontaneous respiration and respiratory challenge showed that f-ATXN1 146Q/2Q mice exhibit a spontaneous respiratory phenotype characterized by elevated respiratory frequency, volumes, and respiratory output. Consequently, the ability of f-ATXN1 146Q/2Q mice to increase ventilation during the challenge is impaired. To investigate the role of mutant ATXN1 expression in neural and skeletal muscle lineages, f-ATXN1 146Q/2Q mice were bred to Nestin-Cre and Acta1-Cre mice respectively. These analyses revealed that the abnormal spontaneous respiration in f-ATXN1 146Q/2Q mice involved two aspects: a behavioral phenotype in which SCA1 mice exhibit increased motor activity during respiratory testing and functional dysregulation of central respiratory control centers. Both aspects of spontaneous respiration were partially ameliorated by removing mutant ATXN1 from neural, but not skeletal muscle, cell lineages.

Central and peripheral mechanisms underlying respiratory deficits in a mouse model of accelerated senescence.

Aging invariably decreases sensory and motor stimuli and affects several neuronal systems and their connectivity to key brain regions, including those involved in breathing. Nevertheless, further investigation is needed to fully comprehend the link between senescence and respiratory function. Here, we investigate whether a mouse model of accelerated senescence could develop central and peripheral respiratory abnormalities. Adult male Senescence Accelerated Mouse Prone 8 (SAMP8) and the control SAMR1 mice (10months old) were used. Ventilatory parameters were assessed by whole-body plethysmography, and measurements of respiratory input impedance were performed. SAMP8 mice exhibited a reduction in the density of neurokinin-1 receptor immunoreactivity in the entire ventral respiratory column. Physiological experiments showed that SAMP8 mice exhibited a decreased tachypneic response to hypoxia (FiO2 = 0.08; 10min) or hypercapnia (FiCO2 = 0.07; 10min). Additionally, the ventilatory response to hypercapnia increased further due to higher tidal volume. Measurements of respiratory mechanics in SAMP8 mice showed decreased static compliance (Cstat), inspiratory capacity (IC), resistance (Rn), and elastance (H) at different ages (3, 6, and 10months old). SAMP8 mice also have a decrease in contractile response to methacholine compared to SAMR1. In conclusion, our findings indicate that SAMP8 mice display a loss of the NK1-expressing neurons in the respiratory brainstem centers, along with impairments in both central and peripheral respiratory mechanisms. These observations suggest a potential impact on breathing in a senescence animal model.

Central Neurogenic Hyperventilation Following Ischemic Stroke in the Pons

Central neurogenic hyperventilation (CNH) is a rare condition that characterized by an increase in the rate and depth of respiration to an extent that produces advanced respiratory alkalosis due to various central nervous disorder. The mechanism of CNH remains unclear. We reported a case of CNH in patients with progressive ischemic stroke in pons, including parabrachial nucleus, which is thought to have disrupted inhibitory impulses to the medullary respiratory center.

Proportions of Hypertension in Stable COPD Patients at the National Respiratory Center Persahabatan Hospital

Background: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. Most of these deaths are related to cardiovascular disease. This is due to systemic inflammation that causes increased vascular stiffness and hypertension. These comorbidities lead to poor quality of life, low exercise tolerance, and an increased risk of hospitalization. This study aims to report the proportion of hypertension among stable COPD patients in the Indonesian population.Methods: This cross-sectional study was conducted at the National Respiratory Center Persahabatan Hospital between February and March 2023. Stable COPD patients admitted to the Asthma and COPD Polyclinic who met the criteria were enrolled. Clinical information, vital signs, spirometry results, and DLCO measurements were collected.Results: There were 84 subjects participating in this study. The result of this study shows a 60.7% proportion of hypertension in stable COPD patients. Hypertension has a significant correlation with pulmonary functional values (P=0.021), severity degree of clinical COPD (P=0.004), Brinkman index (P=0.008), and age (P=0.0001). However, hypertension association with COPD duration (P=0.505) and DLCO (P=0.122) were not significant.Conclusion: The hypertension proportion in stable COPD Indonesian patients is 60.7%. Hypertension shows a significant association with pulmonary function values, severity degree of clinical COPD, Brinkman index, and age.