PubMed · 14999310
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Shaun Holt, Richard Beasley. 2004-01-30. Buteyko pseudoscience.. https://pubmed.ncbi.nlm.nih.gov/14999310/
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In order to identify if there were sex differences in lead (Pb) lung concentrations and in bronchiolar response after its inhalation, a mice inhalation model was conducted. Sixty CD-1 adult mice from each sex inhaled separately, lead acetate 0.1 M for 1 h, thrice weekly during 15 days. Animals were evaluated for Pb-lung concentrations by atomic absorption spectrometry and for morphological evaluation by scanning electron microscopy (SEM). Higher Pb-lung concentrations were determined in females, however, more cell damage was found in males, finding that correlated with an increased loss of the nonciliated bronchiolar cells (NCBC) more sloughing and necrosis. Differences in particle clearance, oxidative stress handling, cytokines pathway activation and cytochrome P450 enzymes activity, all influenced by sex hormones, might be a possible explanation for our findings. The relevance of further studies in this field is stressed, as well as its relation to the different development expected for each sex in disease evolution, possible complications and treatment response.
This study compares the pulmonary response to an inhaled highly soluble hydrochloride (CAD-HCl) with a low soluble sulphate salt (CAD-SO4) of a dicationic amphiphilic drug (CAD). These salts are known to accumulate in the lung. The bioavailability through gastrointestinal uptake is poor. Wistar rats and beagle dogs received repeated 1 h/day inhalation exposures over 1-4 weeks. The focus of this analysis is to appraise the correlation of markers of effects related to pulmonary phospholipidosis and cytotoxicity relative to the concentration of CAD in the lung tissue, alveolar macrophages and serum. Rats and dogs are known to experience remarkable differences in their respiratory minute volumes and respiratory patterns. In order to facilitate dosimetric comparisons, identical exposure paradigms and methodological procedures were selected. Over a wide range of cumulative dosages, the CADs bound to lung tissue and cells in bronchoalveolar lavage (BAL) paralleled, whilst no clear association existed in terms of plasma concentrations. This suggests that analysis of the fractional loading of BAL-cells (mainly alveolar macrophages) with CAD or CAD-surfactant complexes is amenable to monitor the accumulation of CADs in the lung. In terms of the comparative phospholipidosis-inducing potency, the CAD-HCl was more potent as compared to CAD-SO4. Following dosimetric adjustments, rats and dogs appeared to be equally susceptible to phospholipidosis. In summary, when exposed to equivalent concentrations of CADs, dogs did not demonstrate a markedly different susceptibility than rats. With regard to the relative intensity of changes, the increase of phospholipids in BAL-fluid and especially BAL-cells correlated with the cumulative exposure dose. Thus, with regard to probing the extent of CAD-induced 'overloading' of alveolar macrophages pharmacokinetic determinations in BAL-cells are considered superior to determinations in plasma. Additional advantages of using the alveolar macrophage as denominator to normalize pulmonary drug concentrations include comparisons across species, and exposure regimens are feasible based on almost readily available endpoints in both pre-clinical and selected clinical studies.
The assumption that ozone is not only a strong oxidant, but also an important inflammatory mediator, is heavily supported by the ample literature on the pulmonary toxicity and biological effects of environmental ozone and by the recent discovery that antibodies, human neutrophils, and inflammatory lesions catalyze the formation of ozone in vivo. We hypothesized that the pulmonary inflammation in asthma involves a vicious circle of ozone production and recruitment of white blood cells, which produce more ozone. Accordingly, we predicted that electron-rich olefins, which are known ozone scavengers, could be used for prophylactic treatment of asthma. In particular, volatile, unsaturated monoterpenes, could saturate the pulmonary membranes and thereby equip the airways with local chemical protection against either exogenous or endogenous ozone. Here we present experimental evidence using a sensitized rat model to support this hypothesis. Examination of the pulmonary function of sensitized rats that inhaled either limonene (unsaturated, ozone scavenger) or eucalyptol (saturated, inert to ozone) showed that limonene inhalation significantly prevents bronchial obstruction while eucalyptol inhalation does not cause any effect. The anti-inflammatory effect of limonene was also evident from pathological parameters, such as diminished peribronchiolar and perivascular inflammatory infiltrates.