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

To determine the role of hypoxic pulmonary vasoconstriction in pneumococcal pneumonia, hemodynamic measurements were made in 16 dogs before, and within 36 hours after, intrapulmonary administration of type III pneumococcus. Ten dogs with one lobe or more of pneumonia increased their pulmonary vascular resistances and slightly decreased their arterial O2 tensions. Hypoxia increased and hyperoxia decreased their pulmonary vascular resistances. During O2 breathing, arterial PO2 was less during than before the pneumonia and increased when pulmonary perfusion was diverted away from the diseased lung. In 2 dogs breathing air, forcing the cardiac output through the diseased lung caused an increase in vascular resistance that could clearly be reduced by O2 breathing. In 5 dogs, lung mast cell counts showed no decrease in the lobes with pneumonia. In pneumococcal pneumonia, the hypoxic pulmonary pressor mechanism serves to decrease blood flow to the diseased lobes and, thus, to maintain the arterial PO2. Lung mast cells could participate in this response.
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PMID:Preservation of hypoxic pulmonary pressor response in canine pneumococcal pneumonia. 0 Sep 35

Microbial colonization and infection patterns were prospectively evaluated in premature baboons with and without bronchopulmonary dysplasia (BPD) to assess if prolonged hyperoxia would predispose to a different pattern of microbial colonization and/or a higher risk of respiratory infection. Forty baboons were delivered by hysterotomy at 75% of gestation and randomized into two groups. Group I (control or PRN) animals were placed immediately on high-frequency oscillation at 15 Hz; I:E ratio 1:2, and changed to positive-pressure ventilation at 48 to 72 h. They were maintained on clinically appropriate oxygen at minimal ventilator settings for the remainder of the 21-day experimental period. Group II (oxygen-treated or BPD) animals were ventilated with PPV and FIO2 1.0 for 7 days followed by FIO2 0.8 for 14 days. All animals were treated with antibiotics during some portion of the 21-day course. Specimens from nose, oropharynx, trachea, and rectum were cultured for both aerobes and anaerobes throughout the neonatal intensive care unit (NICU) course. A subset of animals from both groups were killed at 21 days and lung, liver, spleen, and gastric contents were cultured quantitatively at autopsy. Findings showed that coagulase-negative staphylococci were the predominant organisms that colonized the neonate in the NICU. Lung infections were seen to evolve through sequential pathogenetic steps: colonization of the upper respiratory tract, with concomitant or subsequent colonization of the trachea with comparable organism and ultimate recovery of the same organisms at autopsy in the lungs of animals with pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bacterial colonization and infection studies in the premature baboon with bronchopulmonary dysplasia. 195 45

The effect of continuous exposure to 80% oxygen on newborn mice with Ureaplasma urealyticum pneumonia was determined. Mice were inoculated intranasally with either U. urealyticum or sterile broth and then housed in either 80% oxygen or room air (21% oxygen). The mice were sacrificed at either 7 or 14 days after inoculation. Significantly more mice in the U. urealyticum group housed in 80% O2 than in the room air-exposed group were culture positive 14 days after inoculation (P = 0.042), but no difference was found at 7 days. The presence of alveolar macrophages, neutrophils, and lymphocytes and alveolar wall thickness were determined. Overall, the group housed in 80% O2 and inoculated with U. urealyticum had severe pulmonary lesions at both time points, while the lesion severity in the room air-exposed group inoculated with U. urealyticum and the group housed in 80% O2 and inoculated with sterile broth was dependent on the time point. Mortality was significantly higher in the group housed in 80% O2 and inoculated with U. urealyticum than it was in all other groups (P less than 0.001). Our results indicate that hyperoxia causes the persistence of U. urealyticum in the lungs of newborn mice, acutely potentiates the inflammatory response, and turns an otherwise self-limited pneumonia into a lethal disease.
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PMID:Hyperoxia potentiates Ureaplasma urealyticum pneumonia in newborn mice. 222 20

