Obstructive sleep apnea (OSA), which is the most common sleep-related breathing disorder, is characterized as frequent upper airway collapse and obstruction. It is a treatable disorder but if left untreated is associated with complications in several organ systems. The health risk to OSA patients shows a strong association with acute cardiovascular events, and with chronic conditions. To the central nervous system, OSA causes behavioral and neuropsychologic deficits including daytime sleepiness, depression, impaired memory, mood disorders, cognition deficiencies, language comprehension and expression deficiencies, all of which are compatible with impaired hippocampal function. Furthermore, there exists a significant correlation between disease severity and cognitive deficits in OSA. Children with severe OSA have significantly lower intelligence quotient (IQ) and executive control functions compared to normal children matched for age, gender and ethnicity. This corroborates the findings of several pediatric studies of cognition in childhood OSA, where deficits are reported in general intelligence and some measures of executive function. In studies of OSA, it is difficult to differentiate the effects of its two main pathologic traits, intermittent hypoxia (IH) and sleep fragmentation. Many OSA studies, utilize IH as the only exposure factor in OSA studies. These approaches simplify research process and attain most of the academic goals. IH, continuous hypoxia and intermittent continuous hypoxia can all result in decreases in arterial O2. There are striking differences to them in the response of physiological systems. There are multiple studies showing that IH treatment in a rodent model of OSA can impair performance of standard water maze tests associated with deficits in spatial learning and memory which most likely are hippocampal-dependent. Cellular damage to the hippocampal cornuammonis 1 (CA1) region likely contributes to neuropsychological impairment among OSA patients, since neural circuits in the hippocampus are important in learning and memory. In this article, studies of hippocampal impairments from IH are reviewed for elucidating the mechanisms and relationships between hippocampal impairments and IH of OSA.
Hippocampus ; physiopathology ; Humans ; Hypoxia ; etiology ; physiopathology ; Sleep Apnea, Obstructive ; etiology ; physiopathology

Animals ; Diaphragm ; physiopathology ; Electrophysiological Phenomena ; physiology ; Hypoxia ; physiopathology ; Male ; Rats ; Rats, Wistar ; Sleep Apnea Syndromes ; physiopathology

Burns ; complications ; immunology ; physiopathology ; Humans ; Hypoxia ; etiology ; immunology ; physiopathology ; Ischemia ; etiology ; immunology ; physiopathology

OBJECTIVETo establish a method for real-time recording the oxygen consumption of mice under normobaric hypoxia.

METHODSThe experimental apparatus was made up of animal container, filling water control system, electronic balance, hose, a computer with weight recording software, etc. The working principle was that the oxygen consumed by animal was replaced by water filling which was controlled by the pneumatic and hydraulic actuator. The water was weighted by an electronic balance and the weight signal was recorded into excel file at the same time. The accuracy and precision of the apparatus were detected by a 10 ml syringe. The oxygen consumption characteristics of 6 acute repetitive hypoxia mice and 6 normal mice were observed.

RESULTSThe P value for the paired t test was 1 and the CV value was 4%. The survival time and total oxygen consumption of acute repetitive hypoxia mice were both significantly increased compared to normal mice (P < 0.05), which were (58.8 +/- 6.8) min and (46.0 +/- 8.7) min respectively for the survival time and (85.1 +/- 8.5) ml and (73.6 +/- 5.4) ml respectively for total oxygen consumption.

CONCLUSIONThe hypoxia tolerance of the acute repetitive hypoxia mice can significantly improved by taking more oxygen in the animal cabin. The accuracy and precision of the apparatus are high and it can be used for the determination of oxygen consumption in hypoxia research.

