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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO2) and carbon dioxide (PCO2) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions, PO2 was significantly lower in the subendocardium (13.5 +/- 4.5 mm Hg) than in the subepicardium (20.7 +/- 2.3 mm Hg), whereas PCO2 did not differ significantly (43 +/- 8.8 and 51 +/- 9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardial PO2 decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardial PO2 was 4.1 +/- 6.3 mm Hg while subepicardial PO2 was 6.7 +/- 15.0 mm Hg (P less than 0.05). PCO2 reached peak values of 56 +/- 25 mm Hg subendocardial and 82 +/- 22 mm Hg subepicardial at 2.67 +/- 0.71 min and 3.43 +/- 0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows while PO2 recovered with different kinetics. Subendocardial PO2 increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.
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PMID:Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia. 309 86

10 patients with juvenile hypertension were investigated during normoxia, hypoxia and hyperoxia in comparison to 10 healthy volunteers. The results of heart rate, stroke volume, cardiac output and blood pressure in supine position as well as in passive orthostasis are significantly different in both groups. It seems that in the initial phase of hypertension the arterial chemoreceptors might be on an enhanced functional state.
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PMID:Orthostatic cardiovascular regulation during hypoxia and hyperoxia in patients with juvenile hypertension. 345 76

The acute effects of intravenously administered hydralazine on pulmonary hemodynamics and ejection radionuclide angiography were evaluated in 9 patients with chronic airflow obstruction (forced expiratory volume in one second, 1.2 +/- 0.8 L, mean +/- SD), pulmonary hypertension (mean pulmonary artery pressure (PAP), 29 +/- 13 mmHg), and sleep hypoxemia (maximal sleep desaturation, 20 +/- 16%). The effect of hydralazine was measured during both normoxia and hypoxia and compared with the effect of hyperoxia. Hydralazine increased cardiac index from 3.7 +/- 0.2 to 4.5 +/- 0.8 L/min/m2 (mean +/- SE, p less than 0.05, n = 9), but there were no significant changes in PAP (29 +/- 4 to 32 +/- 4 mmHg), mean pulmonary vascular resistance index (PVRI) (390 +/- 80 to 360 +/- 80 dyn.s.cm.-5.m2), mean right ventricular stroke work index (12.7 +/- 2.7 to 15.0 +/- 2.2 g.m/m2), and mean pulmonary capillary wedge pressure (12 +/- 1 to 12 +/- 2 mmHg). Mean right ventricular ejection fraction and mean right ventricular end diastolic volume also were not changed after treatment with hydralazine. Hyperoxia was used to assess the reversibility of pulmonary hypertension and to compare this with hydralazine. Hyperoxia increased arterial oxygen saturation (SaO2) from 91 +/- 1 to 96 +/- 1% and decreased the cardiac index from 3.8 +/- 0.1 to 3.1 +/- 0.2 L/min/m2 (p less than 0.02, n = 6) but, as with hydralazine, there was no significant change in PAP (28 +/- 6 to 25 +/- 6 mmHg) and PVRI (350 +/- 120 to 360 +/- 80 dyn.s.cm-5).m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detrimental effects of hydralazine in patients with chronic air-flow obstruction and pulmonary hypertension. A combined hemodynamic and radionuclide study. 632 27

Acute hyperoxia (1 atm) in anesthetized dogs produced a 14% decrease in cardiac output relative to that observed with FIo2 = 0.21 and was associated with 7% decreases in heart rate and stroke volume. Changes in the distribution of peripheral blood flow during hyperoxia, as measured with radioactive labeled microspheres, included decreases in renal cortical flow (-20%), retinal blood flow (-27%), and blood flow to the caudate nucleus, mesencephalon, hippocampus, and cerebellum. Absolute blood flow to intestinal viscera, to respiratory and skeletal muscle, and to fat were unchanged. Simulation of these changes in cardiac output and distribution of blood flow using a digital computer model show a minimal change in the pattern of nitrogen gas elimination, with nitrogen partial pressures in the "slowest" body compartment within 1% of control by 60 min.
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PMID:Peripheral circulatory responses to acute hyperoxia. 661 97

