Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oscillations of arterial pressure during sleep are the hemodynamic hallmark of the sleep apnea syndrome. The mechanism of these transient pressure elevations is incompletely understood. To investigate the role of the arterial chemoreflex in the neurocirculatory responses to apnea, we measured mean arterial pressure (MAP; Finapres) and muscle sympathetic nerve activity (MSNA; peroneal microneurography) during voluntary end-expiratory apnea during exposure to room air, 10.5% O2 in N2 (hypoxemia), and 100% O2 (hyperoxia) in 11 healthy men. While the men breathed spontaneously, MSNA (in bursts/min) rose during hypoxemia and decreased during hyperoxia and MAP remained unchanged. During room air exposure, apnea led to a rise of 94 +/- 54% in MSNA total amplitude and a rise of 6.5 +/- 2.1 mmHg in MAP. MSNA and MAP increased by 616 +/- 158% and 10.8 +/- 2.4 mmHg, respectively, during hypoxemic apnea of equal duration (time-matched responses) and by 98 +/- 41% and 4.9 +/- 2.0 mmHg, respectively, during hyperoxic apnea (P < 0.05 for hypoxemic vs. hyperoxic apnea for both). Thus, in awake healthy humans, activation of the arterial chemoreflex by hypoxemia appears to contribute importantly to the sympathetic and blood pressure responses to apnea.
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PMID:Sympathetic and blood pressure responses to voluntary apnea are augmented by hypoxemia. 786 56

Normobaric hyperoxia has known deleterious effects on survival, presumably due to the generation of superoxide anion and hydrogen peroxide. To investigate the anatomical substrate of the effect of normobaric hyperoxia on the myocardial and striated muscles and the protective effect, if any, of alpha-tocopherol (vitamin E) on these tissues, we administered 95-99% O2 to adult male Wistar rats for 24, 48, 60 and 72 h. The animals were divided into four groups: 1) control I: six rats which breathed room air were used as controls for the ultrastructural studies; 2) control II: 10 rats which breathed 95-99% of O2 for up to 72 h were used as controls for arterial pressure, blood gases/pH, PvO2 and Hb measurements; 3) group A: hyperoxia: 24 rats divided into four subgroups according to the time of exposure to hyperoxia, A24, A48, A60, A72; and 4) group B: alpha-tocopherol/hyperoxia: 24 rats treated with alpha-tocopherol, 15 mg/kg/day, for 14 days before the beginning and throughout the period of hyperoxia, were divided into four subgroups (B24, B48, B60, B72) according to the time of exposure to hyperoxia. Our results showed that: 1) up to the 60th hour, arterial pressure (MAP) was satisfactory; PaO2 > 280 mmHg; PaCO2, pH and Hb were within normal limits; 2) ultrastructural studies of the myocardial apex, the diaphragm and the quadriceps femoris showed dilatation of the sarcoplasmic reticulum/T-tubuli system, swelling of mitochondria, and structural derangement of myofibrils, in particular in the z-bands. The findings were proportionally related to the time of exposure of hyperoxia. They were also more intensely shown on myocardial and diaphragmatic fibers in group A; 3) the survival time (mean +/- SD) was 63.8 +/- 2.5 h in group A and 68.9 +/- 3.8 h in group B. These results suggest that normobaric hyperoxia exerts a cytotoxic effect on the myocardial and striated muscle fibers and that the administration of alpha-tocopherol may delay or change the development of oxygen toxicity.
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PMID:Ultrastructural changes of the myocardial and striated muscle following a challenge of normobaric hyperoxia: the protective effects of alpha-tocopherol. 874 23

We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PET(CO2)) from approximately 40 to approximately 58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PET(CO2) (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16 +/- 3 mmHg) and hyperoxia (17 +/- 2 mmHg PET(CO2)). The increase in cardiac output (Q) at 55 mmHg PET(CO2) was greater in hypoxia (2.61 +/- 0.7 L/min) versus hyperoxia (1.09 +/- 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (> 50 mmHg PET(CO2)) than hyperoxia (> 55 mmHg). MSNA increased earlier during hypoxic hypercapnia (> 45 mmHg) compared with hyperoxic hypercapnia (> 55 mmHg). Thus, in these conscious humans, the dose-response effect of PET(CO2) on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia.
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PMID:Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia. 1256 39

The liver is a target for injury in low flow states. Markers of liver injury are either invasive or not rapidly responding. Magnetic resonance imaging (MRI) may offer a noninvasive alternative to evaluate liver injury due to reduced perfusion. Recently, we reported an MRI method (functional MRI [fMRI]) that enables us to follow liver perfusion by changing the enrichment of inspired gas (air, air-5% carbon dioxide, 95% oxygen-5% carbon dioxide). Rats were subjected to hemorrhagic shock (HS) (bleeding to a MAP of 25 mmHg) and randomized to no resuscitation or resuscitation with Ringer lactate (RL) or adrenaline infusion targeted to a MAP of 50 mmHg or baseline. Significantly decreased fMRI responses to hyperoxia and hypercapnia were observed immediately after HS. Liver enzymes levels, liver histology, and apoptosis assessments were normal immediately after hemorrhage, however, showed significant changes after 6 h. Functional MRI revealed that adrenaline, but not RL infusion, significantly (P < 0.01) improved liver perfusion. Similarly, liver injury, as assessed by liver enzyme levels, liver histology, and apoptosis, was attenuated to a greater extent with adrenaline resuscitation. No significant differences in liver perfusion and injury were noted between resuscitation to low (50 mmHg) versus high (baseline) MAP. This study shows that fMRI enables early assessment of changes in liver perfusion, resulting in liver injury or recovery, and therefore, it may be considered as a noninvasive, rapidly responding tool for following liver outcome subsequent to hemorrhage and resuscitation. Using fMRI, we showed that adrenaline may be preferable to RL as an initial measure to attenuate liver injury after HS.
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PMID:Liver response to hemorrhagic shock and subsequent resuscitation: MRI analysis. 1762 Dec 58

The generation of reactive oxygen species (ROS) plays a major role in endothelial signaling and function. Of the several potential sources of ROS in the vasculature, the endothelial NADPH oxidase (Nox) family of proteins, Nox1, Nox2, Nox4 and Nox5, are major contributors of ROS. Excess generation of ROS contributes to the development and progression of vascular disease. While hyperoxia stimulates ROS production through Nox proteins, hypoxia appears to involve mitochondrial electron transport in the generation of superoxide. ROS generated from Nox proteins and mitochondria are important for oxygen sensing mechanisms. Physiological concentrations of ROS function as signaling molecule in the endothelium; however, excess ROS production leads to pathological disorders like inflammation, atherosclerosis, and lung injury. Regulation of Nox proteins is unclear; however, antioxidants, MAP Kinases, STATs, and Nrf2 regulate Nox under normal physiological and pathological conditions. Studies related to redox regulation of Nox should provide a better understanding of ROS and its role in the pathophysiology of vascular diseases.
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PMID:Redox regulation of Nox proteins. 2088 26