Animals ; Hypoxia ; physiopathology ; Mice ; Monitoring, Physiologic ; instrumentation ; Oxygen Consumption ; physiology

Autophagy is a highly evolutionarily conserved physiological mechanism of organism, including several stages such as autophagosomes formation, the fusion of lysosomes and autophagosomes, and autophagosomes degradation. In physiological conditions, autophagy is responsible for clearing the spoiled organelles and long-lived proteins to maintain the homeostasis of cells and organism. Meanwhile, autophagy is also involved in the formation and development of diseases, but the mechanism has not been confirmed yet. The relationship between autophagy and hypoxic ischemic brain injuries represented by stroke is a research hotpot in recent years, but there is no clear conclusion about autophagy's role and mechanism in hypoxic ischemic brain injuries. We reviewed the activation, function and mechanism of autophagy in hypoxic ischemic brain injuries, in order to provide some perspectives on these researches.
Animals ; Autophagy ; Homeostasis ; Humans ; Hypoxia-Ischemia, Brain ; physiopathology ; Lysosomes

OBJECTIVE: To investigate the effects of simulated hypobaric hypoxia environment at 7 000 m above sea level on cardiac structure and function in rats. METHODS: A total of 96 male SD rats were randomly divided into high-altitude hypobaric hypoxia group (hypoxia group) and normobaric normoxia group (control group). Rats of hypoxia group were placed in a large cabin simulated 7 000 m high-altitude hypobaric hypoxia environment. Operating time 23 h / d, the control circadian ratio of approximately 12 h:12 h. The rats in control group were bred under normobaric normoxia. The hypoxic group was divided into 3 d, 7 d, 14 d, 28 d groups according to hypoxic time, 12 rats in each group. Changes of structure and function of heart due to hypoxia were evaluated by echocardiography and electrocardiogram. Myocardial pathological changes were analyzed by hematoxylin-eosin staining(HE). RESULTS: Compared with the control group at the same time point ①With prolonged exposure to hypobaric hypoxia, the growth ratio of body mass in rats is slower. Arterial oxygen saturation was significantly lower in both 14 d and 28 d (P＜0.05). ② Left ventricular end-diastolic anterior wall thickness (LVAWD) and left ventricular end-diastolic posterior wall thickness (LVPWD) of rats in 28 d were increased significantly (P＜0.05). Left ventricular end-diastolic diameter (LVIDD) and left ventricular internal dimension systole (LVIDS) of rats in 28 d were decreased significantly (P＜0.05, P＜0.01). Left ventricular ejection fraction (EF), fractional shortening of left ventricle (FS), pulmonary vein (PV) peak velocity and PV peak gradient of rats in 7 d were decreased significantly (P＜0.05, P＜0.01). ③The QRS and QT interval period were significantly prolonged in 14 d and 28 d (P＜0.05, P＜0.01). The ST was significantly lower in 3 d and 7 d (P＜0.05, P＜0.01). The amplitude of R wave gradually shifted downward in 7 d, 14 d, 28 d (P＜0.05, P＜0.01). ④The red blood cell (RBC), hemoglobin (HGB), red blood cell distribution width (RDW) in hypoxic group were increased significantly (P＜0.01). The platelet count (PLT) count was decreased significantly in 14 d and 28 d (P＜0.01). The serum creatinine (CR) was increased significantly in 14 d and 28 d (P＜0.05). ⑤Pathological changes such as myocardial edema, sarcolemma condensate, focal degeneration and necrosis with inflammatory cell infiltration could be found at early stage of hypoxia. Myocardial compensatory repair such as myocardial fibroblasts proliferation was significant at end stage of hypoxia. CONCLUSION Left ventricular systolic functions of rats were decreased significantly after exposure to high altitude hypoxia hypobaric. The left ventricular systolic functions would recovery compensatory after one week exposed to high altitude hypoxia hypobaric.
Altitude ; Animals ; Heart ; physiopathology ; Hypoxia ; Male ; Rats ; Rats, Sprague-Dawley

Vascular endothelium plays an important role in regulating vascular homeostasis. Over the past years, it has become clear that endothelial dysfunction is a key event of pathophysiological changes in the initiation and progression of injuries induced by extreme environmental factors. The present review summarizes current understanding of vascular endothelial dysfunction induced by hypoxia, cold and heat, and provides the information for prevention and treatment of environmental exposure injuries.
Endothelium, Vascular ; physiopathology ; Environment ; Humans ; Hypoxia ; physiopathology ; Temperature ; Vascular System Injuries

AIMTo study the effects of different acute hypoxia on blood pressure, heart rate and microvessels and free radical in rabbits.