Blood acid-base balance, blood gases, respiration, ventilation, and renal function were studied in the rainbow trout during and following sustained environmental hyperoxia (PIO2 = 3.50-650 Torr). Animals were chronically fitted with dorsal aortic cannulae for repetitive blood sampling, oral membranes for the measurement of ventilation, and bladder catheters for continuous urine collection. Hyperoxia caused a proportional increase in arterial O2 tension and a stable 60% reduction in ventilation volume (Vw), the latter mainly due to a decrease in ventilatory stroke volume. O2 consumption exhibited a short-term elevation. Arterial CO2 tension (PaCO2) rose within 1 h, causing an immediate drop in arterial pH (pHa), and continued to increase gradually thereafter, reaching a value 2-4x the normoxic control level after 96-192 h. Compensation of the associated acidosis by the accumulation of [HCO3-] in the blood plasma started within 5-6 h, and was complete by 48 h. Therefore, further compensation occurred simultaneously with the gradual rise in PaCO2. The kidney played an important active role in this compensation by preventing excretion of the accumulated [HCO3-]. Upon reinstitution of normoxia, PaCO2 dropped to control levels within 1 h, and restoration of blood acid-base status by reduction of [HCO3-] had commenced by this time. A complete return to control values occurred within 20 h. During hyperoxia, an experimental elevation of the depressed Vw above control normoxic levels caused only a minor and transient reduction in PaCO2 and no change in pHa, but injection of branchial vasodilator 1-isoprenaline (10 mumol/kg) produced a large drop in PaCO2 and rise in pHa. It is concluded that the rise in PaCO2 during hyperoxia is mainly due to internal diffusive and/or perfusive limitation associated with branchial vasoconstriction, rather than to external convective limitation associated with the decreased Vw.
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PMID:Blood acid-base regulation during environmental hyperoxia in the rainbow trout (Salmo gairdneri). 678 12

Cerebral vasoconstrictor responsiveness to 100% oxygen inhalation was measured in 149 subjects, including normal healthy volunteers and those with risk factors for cerebral arteriosclerosis (N = 87). Test results were compared among patients with hemispheric stroke and vertebrobasilar insufficiency (N = 62) with the 133Xe inhalation method. Normal volunteers without risk factors (N = 49), aged 25 to 86 years, showed symmetrical vasoconstriction. Asymptomatic subjects with risk factors (N = 38) and those with vertebrobasilar insufficiency (N = 25) had decreased hemispheric gray matter flow (Fg) values during rest, but vasoconstrictor responsiveness to 100% oxygen inhalation was not significantly reduced. In patients with acute hemispheric infarction, regional vasoconstrictor responsiveness to 100% oxygen inhalation was lost and/or paradoxically reversed; in patients with chronic hemispheric infarction, it was decreased. Testing vasomotor responses during hyperoxia is safe, clinically helpful, and demonstrates impaired vasomotor reactivity in infarcted regions.
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PMID:Cerebral vasomotor responsiveness during 100% oxygen inhalation in cerebral ischemia. 684 19

The hemodynamic effects of breathing 95% oxygen were evaluated in 26 children with congenital heart disease. Aortic, pulmonary arterial, right atrial, and pulmonary arterial wedge pressure, aortic and pulmonary artery oxygen saturation, and blood gas, cardiac index, and heart rate were measured in room air and after each patient had breathed 95% oxygen for 10 (n = 26) and 20 (n = 5) minutes. Measurements were repeated with the patient again breathing room air for 10 (n = 11) and 20 (n = 6) minutes. After 10 minutes of 95% oxygen, arterial partial pressure of oxygen increased from 85 +/- 13 to 420 +/- 89 torr (p less than 0.001). Aortic mean pressure increased from 80 +/- 10 to 83 +/- 10 mm Hg (p less than 0.01), and systemic vascular resistance increased from 20 +/- 7 to 26 +/- 8 U (p less than 0.001). The cardiac index decreased by 21% from 3.96 +/- 0.94 to 3.12 +/- 0.74 liters/min/m2 (p less than 0.001) and the stroke index decreased by 11% (p less than 0.001). A 23% decrease in oxygen consumption (p less than 0.001) was observed, and oxygen transport decreased from 763 +/- 179 to 600 +/- 161 ml O2/min/m2 (p less than 0.001). Cardiac index, stroke index, and systemic vascular resistance did not return to normal until 20 minutes after cessation of oxygen breathing. To determine whether reflex bradycardia is responsible for these oxygen-induced hemodynamic changes, heart rate was kept constant by atrial pacing in a second group of 5 patients. In these children, significant decreases in cardiac index, stroke index, and oxygen consumption, and increases in systemic vascular resistance also occurred with 95% oxygen. Thus, in children with acyanotic congenital heart disease, hyperoxia increases aortic pressure and systemic vascular resistance and decreases cardiac index, stroke index, oxygen consumption, and oxygen transport.
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PMID:Cardiovascular effects of breathing 95 percent oxygen in children with congenital heart disease. 685 98

