This case report outlines the treatment of an 11-year-old female who underwent adenotonsillectomy six years ago for snoring but experienced postoperative inefficacy. Her symptoms worsened two weeks before readmission, with increased snoring and sleep apnea, disabling her from lying down to sleep. She was readmitted on December 1, 2023, and diagnosed with severe obstructive sleep apnea hypopnea syndrome and hypercapnia. Automatic BiPAP alleviated her symptoms, with sleep breathing parameters normalizing during treatment. Follow-up at one month showed significant acceleration in her growth and resolution of her hypersomnolence issue.
Humans ; Female ; Child ; Hypercapnia/complications* ; Sleep Apnea, Obstructive/complications* ; Positive-Pressure Respiration ; Noninvasive Ventilation

BACKGROUNDVery recent studies revealed that obstructive sleep apnoea (OSA) is a contributor of the increased incidence and mortality of cancer in humans, but mechanisms of how OSA promotes tumorigenesis remains largely unknown. We investigated whether intermittent hypoxia with and without hypercapnia plays a role in tumorigenesis.

METHODSFirst, Sprague-Dawley (SD) male rats (12 weeks old) were subjected to different hypoxia exposures: intermittent hypoxia and intermittent hypoxia with hypercapnia; continuous hypoxia and normal air. The systemic application of chronic fast rate hypoxia with or without hypercapnia mimicked severe OSA patients with apnoea/hypopnea index equivalent to 60 events per hour. Then routine blood tests were performed and the levels of brain derived neurotrophic factor (BDNF) and miR-34a were examined.

RESULTSIn contrast to intermittent hypoxia with hypercapnia, both intermittent hypoxia and continuous hypoxia treatments caused significantly higher levels of haematology parameters than normoxia treatments. Compared to normoxia, intermittent hypoxia with hypercapnia exposure resulted in substantial decrease of serum BDNF and, miR-34a in the lower brainstem, while less pronounced results were found in intermittent hypoxia and continuous hypoxia exposure.

CONCLUSIONSThe exposure of intermittent hypoxia with or without hypercapnia, mimicking the situations in severe OSA patients, was associated with, or even promoted tumorigenesis.

Animals ; Brain Stem ; metabolism ; Brain-Derived Neurotrophic Factor ; blood ; metabolism ; Cell Transformation, Neoplastic ; Hypercapnia ; blood ; complications ; Hypoxia ; blood ; complications ; Male ; MicroRNAs ; metabolism ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction

Obstructive sleep apnea syndrome (OSAS) is endangering human health seriously now. We had reviewed some typical animal model which had at least one OSAS character of intermittent hypoxia and/or hypercapnia, upper airway obstruction and sleep structure disorder. However, all of these models could not simulate clinical and pathological features of OSAS completely. Establishing a suitable animal model to study OSAS and related diseases is very important.
Airway Obstruction ; etiology ; Animals ; Disease Models, Animal ; Humans ; Hypercapnia ; etiology ; Hypoxia ; etiology ; Sleep Apnea, Obstructive ; complications

A reduction in diaphragm mobility has been identified in patients with chronic obstructive pulmonary disease (COPD) and has been associated with a decline in pulmonary function parameters. However, little information exists regarding the potential role of diaphragm mobility on hypercapnia in COPD. A new method of assessing the mobility of the diaphragm, using ultrasound, has recently been validated. The purpose of the present study was to investigate the relationship between diaphragm mobility and pulmonary function parameters, as well as that between arterial blood gas values and diaphragm mobility, in COPD patients. Thirty seven COPD patients were recruited for pulmonary function test, arterial blood gas analysis and diaphragm mobility using ultrasound to measure the craniocaudal displacement of the left branch of the portal vein. There were significant negative correlations between diaphragmatic mobility and PaCO2 (r = -0.373, P = 0.030). Diaphragmatic mobility correlated with airway obstruction (FEV1, r = 0.415, P = 0.011) and with ventilatory capacity (FVC, r = 0.302, P = 0.029; MVV, r = 0.481, P = 0.003). Diaphragmatic mobility also correlated significantly with pulmonary hyperinflation. No relationship was observed between diaphragm mobility and PaO2 (r = -0.028, P = 0.873). These findings support a possibility that the reduction in diaphragm mobility relates to hypercapnia in COPD patients.
Aged ; Airway Resistance/physiology ; Carbon Dioxide/blood/physiology ; Diaphragm/physiopathology/*ultrasonography ; Female ; Humans ; Hypercapnia/complications/*physiopathology ; Male ; Middle Aged ; Portal Vein ; Pulmonary Disease, Chronic Obstructive/complications/*physiopathology/ultrasonography ; Pulmonary Gas Exchange ; Respiratory Muscles/physiopathology

OBJECTIVETo study the effect of celecoxib on chronic hypoxia and hypercapnic pulmonary hypertension.

