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

Despite the wide range of insults that can lead to the development of ARDS, a common sequence of pathologic changes can be identified in the lung. These changes can be divided into three phases: the acute, or exudative, phase (up to 6 days), in which hyaline membranes are a characteristic feature; the subacute, or proliferative, phase (4 to 10 days), in which metaplasia of the alveolar lining cells and early evidence of fibrosis are seen; and the chronic phase (8 days and on), when organizing fibrosis is a major finding. Structural changes of chronic pulmonary hypertension are also found in the patients with ARDS of longer duration. The mechanism by which these pulmonary changes occur is unknown. Studies of experimental models of ARDS may offer the best opportunity to elucidate the mechanisms. For example, a single infusion of E. coli endotoxin into sheep mimics the pathophysiologic changes of ARDS, offering a model for study of the initial insult on the lung. In addition, animals exposed to high concentrations of oxygen also show morphologic changes similar to those seen in patients with ARDS. Whether the hyperoxia is responsible for such changes, or whether it potentiates the injury induced by some other insult, is not certain.
 ...
PMID:Pathology of the adult respiratory distress syndrome. 333 56

Injury to the lung during in vivo exposure to hyperoxia results in vascular restructuring and pulmonary hypertension. This study reports the pattern of cellular proliferation that occurs in proximal intrapulmonary arteries over time during vessel wall injury and adaptation to increased partial pressures of oxygen. Although the remodeling of the capillary bed has been emphasized particularly during oxygen injury to the lung, this report identifies significant proliferative changes within the vessel wall of proximal arterial segments isolated from rats exposed to 85% oxygen. An increased incorporation of 3H-thymidine by endothelial cells is the earliest and most dramatic vessel wall response. The labeling index of these cells is increased more than tenfold by the end of 7 days in hyperoxia. Proliferation of medial smooth muscle cells and adventitial fibroblasts is also significantly increased. The increased cell number within these compartments is noted especially for its contribution to the overall vessel wall hypertrophy observed in chronic hyperoxic pulmonary hypertension. This general proliferative response is accompanied by specific shifts in the relative percentages of different actin protein isoforms as identified by two-dimensional gel electrophoresis. Changes in the distribution of actin isoforms are discussed as potential markers of a phenotypic modulation among vascular smooth muscle cells that occurs during the progression of pulmonary vessel wall remodeling.
 ...
PMID:Proliferative changes in the pulmonary arterial wall during short-term hyperoxic injury to the lung. 341 83

Normobaric hyperoxia is known to cause pulmonary hypertension with major restructuring of the walls of large and small pulmonary arteries. This study reports the effects of 21 days of exposure to 87% oxygen on the resting and active mechanical properties and structure of pulmonary arterial segments. Segments from the hilar region, extrapulmonary and proximal preacinar, and selected distal preacinar regions were studied. Resting and active (KCl-induced) tension:circumference curves were determined for each vessel. Morphometric measures were made of vessels fixed at a standard circumference using computerized planimetry. The areas of the media and adventitia as well as vessel wall thickness were increased in hyperoxic vessels. The walls of segments from the hypertensive rats demonstrated an increased stiffness based upon analysis of vessel resting tension:circumference relationships while the tangent modulus (a measure of stiffness normalized to tissue dimensions) was unchanged. Paradoxically, despite medial hypertrophy in the pulmonary vessels remodeled by hyperoxia, active tension was reduced. This study reveals that the resulting hypertensive state is not readily explained by an inherent increase in the maximal contractile capabilities of the remodeled vessel. Rather, obliteration of vessels in combination with increased resting stiffness appear to be the basis for pulmonary hypertension induced in hyperoxia.
 ...
PMID:Mechanical properties and structure of isolated pulmonary arteries remodeled by chronic hyperoxia. 361 98

