Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bis(trifluoromethyl) disulfide (TFD) was originally designed for use as an agricultural fumigant. Inhalation of toxic doses of TFD results in varying degrees of pulmonary edema. The purpose of this study was to determine if exhaustive exercise would potentiate the toxic effects of TFD. One group of treadmill-acclimated rats was exercised to exhaustion following a 10-minute whole-body exposure to TFD. A second group was similarly exposed but not exercised. Two other groups of rats were sham exposed; one was exercised while one remained sedentary following the sham exposure. Twenty-four hours after exposure, the animals were sacrificed; the lungs were removed and weighed, and a portion was collected for histopathologic examination. The remaining lung tissue was allowed to dry to constant weight. There was no difference in endurance times between exposed and sham-exposed rats. There was a significant increase in the amount of pulmonary edema and associated pulmonary pathology in rats exercised following exposure to TFD. Eleven of twelve animals exercised following exposure to TFD and three of twelve animals which remained sedentary following exposure died by 24 hours. The degree of pulmonary pathology in all rats exposed to TFD was profound.
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PMID:The effects of exercise following exposure to bis(trifluoromethyl) disulfide. 181 57

Simple cardiopulmonary functions were studied serially in 26 mountaineers between sea level and an altitude of 25,200 ft. Up to 12,000 ft there was no altitude sickness, though there were complaints of leech bite (26.9%) and blisters (3.8%). One member died of exhaustion, two developed pulmonary oedema, one "flu" (at 15,600 ft) and one pleural rub (at 21,000 ft). Up to 16,000 ft altitude, 4 to 7.7% developed diarrhoea or epistaxis only, but at higher levels 25 to 50% subjects developed several symptoms, besides excessive dyspnea. These included diarrhoea (35-60%), vomiting (30%) abdominal pain (35-60%), rectal bleeding (15%), chest pain (10-40%), dry cough (40-60%), giddiness (30%) and poor memory (7.7%). A small rise in blood pressure was seen (for systolic at lower and diastolic at greater altitudes). After 18,200 ft the steady increase seen in VE slowed and the rise in heart rate and respiratory rate (f) became steeper. After a small rise at 7,800 ft, FVC and FEV1 showed a gradual decline at higher altitudes. After a large initial increase in PEFR up to 12,000 ft, a gradual decline was seen. The mean weight loss during the expedition was 8 +/- 2.7 kg. These changes seem to be due to an incomplete acclimatisation, which future mountaineering teams should take into consideration to avoid health problems and improve performance.
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PMID:Cardiopulmonary functional changes in acute acclimatisation to high altitude in mountaineers. 225 31

The purpose of this study was to determine whether the tachypneic breathing pattern of constant work rate, heavy exercise (CWE) is unique to CWE or whether it represents the usual pattern of the respiratory control system at high levels of ventilation (VI). We compared breathing pattern in ten healthy subjects (age 20-29 years) during CWE and maximal incremental exercise (MIE) on a bicycle ergometer. Work rate was constant at 76% of maximum work rate in CWE and progressively increased by 25 watts/minute until exhaustion during MIE. Breathing pattern was examined at matched levels of VI equivalent to 80% and about 100% of maximum VI during CWE (97.1 and 121.4 L.min-1, respectively). Exercise duration (mean+standard deviation) was 13 +/- 6 and 12 +/- 1 min during CWE and MIE, respectively (P = NS). Tidal volume (VT) fell by an average of 0.20 L towards the end of CWE, but was maintained relatively high and constant towards the end of MIE. At high, but not lower, matched levels of VI breathing pattern during CWE was significantly more rapid and shallow than that during MIE. The tachypnoea of CWE did not correlate with the progressive rise in VI, oxygen uptake or cardiac frequency during CWE. We conclude that (1) CWE is associated with a tachypneic influence that is absent or less during incremental exercise; this tachypnea is most marked at the end of CWE. (2) The tachypnoea of CWE is not part of a generalized rate accelerating process during CWE. The mechanism(s) underlying the tachypnoea are unclear but it may be related to inspiratory muscle fatigue, pulmonary oedema, and/or altered respiratory mechanics.
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PMID:Differential ventilatory control during constant work rate and incremental exercise. 793 15