METHODSSD rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia+ celecoxib group (C). The content of TXB2 and 6-keto-PGF1alpha in plasma and lung were detected by the technique of radioimmunology.

RESULTS(1) Mean pulmonary arteria pressure(mPAP) was significantly higher in rats of B group than those of A group. mPAP was significantly higher in rats of C group than those of B group. Differences of mPAP were not significant in three groups. (2) The content of TXB2 in plasma and lung and the ratio of TXB2/6-keto-PGF1alpha were significantly higher in rats of B group than those of A group. The ratio of TXB2/6-keto-PGF1alpha was significantly higher and the content of 6-keto-PGF1alpha in plasma and lung was significantly lower in rats of C group than those of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A group. WA/TA and PAMT were significantly higher in rats of C group than those of B group. (4) Electron microscopy showed the thickening of vessel wall and the proliferation of collagen fiber in B group and augmentation of smooth muscle cell and abundance of myofilament in pulmonary arterioles in C group.

CONCLUSIONCelecoxib can aggravate hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by increasing the ratio of TXA2/PGI2.

Animals ; Celecoxib ; Chronic Disease ; Cyclooxygenase 2 Inhibitors ; adverse effects ; pharmacology ; Epoprostenol ; blood ; Hypercapnia ; complications ; Hypertension, Pulmonary ; etiology ; physiopathology ; Hypoxia ; complications ; Male ; Pyrazoles ; adverse effects ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Sulfonamides ; adverse effects ; pharmacology ; Thromboxane A2 ; blood

OBJECTIVETo investigate the changes of the endogenous hydrogen sulfide(H2S) system in pulmonary hypertension induced by hypoxic hypercapnia (HHPH) in rats and approach the possible mechanisms.

METHODS20 SD rats were randomly divided into control group (C) and hypoxic hypercapnia group (HH) (n=10). The changes of hemodynamics and the right ventricle/left ventricle + septum (RV/LV + SP) were measured. The ratio of vessel wall area and total area (WA/TA) of arteriae pulmonalis were observed under lightmicroscope. By using TdT-mediated dUTP nick end labeling (TUNEL) and immunocytochemistry techniques, apoptosis index (AI) and expression of Bcl-2, Bax protein in arteriae pulmonalis were tested. Plasma level of H2S and activity of H2S generating enzymes in homogenates of rat lung tissue were evaluated by sensitive modified sulfide electrode method. Cystathionine-gamma-lyase (CSE) mRNA in lung tissues was determined by RT-PCR.

RESULTSThe level of mean pulmonary arterial pressure(mPAP), WA/TA and RV/LV + SP were significantly higher in HH group than those in C group (P < 0.05 or P < 0.01). Compared with those in C group, the AI of arteriae pulmonalis in HH group were significantly lower; the expression of Bcl-2 protein increased while that of Bax protein decreased, and the ratio of Bax/Bcl-2 went up obviously (all P < 0.01). Plasma level of H2S, the activity of H2S generating enzymes and CSE mRNA in HH group were significantly lower than those in C group (all P < 0.01). Plasma level of H2S, the activity of H2S generating enzymes, CSE mRNA each was closely positively related to Al while inversely related to mPAP and Bcl-2/Bax (all P < 0.01).

CONCLUSIONThe endogenous hydrogen sulfide system is closely related to pulmonary hypertension induced by hypoxic hypercapnia. The depression of the H2S/CSE system in HHPH may help increase the ratio of Bcl-2/Bax, inhibit apoptosis of pulmonary artery smooth muscle cells and finally result in the formation of pulmonary hypertension.

Animals ; Apoptosis ; physiology ; Hydrogen Sulfide ; metabolism ; Hypercapnia ; complications ; physiopathology ; Hypertension, Pulmonary ; etiology ; physiopathology ; Hypoxia ; complications ; physiopathology ; Male ; Muscle, Smooth, Vascular ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo investigate the changes of endoplasmic reticulum stress-induced apoptosis in pulmonary tissue of rats with hypoxic pulmonary hypertension.

