No abstract

Inhaled furosemide has been shown to reduce the bronchoconstriction induced by several indirect stimuli, including ultrasonically nebulized distilled water (UNDW). Because the protective effect could be due to the inhibition of the Na(+)-2Cl(-)-K+ cotransport system of bronchial epithelium, we have compared the protective effect of inhaled furosemide with that of inhaled torasemide, a new and more potent loop diuretic, on UNDW-induced bronchoconstriction in a group of 12 asthmatic subjects. UNDW challenge was performed by constructing a stimulus-response curve with five increasing volume outputs of distilled water (from 0.5 to 5.2 ml/min) and the bronchial response expressed as the provocative output causing a 20% fall in FEV1 (PO20UNDW). On different days, each subject inhaled an equal dose (28 mg) of furosemide and torasemide in a randomized, double-blind, placebo-controlled study 5 min prior to an UNDW challenge. Furosemide and torasemide had no significant effect on resting lung function. The geometric mean value of PO20UNDW measured after placebo was 1.73 ml/min. This was significantly lower than that recorded after furosemide (4.25 ml/min; p < 0.025), but not after torasemide (3.05 ml/min; p = 0.07). Inhaled furosemide totally blocked bronchial response to UNDW in five subjects. In two of five subjects the response was also blocked by inhaled torasemide. A remarkable increase in diuresis was noted only after torasemide in most subjects. We conclude that inhaled furosemide has a better protective effect than does inhaled torasemide against UNDW-induced bronchoconstriction. However, the protective effect of furosemide is variable, with some asthmatic patients showing no change in bronchial response to UNDW.(ABSTRACT TRUNCATED AT 250 WORDS)

β-Blockers are competitive antagonists at β-adrenergic receptors (β-AR) and are a life-saving form of treatment in different cardiovascular diseases (CVD). Despite current guidelines supporting the use of selective β₁-blockers in patients with CVD and especially in heart failure (HF), they are still largely underused, mostly as a consequence of the presence of chronic obstructive pulmonary disease (COPD). In primary care, prevalence of COPD in patients with HF is approximately 25%, and it will rise in the next years. In the general population, only 20% of COPD patients with HF are treated with β-blockers. β-Blockers may result in pulmonary adverse effects that are relevant to COPD patients. Bronchoconstriction may be the consequence of: absence of cardioselectivity; loss of cardioselectivity at high doses, and unopposed stimulation of cholinergic muscarinic M₂ receptors. The concern of inducing bronchospasm is the more likely explanation of a poor prescription of β-blockers in patients with CVD also suffering from COPD. However, under carefully controlled conditions, which include close monitoring of lung function and appropriate selection of the drug and titration of the dose on a case-by-case basis, selective β₁-blockers can be safely administered to most patients with COPD. Pneumologists and cardiologists should develop a detailed and standardized protocol to guide the use of selective β₁-blockers in everyday practice, which could significantly reduce the physicians’ mistrust of β-blockers in COPD patients.

No abstract

Recent evidence has suggested that human neoplastic patients show decreased blood histamine levels and cutaneous responses to intradermal histamine. In this study we evaluate the skin response to intradermal injections of histamine and IgE levels in 34 male patients with lung cancer (of which 21 had metastasis) and in 16 control subjects. Analysis of our data does not reveal any difference in the areas of wheal and flare between control subjects and lung cancer patients with or without metastasis. Moreover the evaluation of the different histologic cell type of lung cancer provides the same results. In addition, the sensitivity (Histamine Threshold Concentration) and reactivity (slopes) to histamine is not statistically different. No difference is found for IgE levels between controls and cancer patients. In the light of our finding we believe that in lung cancer patients skin response to intradermal histamine is not decreased, and therefore that the hypothesis concerning the existence of H1-histamine receptor antagonist released by tumour is not confirmed.