Non-invasive continuous positive airway pressure (CPAP) seems to decrease the need for intubation in patients with severe cardiogenic pulmonary oedema (CPO) in the intensive care unit. The goals of our study were to delineate indications for CPAP in the emergency department, and to confirm its usefulness in such a setting. We retrospectively assess the evolution of all patients ventilated under CPAP for an acute hypoxaemic respiratory failure over a 1-year period (n = 64 patients). Hypercarbia and respiratory acidosis were present in most patients with CPO (PaCO2 = 54.4+/-22.3 mmHg; pH = 7.27+/-0.13), according to respiratory exhaustion, although initial PaCO2 was low in the pneumonia group. There was a significant improvement of arterial blood gases after 1 hour of ventilation in the CPO group (PaO2 = 254.1+/-121.0 mmHg; PaCO2 = 44.0+/-12.6 mmHg; pH = 7.34+/-0.08; p < 0.0001 for both parameters). In the pneumonia group, oxygenation was also improved but with the persistence of a significant shunt (PaO2 = 157.6+/-84.4 mmHg). Fifty-four patients (84%) were considered as successfully ventilated under CPAP, with no need for intubation and a favourable evolution, mainly in the CPO group. No side effects were reported. In conclusion, CPAP is a useful and easy-to-use ventilatory device in the emergency department. It is now one of our first line treatments during prehospital and emergency care of patients with CPO.
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PMID:Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department. 982 33

The present work focuses on pulmonary gas exchange during repeated rowing to exhaustion and the recovery of pulmonary diffusion capacity for carbon monoxide (DL) after exercise in healthy young subjects. The components of DL are examined at rest using the single breath method at two different alveolar O2 tensions. Electrical impedance and 99mTechnetium labelled erythrocytes were used to evaluate the recovery of blood distribution. Special attention has been given to the role of the inspiratory muscles as a limiting factor for VO2max and performance. The documentation in this study of a reduced DL several hours after exercise conflicts with the prerequisites of optimal conditions for high metabolic rates in elite athletes. Even low intensity exercise induces a reduction in DL, and together with the fact that a diuretic does not attenuate this decrease, emphasises that the reduction in DM is not due to an interstitial pulmonary edema. The major part of the reduction is due to a decreased CBV reflected in a reduction of VC and a minor part is caused by an injury to the membrane component carried over from exercise. The ability in athletes to repeat exhaustive exercise within 2 h indicates that the slow recovery of DL is not combined with either impaired pulmonary gas exchange or performance. Thus, an acute diffusion limitation and a low pH cause the desaturation in some athletes during exhaustive exercise. Despite the inspiratory muscles having a slower response to endurance training compared with the cardiovascular system, selective training of the inspiratory muscles does not improve either VO2max or performance. This indicates that maximal inspiratory pressure is not a limiting factor for maximal exercise and that the stimuli to increase VA depends on an increased metabolic rate; stressing the role of the peripheral chemoreceptors. Together with the post-exercise decrease in ANP, the reduction in DL may be involved in the mechanism increasing the total blood volume in endurance trained athletes.
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PMID:Pulmonary function after exercise with special emphasis on diffusion capacity. 1091 85

This review summarizes current literature on pulmonary oedema triggered by above-ground exercise in healthy humans from studies that use various imaging techniques to detect oedema. Eleven studies were identified, comprising of 137 subjects (mean age = 28 years). Eighty per cent (n = 110) were males, and 20% (n = 27) were female. The studies were grouped into three different categories according to the severity of the exercise protocol, which were either prolonged, submaximal exercise of 15-min to 2 h in duration at approx. 50-75%VO(2max) and not to exhaustion (PROLONGED, n = 44), a VO(2max) test lasting 16-20 min in which the intensity of exercise was only maximum for about 2 min at the end of the test (GXT, n = 15), and maximum or near maximum effort exercise protocols at or near volitional exhaustion where the goal was to finish in the fastest possible time or maintain the highest possible workload (MAX EFFORT, n = 78). Only 16% of the subjects showed signs of oedema from PROLONGED exercise and no subjects (0%) showed signs of oedema from GXT exercise. Surprisingly, approx. 65% of the subjects showed signs of oedema triggered by MAX EFFORT exercise (chi(2) test of association; P < or = 0.01), which was independent of both sex, the level of hypoxia (inspired PO(2) = 106-118 mmHg vs. 149 mmHg), the timing of the post-exercise imaging (<10, >30 but <60 min, or >60 min) and VO(2max) (approx. 3.0 vs. approx. 4.8 L min(-1)). The data suggests that the chances of triggering pulmonary oedema from exhaustive MAX EFFORT exercise is 4x more compared with PROLONGED exercise. As well, the likelihood of triggering pulmonary oedema may be independent of lung size, sex, moderate levels of hypoxia, and aerobic fitness.
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PMID:Evidence of pulmonary oedema triggered by exercise in healthy humans and detected with various imaging techniques. 1736