METHODSTwenty two male SD rats were randomly divided into control group and 4-week hypoxia-hypercapnia group (n=11). The mean pulmonary arterial pressure (mPAP) and the mean carotid arterial pressure (mCAP) were monitored, and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV + S) were measured. The rattish pathological model were assessed by mPAP, mCAP, RV/(LV+ S), vessel wall area/total area (WA/TA), vessel cavity area/total area (CA/TA) and media thickness of pulmonary arteriole (PAMT). The pulmonary apoptotic cells were detected by Hoechst staining. RT-PCR was used to study the genetic expression of caspasel2, glucose regulated protein 78 (GRP78) and GRP94 in pulmonary tissue. The expression of GRP94 and GRP78 proteins in pulmonary tissue were determined by using immunohistochemistry.

RESULTS(1) (The mPAP, RV/(LV + S), WA/TA and PAMT were respectively higher by 50.5%, 37.3%, 72.5% and 137% in hypoxic group than those in control group, while CA/TA was lower by 41.9% (all P < 0.01). There was not significant difference of mCAP between the two groups. (2) Hoechst staining showed that the pulmonary apoptotic cells in hypoxic group outnumbered markedly than those in control group, and the apoptotic cells were mainly in pulmonary tissue, while they were rare in pulmonary vascular smooth muscle cell. (3) Compared with control group, the expression of pulmonary caspasel2, GRP78 and GRP94 mRNA in hypoxic group were higher by 144%, 137% and 80.7% (all P < 0.05), respectively. (4) The expression of pulmonary GRP78 and GRP94 proteins were up-regulated in hypoxic group, and these proteins mainly localized in pulmonary vascular endothelial cell.

CONCLUSIONThe endoplasmic reticulum stress-induced apoptosis may be one of the mechanism of hypoxic pulmonary hypertension and pulmonary vascular wall remodeling.

Animals ; Apoptosis ; physiology ; Caspase 12 ; metabolism ; Endoplasmic Reticulum Stress ; physiology ; Heat-Shock Proteins ; metabolism ; Hypercapnia ; physiopathology ; Hypertension, Pulmonary ; etiology ; pathology ; physiopathology ; Hypoxia ; complications ; physiopathology ; Lung ; pathology ; Male ; Membrane Glycoproteins ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the effect and mechanism of chimonin on pulmonary arterioles I and III type collagen metabolism in pulmonary hypertension rats induced by chronic hypoxic hypercapnia.

METHODSThirty-six Sprague-Dawley rats were randomly divided into three groups: normal control group(A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group(C). Collagen I, III and their mRNA, Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, content of hydroxyproline in lung homogenate, pulmonary arteriole micromorphometric index were observed.

RESULTSHypoxic hypercapnic rats's mPAP, Hyr of lung homogenate, content of I type collagen and I type collagen mRNA in pulmonary arterioles, were significantly higher than those in control group, pulmonary vessel remodeling of hypoxic hypercapnic rats was significant, those changes in hypercapnia + chimonin group were significantly lower than those in hypoxic hypercapnic group. Blood CO concentration, activity of HO-1 in blood serum and lung homogenate in rats of hypoxic hypercapnic rats were significantly higher than those of control group, and those of hypercapnia + chimonin group were even higher than hypoxic hypercapnic group (P < 0.01). There was no significant difference in mCAP, content of III type collagen and their mRNA in three groups (P > 0.05).

CONCLUSIONChimonin can reduce pulmonary hypertension and pulmonary vessel remodeling induced by hypoxic hypercapnia through inhibiting proliferation of collagen I, the mechanism maybe is up regulating endogenous carbon monoxide system.

Animals ; Arterioles ; metabolism ; Carbon Monoxide ; metabolism ; Chronic Disease ; Collagen Type I ; metabolism ; Collagen Type III ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Hypercapnia ; complications ; physiopathology ; Hypertension, Pulmonary ; etiology ; metabolism ; physiopathology ; Hypoxia ; complications ; physiopathology ; Lung ; blood supply ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the effects of puerarin on pulmonary Vascular remodeling in rats with pulmonary hypertension induced by chronic hypoxia and hypercapnia.

METHODForty male rats (180-220) g of grade two were randomly divided into five groups: normal control group (NC), hypoxia-hypercapnia 1, 2, 3 week groups (LH1, LH2, LH3) and hypoxia-hypercapnia 3-week + puerarin group (LHP3 group, puerarin intraperitoneal injection, 20 mg x kg(-1) x d(-1)). Collagen I, III and their mRNA were observed in pulmonary arterioles by the technique of immunohistochemistry and in situ hybridization.