In spite of the development of various antibiotics, management of elderly patients with pneumonia remains an important problem. It is suggested that adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) often occur in elderly patients with pneumonia. Although neutrophils are suggested to be involved in the genesis of these conditions, details remain unknown. We demonstrated that a highly cytotoxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized from linoleate by human neutrophils, thus it was named leukotoxin. Leukotoxin was detected in lung lavages from patients with ARDS. In these lung lavages, increases in albumin concentration and angiotensin converting enzyme (ACE) activity were also observed. Similar results were observed in lung lavages from rats after exposure to hyperoxia for 60 hours in an experimental model of ARDS. Intravenous administration of leukotoxin (100 mumol/kg) caused lung edema. Albumin concentration and ACE activity were increased in lung lavages of rats receiving leukotoxin. In contrast, these changes were not observed in rats administered with linoleate. Furthermore, administration of leukotoxin (100 mumol/kg) caused coagulation abnormality, i.e., increase in fibrin-fibrinogen degradation products, decrease in fibrinogen, and prolongation of activated partial thromboplastin time and prothrombin time. Administration of linoleate did not induce these changes. It is indicated that O2- was produced by respiratory burst enzyme located in neutrophil plasma membrane, and that hydroxyl radicals derived from O2- by Fenton reaction were responsible for leukotoxin synthesis. From our results, leukotoxin, a product of hydroxyl radicals and linoleate, might be responsible for the genesis of ARDS and DIC.
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PMID:[Leukotoxin and pulmonary injury]. 238 90

Bleomycin is a commonly used antineoplastic agent which produces dose- and time-dependent pneumonitis and fibrosis in humans. The mechanism of bleomycin-induced lung injury is uncertain. However, current data shows that bleomycin can generate reactive oxygen species such as superoxide and hydroxyl radicals. We therefore investigated whether intraperitoneal (i.p.) injection of endotoxin, a protectant for hyperoxia, could modulate the biochemical and morphological estimates of bleomycin-induced lung fibrosis in rats. However, pretreatment with multiple i.p. injections of endotoxin, combined with intratracheal bleomycin instillation, resulted in increased lung collagen content compared to bleomycin treatment alone and controls. Furthermore, morphological estimates of the severity of lung lesions present in the endotoxin-bleomycin treatment group were increased when compared with saline and endotoxin control lung lesions. These data indicate, in the current study design, that endotoxin did not reduce, but instead increased the severity of bleomycin-induced pulmonary fibrosis in rats. The mechanism for this increase in fibrosis may be the result of pre-existing endotoxin-induced cell injury.
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PMID:The effect of endotoxin on bleomycin-induced lung fibrosis in the rat. 241 66

Pulmonary toxicity is an important adverse effect of bleomycin treatment. Very little is known of the mechanisms underlying the development of lung injury, especially after intravenous administration, or how it can be modulated. In this study acute lung injury induced by bleomycin has been examined in rats by assessment of alveolar lavage cell profiles, histological examination, and measurement of the total pulmonary extravascular albumin space. Intratracheal instillation of bleomycin 1.5 mg resulted in a severe pneumonitis with influx of inflammatory cells into the alveoli as assessed by alveolar lavage, oedema of the alveolar walls, and up to an eight fold increase in the total pulmonary extravascular albumin space, maximal at 72 hours. Intravenous bleomycin 0.15-5 mg produced no detectable injury when assessed in these ways. Exposure to hyperoxia (40-90%) after intravenous bleomycin, however, induced lung injury similar to that produced by intratracheal bleomycin. A much more severe injury followed administration of intravenous bleomycin after an exposure to hyperoxia, which itself resulted in lung injury; but lung injury was still detectable after bleomycin when the exposure to hyperoxia was insufficient to induce changes in control animals. Lung injury was not observed when the exposure to hyperoxia preceded bleomycin treatment. These results indicate the importance of oxygen in the pathways leading to acute lung injury following intravenous bleomycin. We conclude that exposure to oxygen might induce lung injury during and after bleomycin treatment, and suggest that in these circumstances oxygen therapy should be kept to a minimum.
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PMID:Development of acute lung injury after the combination of intravenous bleomycin and exposure to hyperoxia in rats. 244 92