This study shows by morphometric and hemodynamic techniques that exposure to hyperoxia at normobaric pressure causes rapid structural remodeling of rat pulmonary arteries and pulmonary hypertension. After 7 days of 90% O2, pulmonary artery cross-sectional area is reduced by a striking loss of intraacinar arteries (control, 13 +/- 1 sq mm; exposed, 8 +/- 1 sq mm; P less than 0.001), the ratio of arteries to alveoli being 4:100 in control rats and 2.5:100 after hyperoxia. The lumen of preacinar and intraacinar arteries is narrowed by a reduction of vessel external diameter (ED) and an increased medial wall thickness (MT). There is a significant reduction in the percent medial thickness [( 2 X 100 X MT]/ED) in both regions. The proportion of muscular and partially muscular intraacinar arteries increases at the expense of nonmuscular ones (P [chi 2] less than 0.01), and fully muscular arteries appear in the alveolar wall where they are not normally found. Intimal thickening occurs in 19% of alveolar duct and 34% of alveolar wall nonmuscular arteries. Right ventricular hypertrophy occurs, the ratio of the left ventricle plus the septum to the right ventricle being significantly reduced (control, 4.07 +/- 0.26; exposed, 3.23 +/- 0.10; P less than 0.02). After 3 days of 87% O2, pulmonary artery pressure is still normal (17.0 +/- 0.9 mmHg) but after 7 days it is significantly increased (26.2 +/- 0.9 mmHg; P less than 0.01), as is pulmonary vascular resistance (control, 0.033 +/- 0.003; exposed, 0.065 +/- 0.015 U/kg; P less than 0.05). Return to air breathing (after 7 days at 87% O2) causes pulmonary vasoconstriction and a further rise of the pulmonary artery pressure (to 38.3 +/- 3.3 mmHg after 60 minutes).
 ...
PMID:Pulmonary artery remodeling and pulmonary hypertension after exposure to hyperoxia for 7 days. A morphometric and hemodynamic study. 623 36

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)
 ...
PMID:Detrimental effects of hydralazine in patients with chronic air-flow obstruction and pulmonary hypertension. A combined hemodynamic and radionuclide study. 632 27

There are several unique aspects of O2 therapy in infants. Inhalation of O2 by preterm infants decreases the frequency of apnea and cyanosis, and increases the ventilatory response to CO2, but the reasons for this are unclear. Immature infants receiving O2 therapy are subject to retinopathy, but we do not know the magnitude or duration of hyperoxia necessary to damage the developing retina. Newborns with persistent pulmonary hypertension, without radiographic signs of pulmonary disease, frequently remain hypoxemic despite breathing 100% O2. In these infants, the unresponsiveness of teh postnatal pulmonary circulation to high concentrations of inspired O2 needs elucidation. Babies with respiratory failure who are treated with O2 and mechanical ventilation often acquire chronic pulmonary disease. The etiologic importance of O2 compared to postive airway pressure in the development of this condition remains controversial. Some laboratory studies suggest that newborn animals are resistant to pulmonary injury from O2; other studies indicate that youth offers no protection. The results of experiments carried out with newborn mice and lambs provide evidence that diet may be an important element in the susceptibility of newborn animals to pulmonary O2 toxicity.
 ...
PMID:Special considerations in oxygen therapy of infants and children. 677 80

20 anesthetized mechanically ventilated dogs received an infusion of epinephrine, 2 micrograms/kg/min, for 4 h. 10 dogs were ventilated with air for the entire 4-hour period and 10 were ventilated with oxygen for the first hour and then air for 3 h. During the first hour of the epinephrine infusion in the group ventilated with oxygen, as compared to the group ventilated with air, the heart rate decreased (it increased in the dogs ventilated with air); the cardiac output increased less; the systemic vascular resistance decreased less; the pulmonary vascular resistance decreased more; and the pulmonary artery wedge pressure increased (it decreased in the dogs ventilated with air). During the next 3 h when the animals were ventilated with air, the effects of oxygen on the hemodynamic changes induced by epinephrine persisted for variable periods. The epinephrine-induced pulmonary arteriovenous shunt was significantly less at all times in the group ventilated with oxygen, not only during the oxygen breathing but following it for 3 h. Oxygen breathing has been known to exert powerful effects on the heart, and the pulmonary and systemic circulations in normal man and animals and in patients with pulmonary hypertension and acute respiratory failure. This study demonstrates that oxygen breathing significantly alters the cardiovascular effects of epinephrine during oxygen breathing and reduces the epinephrine-induced pulmonary shunt during and for several hours after oxygen is discontinued. These finding add further evidence that hyperoxia affects, by unknown mechanisms, the autonomic regulation of the cardiovascular system.
 ...
PMID:The cardiovascular action of oxygen breathing: effect on adrenergic stimulation. 687 16