Exposure to heat disturbs the homeostasis of body water, serum osmosis, and core temperature, resulting in the development of heat cramp, heat syncope, heat exhaustion, and heat stroke. Commonly coexisting risks are humidity, windlessness, infrared radiation, physical exertion, continuous work, chemical protective clothing, and lack of acclimatization. Exposure to cold constricts peripheral arteries and reduces metabolism, resulting in the development of chilblains, frostbite, immersion foot, and hypothermia. Wind, water immersion, and alcohol drinking will aggravate the symptoms. Exposure to abnormal pressure underwater or inside caissons or air cabins compresses or distends closed cavities inside the body, resulting in squeeze, nitrogen narcosis, oxygen intoxication, decompression sickness, reverse block, lung edema, and arterial gas embolism. Multifaceted preventive measures and on-site emergency care should be undertaken.
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PMID:[Disorders caused by heat, cold, and abnormal pressure]. 2460 19

It is known that intracranial hemorrhage (ICH) is accompanied by the development of neurogenic pulmonary edema and insufficiency of surfactant function. The present study was undertaken for evaluation of the role of vagal afferents in the mechanisms of ICH effects on pulmonary surfactant and water balance of the lung. We explored the surface activity and biochemical composition of surfactant, as well as blood supply, total, intravascular and extravascular fluid content in lung after ICH, simulated by intraventricular administration of autologous blood against the background of bilateral blockade of capsaicin-sensitive vagal affere its. The blockade was caused by the capsaicin application (50 mcmol) on the cervical part of the nerves. Intracerebralhemorrhage was accompanied by the decrease of surfactant activity which appeared by the enhancement of minimal, maximal and static surface tension of bronchoalveolar lavage fluid (BAL), the reduction of total phospholipids including their main fraction phosphatidylcholine, the increase of lysophosphatidyicholine content and hyperhydration of the lung. The level of total proteins in BAL elevated, confirmed the enhanced permeability of the alveolar-blood barrier. The exhaustion of neuropeptides in capsaicin-sensitive vagal afferents led to the partial restoration of surface active properties of lung, normalization of phospholipids and protein contents and water balance parameters. The obtained results suggest that capsaicin-sensitive vagal afferents play a pivotal role in the disturbances of surfactant function and water balance of the lung after ICH.
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PMID:[Surfactant and water balance of lung in intracerebral hemorrhage at conditions of capsaicin blockade of vagus nerve]. 2601 24

We report a case of fatal hyponatremic encephalopathy in a child who was forced to exercise as a form of punishment. A 9-year-old girl with attention-deficit/hyperactivity disorder was forced to run repeated 50-ft sprints to the point of exhaustion by her grandmother as punishment for taking candy from a classmate. After more than 3 hours of forced running, the child collapsed, began to vomit, and had repeated clonic seizures. Upon presentation to the emergency department, she was nonresponsive with a Glasgow Coma Scale score of 11 and had noncardiogenic pulmonary edema with serum sodium of 117 mEq/L. She was treated with antiepilectic medications and transferred to a university children's hospital where she later died. On postmortem examination, she was found to have massive cerebral edema with transtentorial herniation and pulmonary edema. Her clinical presentation closely resembled exercise-associated hyponatremic encephalopathy seen in adult endurance athletes. This appears to be the first report of fatal exercise-associated hyponatremia in a child.
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PMID:Fatal Hyponatremic Encephalopathy as a Result of Child Abuse From Forced Exercise. 2660 Feb 33

In acute hypoxemic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) patients, spontaneous breathing is associated with multiple physiologic benefits: it prevents muscles atrophy, avoids paralysis, decreases sedation needs and is associated with improved hemodynamics. On the other hand, in the presence of uncontrolled inspiratory effort, severe lung injury and asynchronies, spontaneous ventilation might also worsen lung edema, induce diaphragm dysfunction and lead to muscles exhaustion and prolonged weaning. In the present review article, we present physiologic mechanisms driving spontaneous breathing, with emphasis on how to implement basic and advanced respiratory monitoring to assess lung protection during spontaneous assisted ventilation. Then, key benefits and risks associated with spontaneous ventilation are described. Finally, we propose some clinical means to promote protective spontaneous breathing at the bedside. In summary, early switch to spontaneous assisted breathing of acutely hypoxemic patients is more respectful of physiology and might yield several advantages. Nonetheless, risk of additional lung injury is not completely avoided during spontaneous breathing and careful monitoring of target physiologic variables such as tidal volume (Vt) and driving transpulmonary pressure should be applied routinely. In clinical practice, multiple interventions such as extracorporeal CO2 removal exist to maintain inspiratory effort, Vt and driving transpulmonary pressure within safe limits but more studies are needed to assess their long-term efficacy.
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PMID:Spontaneous breathing: a double-edged sword to handle with care. 2882 67


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