RESULTLight microscopy showed media thickness of pulmonary arterioles was much higher in LH3 group than that of NC group, and, vessel cavity turned more straiter in LH3 group than that of NC group. Howerer, the damage of pulmonary arterioles in LHP3 group was much slighter than that of LH3 group. The levels of plasma ET-1 and lung homogenates Hyr and MDA were much higher in rats of LH3 group than those of NC group (P < 0.01), and lower in LHP3 group than LH3 groups (P < 0.01). The activities of SOD in lung homogenates were significantly lowered in hypoxic and hypercapnic groups compared with control group (P < 0.01), but higher in LHP3 group than that of LH3 group. Plasma NO content of group LH was lower than that of group NC (P < 0.01), it was highter in group LHP3 than that of group LH3 (P < 0.01). Expression of collagen I and collagen I mRNA in pulmonary arterioles were significantly higher in rats of LH groups than those of NC group (P < 0.01), and they were lower in rats of LHP3 group than those of LH3 group (P < 0. 01). Expression of collagen III and collagen III mRNA were not significant difference among three groups.

CONCLUSIONPuerarin could improve pulmonary vascular remodeling in rats with pulmonary hypertension by inhibiting the deposition of collagen.

Animals ; Hypercapnia ; complications ; Hypertension, Pulmonary ; drug therapy ; Hypoxia ; complications ; Isoflavones ; pharmacology ; Male ; Oxidative Stress ; drug effects ; Pulmonary Artery ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley

BACKGROUNDAlthough severe encephalopathy has been proposed as a possible contraindication to the use of noninvasive positive-pressure ventilation (NPPV), increasing clinical reports showed it was effective in patients with impaired consciousness and even coma secondary to acute respiratory failure, especially hypercapnic acute respiratory failure (HARF). To further evaluate the effectiveness and safety of NPPV for severe hypercapnic encephalopathy, a prospective case-control study was conducted at a university respiratory intensive care unit (RICU) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) during the past 3 years.

METHODSForty-three of 68 consecutive AECOPD patients requiring ventilatory support for HARF were divided into 2 groups, which were carefully matched for age, sex, COPD course, tobacco use and previous hospitalization history, according to the severity of encephalopathy, 22 patients with Glasgow coma scale (GCS) < 10 served as group A and 21 with GCS = 10 as group B.

RESULTSCompared with group B, group A had a higher level of baseline arterial partial CO2 pressure ((102 +/- 27) mmHg vs (74 +/- 17) mmHg, P < 0.01), lower levels of GCS (7.5 +/- 1.9 vs 12.2 +/- 1.8, P < 0.01), arterial pH value (7.18 +/- 0.06 vs 7.28 +/- 0.07, P < 0.01) and partial O(2) pressure/fraction of inspired O(2) ratio (168 +/- 39 vs 189 +/- 33, P < 0.05). The NPPV success rate and hospital mortality were 73% (16/22) and 14% (3/22) respectively in group A, which were comparable to those in group B (68% (15/21) and 14% (3/21) respectively, all P > 0.05), but group A needed an average of 7 cm H2O higher of maximal pressure support during NPPV, and 4, 4 and 7 days longer of NPPV time, RICU stay and hospital stay respectively than group B (P < 0.05 or P < 0.01). NPPV therapy failed in 12 patients (6 in each group) because of excessive airway secretions (7 patients), hemodynamic instability (2), worsening of dyspnea and deterioration of gas exchange (2), and gastric content aspiration (1).

CONCLUSIONSSelected patients with severe hypercapnic encephalopathy secondary to HARF can be treated as effectively and safely with NPPV as awake patients with HARF due to AECOPD; a trial of NPPV should be instituted to reduce the need of endotracheal intubation in patients with severe hypercapnic encephalopathy who are otherwise good candidates for NPPV due to AECOPD.

Aged ; Brain Diseases ; therapy ; Carbon Dioxide ; blood ; Case-Control Studies ; Female ; Glasgow Coma Scale ; Humans ; Hypercapnia ; therapy ; Male ; Middle Aged ; Oxygen ; blood ; Positive-Pressure Respiration ; adverse effects ; Prospective Studies ; Pulmonary Disease, Chronic Obstructive ; complications