Background: Blood pH and bicarbonate estimations are basal acid-base laboratory tests that are performed in infants with infantile hypertrophic pyloric stenosis (IHPS). This study aimed to define the clinical value of...Background: Blood pH and bicarbonate estimations are basal acid-base laboratory tests that are performed in infants with infantile hypertrophic pyloric stenosis (IHPS). This study aimed to define the clinical value of pCO<sub>2</sub> and BE in infants suspected to have IHPS. Methods: We collected data from 80 “surgical” infants younger than 100 days with prolonged nonbilious vomiting who were suspected to have IHPS. In 65 infants, pyloric stenosis was confirmed, and 15 infants had nonsurgical conditions. Capillary blood was tested for standard acid-base parameters and lactate. The two groups were compared. Results: Eighty-eight percent of the IHPS infants had elevated standard bicarbonate levels (st bicarb) > 25 mmol/l, and 60% had BE > 3.5 mmol/l;12% of the infants showed hypercapnia (pCO<sub>2</sub> ≥ 50 mmHg) associated with markedly increased standard bicarbonate and BE. Infants with nonsurgical vomiting were older at admission (p = 0.002), had a longer duration of vomiting (p < 0.001), were older (p = 0.002) and weighted more at admission (p = 0.004), had lower pCO<sub>2</sub> (p = 0.021), lower st bicarb (p < 0.001) and lower BE (p = 0.001). In addition, nonsurgical infants showed a trend to anemia (p = 0.002). Conclusions: In infants with IHPS/nonbilious vomiting, acid-base analysis (ABA) is equivocal or inconclusive. These findings may be misleading and could result in a false clinical decision. Nonsurgical vomiting is associated with a lower degree of alkalosis, normocapnia to slight hypercapnia and a base deficit. However, even infants with IHPS may present with a negative BE. In infants with IHPS and severe alkalosis, hypercapnia carries a risk for respiratory depression. Monitoring the infant’s respiration allows for the early detection of respiratory deterioration.展开更多
Objective: To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension. Method...Objective: To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension. Methods: 1) 40 SD rats were randomly divided into four groups: normoxic control group (N), hypoxia hypercapnia group (HH), endoplasmic reticulum stress (ERS) inhibitor 4-phenyl butyric acid group (4-PBA), ERS pathway agonist tunicamycin group (TM). 2) The mean pulmonary arterial pressure (mPAP) and the right ventricular hypertrophy index (RV/(LV + S)) were measured in each group. 3) Identification of pulmonary artery smooth muscle cells (PASMCs) in each group by immunofluorescence α-SMA. 4) Morphological changes of lung tissue and pulmonary artery were observed by electron microscope. 5) The apoptotic index of PASMCs in each group was detected by TUNEL. 6) Reverse transcription polymerase chain reaction (RT-PCR) and Western Blot (WB) were used to detect the expression of ERS related protein and mRNA (GRP78, CHOP, JNK, Caspase-12) in each group. Results: 1) Compared with the N group, the mPAP, RV/(LV + S) and vascular wall area (WA)/total area (TA) value of HH group, 4-PBA group and TM group were increased (P < 0.01), and the vascular lumen area (LA)/TA values, PASMCs apoptosis index were significantly decreased. GRP78, CHOP, JNK, Caspase-12 expression were increased, and the differences were statistically significant. 2) Compared with the HH group, the mPAP, RV/(LV + S) and WA/TA of 4-PBA group were decreased (P < 0.01);the LA/TA value and PASMCs apoptosis index were increased (P < 0.05);and the mRNA and protein expression of CHOP, JNK, Caspase-12 and GRP78 had a significant decrease (P < 0.05). 3) Compared with the HH, the mPAP, RV/(LV + S) and WA/TA of TM group were increased (P P P < 0.01);and? PASMCs apoptotic index was increased (P < 0.01). Meanwhile, the mRNA expression of Caspase-12, CHOP, JNK and GRP78 was increased to varying degrees (P < 0.05), and the protein expression of Caspase-12, CHOP and JNK was also increased significantly (P Conclusion: Hypoxia and hypercapnia induced pulmonary vascular remodeling may be related to the proliferation of PASMCs, and ERS related factors (JNK, Caspase12 and CHOP) are involved in the regulation of hypoxic hypercapnia.展开更多