Gill ventilation frequency (fG), the pressure amplitude (PBC) and stroke volume (VS) of buccal ventilation cycles, the frequency of air breaths (fL), water flow over the gills (VW), gill oxygen uptake (MGO2), oxygen utilization (U), and heart frequency (fH) have been measured in unanaesthetized, air breathing Rana catesbeiana tadpoles (stage XVI-XIX). The animals were unrestrained except for ECG leads or cannulae, and were able to surface voluntarily for air breathing. They were subjected to aquatic normoxia, hyperoxia and three levels of aquatic hypoxia, and their respiratory responses recorded in the steady state. The experiments were performed at 20 +/- 0.5 degrees C. In hyperoxia there was an absence of air breathing, and fG, PBC and VW fell from the normoxic values, while U increased, resulting in no significant change in MGO2. Animals in normoxia showed a very low fL which increased in progressively more hypoxic states. VW increased from the normoxic value in mild hypoxia (PO2 = 96 +/- 2 mm Hg), but fell, associated with a reduction in PBC, in moderate (PO2 = 41 +/- 1 mm Hg) and severe (PO2 = 21 +/- 3 mm Hg) hypoxia in the presence of lung ventilation. Gill MGO2 was not significantly different from the normoxic value in mild hypoxia but fell in moderate hypoxia, while in severe hypoxia oxygen was lost to the ventilating water from the blood perfusing the gills. There was no significant change in fH from the normoxic value in either hypoxia or hyperoxia. These data indicate, that in the bimodally breathing bullfrog tadpole, aquatic PO2 exerts a strong control over both gill and lung ventilation. Furthermore, there is an interaction between gill and lung ventilation such that the onset of a high frequency of lung ventilation in moderate and severe hypoxia promotes a suppression of gill ventilation cycles.
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PMID:Gill and lung ventilation responses to steady-state aquatic hypoxia and hyperoxia in the bullfrog tadpole. 697 6

Lipid peroxidation and some parameters of hemostasis were studied during exposure to various hyperoxia schemes combined with heparin therapy before and after treatment in 124 patients aged 16 to 69 with CNS involvement which developed as a result of atherosclerosis and essential hypertension, 60 of whom presented with initial manifestations of cerebral circulation insufficiency (IMCCI), 33 with posthypoxic encephalopathies (PE), and 31 with ischemic stroke (IS). Hyperoxia mechanisms were differently directed in the studied groups of patients, this necessitating a differentiated approach to the choice of schemes of hyperbaric oxygenation. Use of a short course of hyperbaric oxygenation (up to 3 sessions at 1.2 to 1.25 atA) is recommended for patients with IMCCI and PE. For patients with IS in the acute period hyperbaric oxygenation at 1.4 atA is advisable combined with heparin therapy in doses of 150 to 300 U/kg b.w. a day.
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PMID:[Effects of hyperoxia regimes on the state of lipid peroxidation and hemostasis in patients with lesions of the central nervous system]. 789 81

Hemodynamic consequences of the withdrawal of arterial chemoreceptor drive (ACD) by brief systemic hyperoxia were studied in 16 mild hypertensive subjects (HT) and in 16 healthy subjects (NT) in horizontal position at resting metabolic rate. In another 9 mild HT and match NT measurements were made in resting sitting position and during steady-state mild physical exercise on cycloergometer, (30% of VO2 max.) Tidal volume, minute ventilation, end tidal CO2 and O2 concentration, K+, Na+, pO2, pCO2 values in blood were recorded. Impedance reography was used for recording stroke volume (SV) and arm blood flow (ABF). Cardiac output (CO), ABF and arterial blood pressure (ABF) values were used for calculation of the total peripheral resistance (TPR) and vascular resistance in the arm (AVR). To assess the neurogenic circulatory response to withdrawal of ACD in HT attenuated by opposite peripheral effects of high oxygen, the values of AVR, ABP, TPR and AVR changes during brief hyperoxia in NT, assumed to be of peripheral origin, were subtracted from respective values in HT, assumed to be of mixed neurogenic and peripheral origin. In HT hyperoxia applied in sitting position produced a brief decrease in systolic and diastolic ABP by 5.4 +/- 0.8% and 3.4 +/- 1.1% respectively, of TPR by 12.4 +/- 3% and of AVR by 4.7 +/- 4.6%. Decrease in AVR during hyperoxia was significantly greater in sitting than in horizontal position. In NT hyperoxia produced opposite effects in ABP, TPR and AVR, as compared to those in HT. In HT subjects during steady-state exercise the TPR decreased by 21 +/- 3.7% reaching a value no different from that in NT. We suggest, that in primary hypertension neurogenic sympathoexcitatory ACD is augmented and interacts with the peripheral mechanisms related to tissue oxygen supply.
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PMID:Hemodynamic responses to brief hyperoxia in healthy and in mild hypertensive human subjects in rest and during dynamic exercise. 880 52


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