METHODSThe experiment model was carried out with acute hypoxia on two groups of rabbits, using artificial inspiration 12.5% O2 and 87.5% N2, 8.5% O2 and 91.5% N2 (equivalent to altitudes of some 4 000 m and 6 500 m) keeping hypoxia for 5, 10, 15, 20 min. During the course of it, the changes of blood pressure, heart rate and microvessels response, superoxide dismutase (SOD), malondialdehyde (MDA) were recorded accordingly.

RESULTS(1) systolic pressure was slightly up, then down in 5 mins. Diastolic pressure was significantly down (P < 0.05) in 20 min. (2) Heart rate showed reduced and prolonged, particularly in 8.5% hypoxia group (P < 0.05). (3) Vas bores of microvessle expanded (P < 0.05) and the blood stream became slow gradually (P < 0.05, P < 0.01) in following acute hypoxia time. (4) SOD was significantly down (P < 0.05), MDA was significantly increased (P < 0.05) in 20 mins.

CONCLUSIONAcute hypoxia could cause the blood pressure and heart rate to decrease, vas bore of microvessle to expand, the blood circulation to slow down and free radicals would increase.

Animals ; Blood Pressure ; Free Radicals ; metabolism ; Heart Rate ; Hypoxia ; metabolism ; physiopathology ; Microvessels ; physiopathology ; Rabbits

Activation of peripheral respiratory chemoreceptors provokes respiratory and cardiovascular reflexes, providing a novel understanding of pathogenic mechanism of hypertension. Here we hypothesize that activation of peripheral respiratory chemoreceptors by hypoxia causes enhanced cardiorespiratory activity in conscious spontaneously hypertensive rats (SHRs). Using whole body plethysmography in combination with radio telemetry, pulmonary ventilation, arterial blood pressure and heart rate were examined in SHRs and Wistar-Kyoto (WKY) rats. We found that exposure to hypoxia induced greater increases in tidal volume and minute ventilation volume in SHRs compared to WKY rats. In addition, hypoxia caused a robust increase in arterial blood pressure and heart rate in SHRs relative to WKY counterparts. After carotid body denervation, the hypoxic ventilatory response was significantly decreased in both SHRs and WKY rats, but without significant difference between the two strains; moreover, the differences of arterial blood pressure and heart rate changes during hypoxic exposure were statistically insignificant between SHRs and WKY rats. It is concluded that hypoxia remarkably potentiates cardiorespiratory activity in the SHRs, suggesting an enhanced sensitivity of carotid bodies to hypoxia.
Animals ; Blood Pressure ; Heart Rate ; Hypertension ; physiopathology ; Hypoxia ; physiopathology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY

AIMTo study the effect of chronic hypoxic hypercapnia on expression of COX-2 mRNA in pulmonary arterioles.

METHODSSD rats were randomly divided into two groups: control group and hypoxic hypercapnic group. COX-2 mRNA was observed in pulmonary arterioles by the technique of in situ hybridization.

RESULTSmPAP, weight ratio of right ventricle (RV) to left ventricle plus septum (LV + S) and COX-2 mRNA in pulmonary arterioles were much higher in rats of hypoxic hypercapnic group than those of control group. Light microscopy showed that vessel smooth muscle cell hypertrophy and vessel cavity straightness were found in hypoxic hypercapnic group.

CONCLUSIONChanges of expressions of COX-2 mRNA may regulate hypoxic hypercapnic pulmonary hypertension.

Animals ; Cyclooxygenase 2 ; genetics ; metabolism ; Hypercapnia ; metabolism ; physiopathology ; Hypoxia ; metabolism ; physiopathology ; Male ; Pulmonary Artery ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley