Respiratory medicine: fighting for survival.
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Biomedical subjects
Publications and source records attributed to A Woodcock.
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In a patient who had a sudden onset of bilateral diaphragmatic paralysis after forceful neck manipulation complete, though gradual, recovery in lung function and transdiaphragmatic pressures was seen over three years. This is a previously unrecognised risk of neck osteopathy.
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In a canine model of acute ischemic lung injury, a hypertonic citrate solution (HTC) widely used for renal preservation in the United Kingdom, was compared with modified Euro-Collins' solution (ECS) currently the most widely clinically used pulmonary perfusate. Ten beagle dogs underwent left thoracotomy and exclusion of the left lung in situ. The lung was flushed with 30 ml/kg of either HTC or ECS and subjected to 60 min of warm ischemia. The circulation to the lung was then restored, the contralateral lung excluded, and the animal ventilated at a fixed FiO2 of 0.4 for 4 hr. Lung function was assessed by arterial oxygenation and hemodynamic measurements and, following sacrifice, by lung weight gain, bronchoalveolar lavage, and ultrastructural studies. Flush perfusion with HTC was associated with significantly less severe reperfusion injury, as determined by superior arterial oxygenation (PaO2 at 1 hr: HTC--152 mmHg [(95% confidence interval) CI] [122-182], ECS--59 [47-70]; PaO2 at 4 hr: HTC--124 [100-149], ECS--51 [42-61]), lower pulmonary vascular resistance index (PVRI at 4 hrs: HTC--838 dynes sec cm-5m-2 [651-1075], ECS--1233 [963-1588]); and lower lung weight (HTC--85 g [66-107], ECS--146 [114-184]). Bronchoalveolar lavage studies demonstrated an influx of neutrophils following reperfusion that was significantly less marked in the HTC group (increase in % neutrophils: HTC 24 [19-29], ECS 77 [72-82]). Lung injury assessed by electron microscopy tended to be less severe in the HTC animals. We conclude that HTC may offer an alternative superior to ECS for lung preservation.
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Bedding has been constructed with a vapour-permeable waterproof fabric that is impermeable to house dust mite antigen (Der p1). Der p1 levels per gram of mattress dust after 12 weeks' use of the new covering were 1% of levels in control samples from mattresses cleaned conventionally.
A total of 47 poor-risk small-cell lung cancer patients (elderly, poor performance status, recent myocardial infarction, or extensive-stage disease with biochemical abnormalities) were treated with a regimen of bolus ifosfamide at 1.5 g/m2 with equidose mesna as a 30-min infusion, followed by 100 mg oral etoposide daily for 8 days. Therapy was repeated every 3 weeks. The overall response rate was 60% (75% for limited-stage and 48% for extensive-stage disease), and the overall median survival was 7 months. Patients' performance status significantly improved with therapy (P less than 0.0001). Despite the poor-risk factors, the Manchester prognostic score was applied and verified. The median survival was 8 months for patients with a good prognosis, 6 months for those with an intermediate prognosis and 2.5 months for poor-prognosis patients (P = 0.0002). Therapy was well tolerated. The median WHO grade of haematological toxicity was 2 (range, 0-4). Only 10/226 (4%) courses were delayed due to leukopenia. Blood transfusions followed 18/226 (8%) courses. Intravenous antibiotics were given following 15/226 (7%) courses. No patient required platelet support. Poor-risk patients who have a good or intermediate Manchester prognostic score may benefit from this low-toxicity regimen.
The single-flush technique of lung preservation is thought to be enhanced by prostaglandin treatment. In order to test this hypothesis, ten beagle dogs underwent thoracotomy and in situ flush perfusion of the excluded left lung with 30 ml/kg of cold, modified Euro-Collins' solution. Group 1 (n = 5) received pretreatment with 30 ng/kg/min of PGI2 by infusion and as an additive to the flush (20 micrograms/L). Group 2 (n = 5) received no PGI2 and served as controls. Following 60 min of warm ischemia, the left lung was reperfused, the contralateral lung excluded, and the animal ventilated at a fixed FiO2 of 0.4 for 4 hr. The severity of reperfusion injury was assessed by arterial oxygenation and hemodynamic measurements and, following sacrifice, by lung weight gain and bronchoalveolar lavage and ultrastructural studies. PGI2 therapy resulted in significant amelioration of reperfusion injury, with superior oxygenation at both 1 and 4 hr (PaO2 at 1 and 4 hr, respectively; PGI2: 145 mmHg +/- 17.0 and 114 +/- 11.2; no PGI2: 59 mmHg +/- 5.8 and 51 +/- 4.5; P less than 0.01 at both times), lower pulmonary vascular resistance index at 4 hr (PVRI; PGI2: 913 dynes sec cm-5m-2 +/- 91; no PGI2: 1239 +/- 68; P less than 0.05) and lower lung weight (PGI2: 76 g +/- 4; no PGI2: 146 +/- 10; P less than 0.001). Bronchoalveolar lavage studies revealed an influx of neutrophils following reperfusion that was less marked in the PGI2 group (increase in % neutrophils; PGI2: 50.4 +/- 6.7; no PGI2: 76.9 +/- 6.0; P less than 0.05). Lung injury score assessed by electron microscopy was lower in the PGI2 group (PGI2: 5.2 +/- 1.1; no PGI2; 8.1 +/- 0.5; P less than 0.05). It is concluded that PGI2 treatment is protective against ischemic lung injury in this model.
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Nutritional selenium deficiency disease, due to low soil selenium content, is well recognized in British livestock. The adequacy of the selenium status of 25 healthy human volunteers, 50 blood donors, 94 general medical patients and 106 allergy clinic patients was investigated in 1987/8 by measuring serum selenium concentration and platelet glutathione peroxidase activity. Mean serum selenium concentration for the entire study population was 92 micrograms/l. Significant linear correlations between serum selenium concentration and peroxidase activity indicate that a substantial proportion of both healthy volunteers and medical patients are of low selenium nutritional status. Twenty-five per cent of healthy volunteers and 50 per cent of medical patients had serum selenium values below those required for full expression of selenium-dependent enzyme activity. Deficiency of the antioxidant activities of selenium and selenium-dependent enzymes may be relevant to geographical differences in morbidity from a wide range of human disease states.
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Quantitative studies on sunburn cell (SBC) production in mouse epidermis are reported. Ultraviolet radiation (UVR), 260-300 nm, produced a dose related effect with respect to SBC formation. Maximal spectral reactivity was at wavelengths shorter than 300 nm. In 8-methoxypsoralen (8-MOP) photosensitization, SBCs were also produced and this response is dose related with respect to long wave UVR dose. In fluorescein photosensitization, provoked by 487 nm light, SBCs were not produced. The response in 8-MOP photosensitization and 254 nm UVR (given alone) differed in respect of time course, but it is considered that both may perhaps to initiated by a DNA lesion.