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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
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PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

Extensive and severe bronchiectasis was found in 7 heroin-addicted individuals with pulmonary symptoms whose chest roentgenograms were not suggestive of severe airway disease. Abnormalities consisted of varicose and cylindrical alterations. Pulmonary function tests revealed airflow obstruction, decreased lung volumes, and diffusion capacity impairment. Arterial blood gas analysis demonstrated mild hypoxemia in all patients and chronic hypocapnia in 4. Serial pulmonary function tests in 2 patients revealed only modest improvement in the degree of airflow obstruction. The occurence of bronchiectasis appeared to be related to episodes of heroin-induced pulmonary edema and infection.
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PMID:Bronchiectasis: a cause of pulmonary symptoms in heroin addicts. 47 3

A retrospective clinico-pathological analysis of 78 cases of fatal subarachnoid hemorrhage (SAH) was carried out: 71% had a pathological diagnosis of pulmonary edema (PE), and of these 31% had a clinical diagnosis of PE. Patients with pathological PE were younger and died sooner after their SAH than those without. The incidence of PE fell with the passage of time following SAH, while the occurrence of pneumonia and embolism increased. There were hypoxemia and hypocapnia in both groups, more severe in the group that had pathological PE. The pathophysiology of neurogenic PE is discussed and possible therapeutic approaches indicated.
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PMID:Pulmonary edema following fatal aneurysm rupture. 69 Jun 77

A case of acute pulmonary complication following intra-arterial infusion of Lipiodol-Adriamycin emulsion for hepatocellular carcinoma was reported. Intra-arterial infusion chemotherapy was performed on a 75-year-old male with Lipiodol-Adriamycin emulsion (Lipiodol 8 ml + Adriamycin 40 mg). Severe dyspnea and cyanosis started about 30 minutes after the infusion, and blood gas analysis revealed hypoxemia and hypocapnia. Chest X-ray revealed diffuse infiltrative shadow throughout the both lungs. He was on positive end-expiratory pressure breathing for 4 days. Clinical symptoms and chest X-ray improved rapidly in the course of two weeks, he became almost asymptomatic. We concluded that the nature of this pulmonary damage was pulmonary edema due to the large amount of Adriamycin that flowed into pulmonary artery via arterio-venous shunt present in the hepatocellular carcinoma.
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PMID:[Pulmonary complication following intra-arterial infusion of lipiodol-adriamycin emulsion for hepatocellular carcinoma, report of a case]. 215 47

A 4 hr intravenous infusion of Escherichia coli endotoxin in a total dose of 100 mg/kg produced significant morphological and functional pulmonary alterations in pentobarbitone anesthetized rats. Lung vascular permeability index was increased from 2.11 +/- 0.34 in normal rats to 4.82 +/- 0.65 in untreated endotoxemic rats. Treatment of endotoxemic rats with recombinant human superoxide dismutase (r-HSOD) in doses of 0.1, 0.215, and 0.464 mg/kg.min i.v., infused concomitantly with endotoxin, dose-dependently reduced the permeability index to 3.28 +/- 0.96, 2.83 +/- 0.55 (P less than 0.05), and 2.16 +/- 0.65 (P less than 0.05). The wet lung weight was 523 +/- 15 and 664 +/- 46 mg/100 g bwt in normal and in untreated endotoxemic rats, respectively. r-HSOD dose-dependently inhibited the endotoxin-induced increase in wet lung weight to 617 +/- 40, 577 +/- 31, and 559 +/- 39 (P less than 0.05) mg/100 g bwt. r-HSOD (0.464 mg/kg.min) did not affect permeability index and wet lung weight in normal, nonintoxicated rats. Endotoxin infusion produced a significant increase in respiratory rate (max. +69%) and blood gas alterations, indicating a hyperventilatory hypocapnia in endotoxemic control rats. Infusion of r-HSOD (0.464 mg/kg.min) significantly inhibited the endotoxin-induced tachypnoe (max. +13%) and blunted the alterations in arterial hydrogen carbonate content and carbon dioxide tension. In conclusion, infusion of r-HSOD dose-dependently and significantly inhibited pulmonary edema formation and hyperventilatory dyspnoe in endotoxemic rats.
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PMID:Effects of recombinant human superoxide dismutase on increased lung vascular permeability and respiratory disorder in endotoxemic rats. 217 95