Pulmonary arterial hypertension (PAH) is a serious disease which is characterized by increased vascular resistance and pressure. We have previously hypothesized that panax notoginseng saponins (PNS) might attenuate pu...Pulmonary arterial hypertension (PAH) is a serious disease which is characterized by increased vascular resistance and pressure. We have previously hypothesized that panax notoginseng saponins (PNS) might attenuate pulmonary vasoconstriction under hypoxia and hypercapnia condition. This study aims to investigate the effect of notoginsenoside R<sub>g1</sub>, a main ingredient of PNS, with various concentrations (8, 40, 100 mg/L, respectively) on extracellular signal regulated kinase (ERK1/2) signaling pathway in pulmonary arterial smooth muscle cells (PASMCs). In addition, PASMCs were randomly divided into six groups: SD rat under normoxic condition as control group (N group), hypoxia hypercapnia group (H group), DMSO control group (HD group), R<sub>g1</sub>-treatment groups (R<sub>gL</sub>R<sub>gM</sub> and R<sub>gH</sub> group). Western-blot and RT-PCR were used to test the expression of p-ERK protein and the expression of ERK1 mRNA and ERK2 mRNA. This study provided the evidence that the expression of p-ERK protein and the expression of ERK1 mRNA and ERK2 mRNA in HD group and H group were obviously higher than that in N group (P < 0.01), Whereas the level of ERK1/2 mRNA in R<sub>g1</sub>-treatment groups was significantly lower than that in HD group and H group (P < 0.01), and the proper concentration of R<sub>g1</sub> is 40 mg/L. These results suggested that notoginsenoside R<sub>g1</sub> can attenuate pulmonary vasoconstriction which may lead to HHPV through reducing the expression of ERK1/2.展开更多
The changes of the structure and content of the erythrocyte membrane band 3 protein and its function of anion transport and blood gases inside and out of the erythrocytes were observed under isobaric hypoxia and hypox...The changes of the structure and content of the erythrocyte membrane band 3 protein and its function of anion transport and blood gases inside and out of the erythrocytes were observed under isobaric hypoxia and hypoxia-hypercapnia in rats. It was found t展开更多
Notoginsenoside R1, the main active ingredient of Panax notoginseng saponins (PNS), has been proposed to play fatal roles in the development of hypoxic hypercapnia-induced pulmonary vasoconstriction (HHPV). Subsequent...Notoginsenoside R1, the main active ingredient of Panax notoginseng saponins (PNS), has been proposed to play fatal roles in the development of hypoxic hypercapnia-induced pulmonary vasoconstriction (HHPV). Subsequently, pulmonary arterial smooth muscle cells (PASMCs) lead to pulmonary vascular system remodeling and chronic pulmonary disease in the development of HHPV. Despite considerable studies have contributed to pulmonary disease, the mechanism of how Notoginsenoside R1 affects HHPV remains unclear. In this view, we will discuss the effect of notoginsenoside R1 by investigating the expression of p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway in PASMCs under hypoxia and hypercapnia condition. The third order PASMCs of Sprague Dawley (SD) rats were cultured with various concentrations (8, 40, 100 mg/L, respectively) of Notoginsenoside R1. Our data showed that the protein and mRNA expression levels of p-38 MAPK were higher in hypoxic hypercapnia group compared with hypoxic DMSO and normoxia control groups (p 1 treatment groups, the level of p-p38 MAPK protein and p38 MAPK mRNA were significantly decreased with different degrees (p 1 treatment may contribute to attenuate HHPV via decreasing the protein and mRNA expression levels of p-38 MAPK.展开更多
BACKGROUND In the obese patient population,some patients have severe obstructive sleep apnea(OSA)with daytime hypoventilation.Such patients are generally identified on the basis of the presence or absence of daytime h...BACKGROUND In the obese patient population,some patients have severe obstructive sleep apnea(OSA)with daytime hypoventilation.Such patients are generally identified on the basis of the presence or absence of daytime hypercapnia,and the condition is called obesity hypoventilation syndrome.However,mechanisms for such daytime hypoventilation remain unclear.AIM To investigate metabolic syndrome and daytime hypercapnia association based on hypercapnia prevalence in obese OSA patients in a nested case-control study.METHODS Consecutive obese patients(body mass index≥30 kg/m2)who underwent polysomnography due to suspected OSA were included.Among them,patients with severe OSA(apnea hypopnea index≥30/h)were divided into two groups according to the presence or absence of hypercapnia during wakefulness(arterial partial pressure of carbon dioxide≥or<45 Torr,respectively).The characteristics and clinical features of these two groups were compared.RESULTS Among 97 eligible patients,25 patients(25.8%)had daytime hypercapnia.There were no significant differences in age,gender,body mass index,apnea-hypopnea index,and Epworth Sleepiness Scale scores between the two groups.However,patients with hypercapnia had a significantly lower arterial partial pressure of oxygen level(75.8±8.2 torr vs 79.9±8.7 torr,P=0.042)and higher arterial partial pressure of carbon dioxide level(46.6±2.5 torr vs 41.0±2.9 torr,P<0.001).Additionally,patients with hypercapnia were more likely to have metabolic syndrome(72.0%vs 48.6%,P=0.043)and a higher metabolic score(the number of satisfied criteria of metabolic syndrome).In multivariate logistic regression analysis,the presence of metabolic syndrome was associated with the presence of hypercapnia(OR=2.85,95%CI:1.04-7.84,P=0.042).CONCLUSION Among obese patients with severe OSA,26%of patients had hypercapnia during wakefulness.The presence of metabolic syndrome was independently correlated with the presence of daytime hypercapnia.展开更多