Nifedipine is a potent slow channel calcium antagonist and systemic vasodilator recently reported to attenuate hypoxic pulmonary vasoconstriction in man. Other systemic vasodilators have also been shown to attenuate hypoxic pulmonary vasoconstriction, but their effects in some species may be mediated by reflex beta-adrenergic discharge. We evaluated the effect of nifedipine on the relation between pulmonary arterial pressure and blood flow during hyperoxia (inspired partial pressure of oxygen [PO2] 200 mm Hg) and hypoxia (inspired PO2 50 mm Hg) in denervated ventilated pig lungs perfused in situ with the animal's own blood. Ten lungs were ventilated with alternating 15 minute periods of hyperoxia and hypoxia. Hypoxia shifted the pulmonary artery pressure (x axis)-blood flow (y axis) relationship to the right and decreased its slope, indicating vasoconstriction. Nifedipine, given as a 0.1, 1, or 10 microgram/kg bolus into the pulmonary artery, caused a dose-dependent reduction of hypoxic pulmonary vasoconstriction. It is concluded that nifedipine is a potent pulmonary vasodilator acting locally within the lung and that it might be useful in the therapy of hypoxic pulmonary hypertension from chronic lung disease in man.
 ...
PMID:Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. 712 46

Pulmonary and intracardiac hemodynamic findings are reported. They were obtained by means of catheterization of right cardiac departments and the pulmonary artery with thermodilution in 57 patients with chronic nonspecific pulmonary diseases (CNPD), under conditions of resting, rationed bicycle-ergometric exercise, hypo- and hyperoxia, and nitroglycerin administration. Changes in pulmonary and intracardiac hemodynamics which reflect the ongoing exhaustion of compensatory mechanisms in the external respiration apparatus, the pulmonary vascular system and the heart, are shown to precede the formation of right ventricular hypertrophy in obstructive CNPD A classification of secondary pulmonary hypertension, based on clinical and instrumental signs, is offered.
 ...
PMID:[Pulmonary hypertension in chronic nonspecific lung diseases]. 716 25

The etiology of shocklung is diverse. All causes lead to a lesion of the alveolar-capillary membrane with interstitial and subsequent alveolar edema. The clinical manifestations, although variable, are progressive and can be divided into 3 stages, which are the expression of a decrease in pulmonary compliance and of hypoxemia due to a ventilation-perfusion defect (shunt effect). The diagnosis of shocklung must be differentiated from pulmonary edema of cardiac origin by right heart catheterization and demonstrate a normal capillary pressure, a pulmonary hypertension with increased pulmonary resistance and a normal or increased cardiac output. A decreased PaO2 is the first sign of a ventilation-perfusion imbalance. The problem of alveolar-capillary O2 transfer is better defined by the alveolar-arterial O2 difference, the calculation of quantity of the intrapulmonary shunt and the hyperoxia curve. The daily analysis of the hyperoxia curve allows for a better appreciation of the clinical status than the clinical and radiological signs. The prognosis of the shockening is poor inspite of better reanimation technics. The mortality is about 50% and depends on 3 factors: etiology, early diagnosis and correction of the primary insult.
 ...
PMID:[The adult respiratory distress syndrome. Clinical signs, radiology and biological data (author's transl)]. 736 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>