The potential protective effects of ICRF 187, Didox, Amidox and VF 165 were investigated in models of bleomycin, or bleomycin and hyperoxia induced lung injury. ICRF 187, a bispiperazinedione compound, is a strong chelating agent which blocks a number of free radical mediated processes. The polyhydroxyphenyl derivatives, Didox, Amidox and VF 165, demonstrate degrees of Fe chelating activities and free radical scavenging abilities. Hamsters treated with 5.0 U/kg bleomycin followed by treatment with ICRF 187 or Didox exhibited similar mortality to the bleomycin alone treated group. In a second study, a low dose of bleomycin (1.2 U/kg) was used followed by exposure to 70% oxygen. Treatment with ICRF 187, Didox, Amidox, or VF 165 failed to protect against lung injury; with the ICRF 187 and Amidox groups exhibiting significantly increased rates of mortality over that seen in animals treated only with bleomycin and hyperoxia. No animals treated with the agents alone died. Histopathology documented that all bleomycin-treated hamsters died of severe pneumonitis. Additionally, in the agent-treated groups there was a prominent proliferation of type II pneumocytes, which demonstrated marked anaplasia, a feature not typical of early bleomycin and hyperoxia lung injury. In conclusion, ICRF 187 and the polyhydroxyphenyl derivative, Amidox, paradoxically increase bleomycin- and hyperoxia-induced lung injury. The possible mechanisms of this interaction include: (1) increased availability of Fe to bleomycin; (2) interference with the healing process; or (3) inhibition of endogenous protective effects of SOD.
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PMID:ICRF 187 and polyhydroxyphenyl derivatives fail to protect against bleomycin induced lung injury. 247 96

Diffuse alveolar damage (DAD) is usually considered a generalized lung process. During five years the authors observed 83 patients with generalized DAD in 827 adult autopsies (10.1%) and 10 patients with identical, but localized, lesions. The authors propose the term regional alveolar damage (RAD) to designate localized "DAD." RAD was unilateral in six patients and most frequently involved the upper lobe. All ten patients had chronic systemic diseases and presented with life-threatening illnesses. The probable causes of RAD were multifactorial and included hypotensive shock, septicemia, pneumonia, hyperoxia, and pancreatitis. All patients developed respiratory failure, requiring supplemental oxygen and, in nine patients, mechanical ventilation. Chest roentgenograms revealed alveolar or combined alveolar and interstitial infiltrates that corresponded to the lesions found at autopsy. The reasons for localization of RAD within the lung are unclear, but the presence of proliferative lesions and frequent involvement of the upper lobe suggests that RAD is not simply an early phase of DAD and implicates additional pathogenetic factors.
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PMID:Regional alveolar damage (RAD). A localized counterpart of diffuse alveolar damage. 266 70

Guinea pigs were inoculated by the respiratory route with wild-type (Cyr) or vaccine (Oka) strain varicella zoster virus (VZV). Wild-type cell-free virus obtained by sonication produced neutralizing antibody responses in steroid-treated animals when given via the intratracheal route, and induced neutralizing antibody as well as a pneumonitis in normal animals when given via the intrabronchial (i.b.) route. A humoral response also followed i.b. instillation of cell-associated wild-type or vaccine strain VZV. Prior i.b. administration of thioglycollate or exposure to hyperoxia altered the number and function of pulmonary macrophages, respectively, but viral susceptibility of the guinea pigs was not enhanced. Both strains of VZV could be isolated from bronchial washings up to 48 hours after i.b. instillation of cell-associated virus, but neither strain was isolated thereafter from cultures of bronchial washings or explanted lung tissues.
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PMID:Inoculation of guinea pigs with varicella-zoster virus via the respiratory route. 301 Sep 8

Pulmonary insults caused by transfusion, radiation, and hyperoxia share many clinical features with insults caused by serious pulmonary infections. The major objective in evaluating these patients is to establish the diagnosis with as much certainty as possible. Unfortunately, there are no clinical aspects or laboratory tests that are pathognomonic for these diseases; therefore, it is often necessary to rely on a knowledge of those features which help to distinguish these disorders from infectious etiologies. For example, patients suffering from transfusion-related acute lung injury (TRALI) experience onset of insult within 6 hours of a transfusion and have the presence of leukoagglutinins in their serum. Patients with radiation injuries frequently have roentgenographic infiltrates that conform to the ports of radiation. Despite extensive animal and human studies, factors distinguishing hyperoxic injury from infectious disorders remain poorly defined. These clinical features and others are reviewed to identify the essential components in the diagnosis of TRALI, acute radiation pneumonitis, and hyperoxic pneumonitis.
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PMID:Pulmonary insults due to transfusions, radiation, and hyperoxia. 305 15


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