Background Therapeutic hypercapnia （TH） has been demonstrated to protect several organs ischemia-reperfusion injury.The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusi...Background Therapeutic hypercapnia （TH） has been demonstrated to protect several organs ischemia-reperfusion injury.The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusion injury （HIRI）.Methods Thirty adult male Wistar rats weighing （250 ± 20） g were randomized into 3 groups （n=10 in each）, group C （control group）, group A （hypercapnia group） and group B （CO2 preconditioning group）.A segmental ischemia of the liver was induced by interrupting the blood vessels including the bile duct to the median and left lateral lobes for 60 minutes and all the animals were sacrificed after 240 minutes observation period of reperfusion.Mean arterial pressure （MAP）and the blood gases were measured before ischemia （baseline） and at 30, 60, 120, 180 and 240 minutes after reperfusion.Arterial blood samples were obtained for determination of serum levels of TNF-α, IL-10, serum aspartate aminotransferase （AST） and alanine aminotransferase （ALT）.The histopathology of liver tissues was evaluated by light microscopy.The NF-κB expression and apoptotic hepatocytes were respectively determined by immunohistochemistry and TUNEL assay.Results The serum levels of liver enzymes and TNF-α were significantly decreased while the IL-10 level was significantly increased in groups A and B than in group C （P 〈0.05）, and group B surpassed group A （P 〈0.05）.The histopathological scores, the NF-κB immunohistochemical score （IHS） and apoptotic index were significantly lower in groups A and B than in group C （P 〈0.05）, and the decrease in group B was more obvious than in group A （P〈0.05）.Conclusion Therapeutic hypercapnia attenuates ischemia-reperfusion injury to the liver.Moreover, the effects of CO2preconditioning are outstandingly notable.展开更多
Background Very 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 larg...Background Very 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.Methods First,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.Results In 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.Conclusions The exposure of intermittent hypoxia with or without hypercapnia,mimicking the situations in severe OSA patients,was associated with,or even promoted tumorigenesis.展开更多
文摘Background: Blood pH and bicarbonate estimations are basal acid-base laboratory tests that are performed in infants with infantile hypertrophic pyloric stenosis (IHPS). This study aimed to define the clinical value of pCO<sub>2</sub> and BE in infants suspected to have IHPS. Methods: We collected data from 80 “surgical” infants younger than 100 days with prolonged nonbilious vomiting who were suspected to have IHPS. In 65 infants, pyloric stenosis was confirmed, and 15 infants had nonsurgical conditions. Capillary blood was tested for standard acid-base parameters and lactate. The two groups were compared. Results: Eighty-eight percent of the IHPS infants had elevated standard bicarbonate levels (st bicarb) > 25 mmol/l, and 60% had BE > 3.5 mmol/l;12% of the infants showed hypercapnia (pCO<sub>2</sub> ≥ 50 mmHg) associated with markedly increased standard bicarbonate and BE. Infants with nonsurgical vomiting were older at admission (p = 0.002), had a longer duration of vomiting (p < 0.001), were older (p = 0.002) and weighted more at admission (p = 0.004), had lower pCO<sub>2</sub> (p = 0.021), lower st bicarb (p < 0.001) and lower BE (p = 0.001). In addition, nonsurgical infants showed a trend to anemia (p = 0.002). Conclusions: In infants with IHPS/nonbilious vomiting, acid-base analysis (ABA) is equivocal or inconclusive. These findings may be misleading and could result in a false clinical decision. Nonsurgical vomiting is associated with a lower degree of alkalosis, normocapnia to slight hypercapnia and a base deficit. However, even infants with IHPS may present with a negative BE. In infants with IHPS and severe alkalosis, hypercapnia carries a risk for respiratory depression. Monitoring the infant’s respiration allows for the early detection of respiratory deterioration.
