Clinical science
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1. The effect of oral magnesium aspartate hydrochloride on monocrotaline (MCT)-induced pulmonary arterial hypertension was evaluated in rats. 2. A single subcutaneous injection of MCT, a pyrrolizidine alkaloid of plant origin, induces significant morphological changes in pulmonary vessels, pulmonary arterial hypertension and right ventricular hypertrophy in rats by 3 weeks. 3. ⋯ Pulmonary artery pressure, right ventricular hypertrophy, lung pathology, organ weights and serum electrolytes were assessed 3 weeks after a single subcutaneous injection of MCT. Seventy-five per cent of the rats treated with MCT and oral Mg2+ (12 out of 16) showed significant reduction in pulmonary arterial hypertension, arterial pathology and right ventricular hypertrophy. 5. Our data indicate that Mg2+ attenuates experimentally induced pulmonary hypertension, possibly either by modulating the intracellular Ca2+ level and/or by directly affecting the pulmonary endothelial cell-smooth muscle cell complex involved in metabolism and maintenance of pulmonary vascular resistance.
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1. Incomplete mixing of alveolar gas may be expressed as an equivalent alveolar dead space serving a remaining alveolar space in which mixing is regarded as complete. Calculation of this dead space during multiple-breath, inert gas wash-in or wash-out leads to an estimate of 'multiple-breath alveolar mixing efficiency' (MBME). 2. ⋯ Patients with CAL showed a big increase in the volume of the conducting airways or 'series dead space' (VDS) for both gases, and VDS was always bigger for SF6 than for He. This very large VDS appears to be the main reason for wash-in delay in these patients, followed by impaired diffusive mixing in the peripheral air spaces. Ventilation maldistribution may play little part in the mixing defect.(ABSTRACT TRUNCATED AT 250 WORDS)
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Letter Randomized Controlled Trial Clinical Trial
Dihydroxyphenylglycol and dihydroxymandelic acid during intravenous infusions of noradrenaline.
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Beat to beat changes in cardiac output during standardized Valsalva's manoeuvres were recorded using electrical bioimpedance cardiography in 13 normal subjects. Cardiac output increased by 12 +/- 5% after 1 s of straining solely because of an increase in heart rate. ⋯ There was a sustained increased in cardiac output (maximum +17 +/- 4%) in the late post strain period. The mean coefficient of variation in impedance measurements of cardiac output was 6.8% during all parts of Valsalva's manoeuvre, with no single value exceeding 10%.