The effects of "hypocirculation" and "hypercirculation" of the lungs are small. Hypocirculation has an influence of the ventilation/perfusion ratio, and can thus contribute to hypocapnia. In the early stages, hypercirculation--in particular via a left-to-right shung, leads to an increase in diffusion capacity; after a course of many years, a "counter-situation" occurs. Progressive pulmonary hypertension, as is exemplified for mitral stenosis, leads to measurable restrictive and obstructive impairment of function, and possible to unspecific hyper-reaction, as also, over the long-term, to a diminishement in membrane diffusion capacity. Chronic left heart failure is characterised by interstitial oedema at the level of the alveolar and bronchial capillary beds. The results are measurable restrictions in the static volumes, and in particular of the obstruction parameters and the closing volume that involve the small airways. In the individual case, no statement as to the extent of left heart failure is possible. In the passive pulmonary hypertension phase, diffusion capacity increases; in the further course of the disease, with development of interstitial and alveolar oedema, it decreases again. In acute left heart failure, the persistance and/or extent of pulmonary oedema is not determined solely by the magnitude of the pulmonary venous pressure. Permeability oedema--brought about by mediators--would appear to be significant on the basis of animal experiments. Not infrequently, left cardiac failure leads to small pleural effusions which occur in combination with substantial atelectasia, the aetiology of which is unclear. Interpretation difficulties are caused by the clinical findings and function-analytical data obtained in patients with a combination of chronic lung disease and reducted volume storage capacity of the pulmonary circulation and of the left heart failure, a common situation in the elderly patient. Diminished pulmonary function parameters that fail to adequate respond to bronchodilators may be an expression of left ventricular failure.
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PMID:[The lung in heart diseases]. 219 2

Methotrexate, an antifolate cytotoxic drug, is used in anticancer chemotherapy as well as an immuno suppressive in rheumatoid arthritis. It is responsible for numerous secondary effects, amongst which is a characteristic acute pneumonia known since 1969. This pneumonitis has been described in detail, up to the present time in 78 cases gathered in this review. The prevalence of this complication is estimated at around 7%. This pneumonia may occur whatever the age, indication for which methotrexate is prescribed, the route of administration of the product (including the intra-thecal route) and the dose. It includes dyspnoea, fever, (sometimes quite marked) and frequently an acute reversible respiratory failure. Radiologically the opacities are usually diffuse interstitial and symmetrical with a basal predominance with sometimes some confluence and occasionally a pleural reaction. In a small number of cases a transient mediastinal adenopathy has been described. Respiratory function tests show a rapidly developing restrictive syndrome accompanied by hypoxia and hypocapnia. Broncho-alveolar lavage is characterised by hypercellularity with a frank and apparently transitory lymphocytosis. Histologically the most frequent lesion sighted is an extensive acute granulomatous reaction with or without oedema. Most often the outcome is favourable (75% of cases). However 6 deaths due to respiratory failure have been reported. Even though there has not been any formal test, steroid therapy in high dosage seems to accelerate recovery. Progress to an irreversible pulmonary fibrosis is possible but rare. The mechanism of this drug related acute pneumonia is not known but would seem to resemble that of other granulomatosis. Besides this rapidly progressive pneumonitis, methotrexate is responsible for a very small number of cases of severe pulmonary oedema and of acute painful pleurisies.
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PMID:[Pneumopathy caused by methotrexate]. 225 35

In this experimental study, we investigated pathophysiology of respiratory failure with acute pancreatitis. Pancreatitis was induced by injection of 15% Na-taurocholate 1 ml/kg into the main pancreatic duct of the dogs. Experimental dogs were divided into two groups based on the value of Respiratory Index (R-Index). Group A included 9 dogs in whom respiratory failure was not recognized (R-Index less than 0.5) and Group B included 9 dogs with respiratory failure (R-Index less than 0.5). All the dogs were sacrificed 12 hours after induction of pancreatitis, and histological findings were examined. Quantity of water in the lung (Qwl) was also measured by gravimetric method. Group B showed severe hypoxia with hypocapnia, and increase of A-aDO2, R-Index, and decrease of a/A PO2. Qwl in Group B increased significantly comparing with Group A. In biochemical study, increase of serum lipase, triglyceride, free fatty acid, and angiotensin converting enzyme were observed in Group B. These results indicate that respiratory failure with acute pancreatitis is due to lung edema following injury of the capillary of the lung. The role of free fatty acid liberated by lipolysis was suggested in the mechanism of pulmonary damage with acute pancreatitis.
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PMID:[Experimental study of respiratory failure with acute pancreatitis in dogs]. 241

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

Intravenous infusion of free fatty acid (FFA) produces an increase in the alveolar surfactant pool of the rabbit and pulmonary edema, hyperventilation, hypoxemia and hypocapnia. Previous studies suggested that alveolar PCO2 would be a regulator of intracellular storages of surfactant. In order to study the role of hypocapnia in the increase of lung surfactant in our experiments we administered 20 mg FFA X kg-1 X min-1 i.v. to rabbits breathing room air (n = 10) or 5% CO2, 21% O2, 74% N2 (n = 7). Disaturated phosphatidylcholine (DSPC) was determined in bronchial-alveolar lavage fluid as index of alveolar surfactant content, 5% CO2 in the inspired air prevented the hypocapnia and blocked the increase in DSPC induced by FFA (p less than 0.01). Pulmonary edema post-FFA was not changed by 5% CO2 administration. We conclude that hypocapnia produced by hyperventilation during FFA infusion would be an important factor in the increase of DSPC observed after FFA infusion.
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PMID:Role of hypocapnia in the alveolar surfactant increase induced by free fatty acid intravenous infusion in the rabbit. 308 86


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