文摘Objective: To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension. Methods: 1) 40 SD rats were randomly divided into four groups: normoxic control group (N), hypoxia hypercapnia group (HH), endoplasmic reticulum stress (ERS) inhibitor 4-phenyl butyric acid group (4-PBA), ERS pathway agonist tunicamycin group (TM). 2) The mean pulmonary arterial pressure (mPAP) and the right ventricular hypertrophy index (RV/(LV + S)) were measured in each group. 3) Identification of pulmonary artery smooth muscle cells (PASMCs) in each group by immunofluorescence α-SMA. 4) Morphological changes of lung tissue and pulmonary artery were observed by electron microscope. 5) The apoptotic index of PASMCs in each group was detected by TUNEL. 6) Reverse transcription polymerase chain reaction (RT-PCR) and Western Blot (WB) were used to detect the expression of ERS related protein and mRNA (GRP78, CHOP, JNK, Caspase-12) in each group. Results: 1) Compared with the N group, the mPAP, RV/(LV + S) and vascular wall area (WA)/total area (TA) value of HH group, 4-PBA group and TM group were increased (P < 0.01), and the vascular lumen area (LA)/TA values, PASMCs apoptosis index were significantly decreased. GRP78, CHOP, JNK, Caspase-12 expression were increased, and the differences were statistically significant. 2) Compared with the HH group, the mPAP, RV/(LV + S) and WA/TA of 4-PBA group were decreased (P < 0.01);the LA/TA value and PASMCs apoptosis index were increased (P < 0.05);and the mRNA and protein expression of CHOP, JNK, Caspase-12 and GRP78 had a significant decrease (P < 0.05). 3) Compared with the HH, the mPAP, RV/(LV + S) and WA/TA of TM group were increased (P P P < 0.01);and? PASMCs apoptotic index was increased (P < 0.01). Meanwhile, the mRNA expression of Caspase-12, CHOP, JNK and GRP78 was increased to varying degrees (P < 0.05), and the protein expression of Caspase-12, CHOP and JNK was also increased significantly (P Conclusion: Hypoxia and hypercapnia induced pulmonary vascular remodeling may be related to the proliferation of PASMCs, and ERS related factors (JNK, Caspase12 and CHOP) are involved in the regulation of hypoxic hypercapnia.
文摘Pulmonary arterial hypertension (PAH) is a serious disease which is characterized by increased vascular resistance and pressure. We have previously hypothesized that panax notoginseng saponins (PNS) might attenuate pulmonary vasoconstriction under hypoxia and hypercapnia condition. This study aims to investigate the effect of notoginsenoside R<sub>g1</sub>, a main ingredient of PNS, with various concentrations (8, 40, 100 mg/L, respectively) on extracellular signal regulated kinase (ERK1/2) signaling pathway in pulmonary arterial smooth muscle cells (PASMCs). In addition, PASMCs were randomly divided into six groups: SD rat under normoxic condition as control group (N group), hypoxia hypercapnia group (H group), DMSO control group (HD group), R<sub>g1</sub>-treatment groups (R<sub>gL</sub>R<sub>gM</sub> and R<sub>gH</sub> group). Western-blot and RT-PCR were used to test the expression of p-ERK protein and the expression of ERK1 mRNA and ERK2 mRNA. This study provided the evidence that the expression of p-ERK protein and the expression of ERK1 mRNA and ERK2 mRNA in HD group and H group were obviously higher than that in N group (P < 0.01), Whereas the level of ERK1/2 mRNA in R<sub>g1</sub>-treatment groups was significantly lower than that in HD group and H group (P < 0.01), and the proper concentration of R<sub>g1</sub> is 40 mg/L. These results suggested that notoginsenoside R<sub>g1</sub> can attenuate pulmonary vasoconstriction which may lead to HHPV through reducing the expression of ERK1/2.
文摘The changes of the structure and content of the erythrocyte membrane band 3 protein and its function of anion transport and blood gases inside and out of the erythrocytes were observed under isobaric hypoxia and hypoxia-hypercapnia in rats. It was found t
文摘Notoginsenoside R1, the main active ingredient of Panax notoginseng saponins (PNS), has been proposed to play fatal roles in the development of hypoxic hypercapnia-induced pulmonary vasoconstriction (HHPV). Subsequently, pulmonary arterial smooth muscle cells (PASMCs) lead to pulmonary vascular system remodeling and chronic pulmonary disease in the development of HHPV. Despite considerable studies have contributed to pulmonary disease, the mechanism of how Notoginsenoside R1 affects HHPV remains unclear. In this view, we will discuss the effect of notoginsenoside R1 by investigating the expression of p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway in PASMCs under hypoxia and hypercapnia condition. The third order PASMCs of Sprague Dawley (SD) rats were cultured with various concentrations (8, 40, 100 mg/L, respectively) of Notoginsenoside R1. Our data showed that the protein and mRNA expression levels of p-38 MAPK were higher in hypoxic hypercapnia group compared with hypoxic DMSO and normoxia control groups (p 1 treatment groups, the level of p-p38 MAPK protein and p38 MAPK mRNA were significantly decreased with different degrees (p 1 treatment may contribute to attenuate HHPV via decreasing the protein and mRNA expression levels of p-38 MAPK.
文摘BACKGROUND In the obese patient population,some patients have severe obstructive sleep apnea(OSA)with daytime hypoventilation.Such patients are generally identified on the basis of the presence or absence of daytime hypercapnia,and the condition is called obesity hypoventilation syndrome.However,mechanisms for such daytime hypoventilation remain unclear.AIM To investigate metabolic syndrome and daytime hypercapnia association based on hypercapnia prevalence in obese OSA patients in a nested case-control study.METHODS Consecutive obese patients(body mass index≥30 kg/m2)who underwent polysomnography due to suspected OSA were included.Among them,patients with severe OSA(apnea hypopnea index≥30/h)were divided into two groups according to the presence or absence of hypercapnia during wakefulness(arterial partial pressure of carbon dioxide≥or<45 Torr,respectively).The characteristics and clinical features of these two groups were compared.RESULTS Among 97 eligible patients,25 patients(25.8%)had daytime hypercapnia.There were no significant differences in age,gender,body mass index,apnea-hypopnea index,and Epworth Sleepiness Scale scores between the two groups.However,patients with hypercapnia had a significantly lower arterial partial pressure of oxygen level(75.8±8.2 torr vs 79.9±8.7 torr,P=0.042)and higher arterial partial pressure of carbon dioxide level(46.6±2.5 torr vs 41.0±2.9 torr,P<0.001).Additionally,patients with hypercapnia were more likely to have metabolic syndrome(72.0%vs 48.6%,P=0.043)and a higher metabolic score(the number of satisfied criteria of metabolic syndrome).In multivariate logistic regression analysis,the presence of metabolic syndrome was associated with the presence of hypercapnia(OR=2.85,95%CI:1.04-7.84,P=0.042).CONCLUSION Among obese patients with severe OSA,26%of patients had hypercapnia during wakefulness.The presence of metabolic syndrome was independently correlated with the presence of daytime hypercapnia.
文摘Background Therapeutic hypercapnia （TH） has been demonstrated to protect several organs ischemia-reperfusion injury.The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusion injury （HIRI）.Methods Thirty adult male Wistar rats weighing （250 ± 20） g were randomized into 3 groups （n=10 in each）, group C （control group）, group A （hypercapnia group） and group B （CO2 preconditioning group）.A segmental ischemia of the liver was induced by interrupting the blood vessels including the bile duct to the median and left lateral lobes for 60 minutes and all the animals were sacrificed after 240 minutes observation period of reperfusion.Mean arterial pressure （MAP）and the blood gases were measured before ischemia （baseline） and at 30, 60, 120, 180 and 240 minutes after reperfusion.Arterial blood samples were obtained for determination of serum levels of TNF-α, IL-10, serum aspartate aminotransferase （AST） and alanine aminotransferase （ALT）.The histopathology of liver tissues was evaluated by light microscopy.The NF-κB expression and apoptotic hepatocytes were respectively determined by immunohistochemistry and TUNEL assay.Results The serum levels of liver enzymes and TNF-α were significantly decreased while the IL-10 level was significantly increased in groups A and B than in group C （P 〈0.05）, and group B surpassed group A （P 〈0.05）.The histopathological scores, the NF-κB immunohistochemical score （IHS） and apoptotic index were significantly lower in groups A and B than in group C （P 〈0.05）, and the decrease in group B was more obvious than in group A （P〈0.05）.Conclusion Therapeutic hypercapnia attenuates ischemia-reperfusion injury to the liver.Moreover, the effects of CO2preconditioning are outstandingly notable.
基金This study was supported by a grant from the National Natural Science Foundation of China （No. 81241004）.
文摘Background Very 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.Methods First,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.Results In 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.Conclusions The exposure of intermittent hypoxia with or without hypercapnia,mimicking the situations in severe OSA patients,was associated with,or even promoted tumorigenesis.
