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Biomedical subjects

L Allegra

Publications and source records attributed to L Allegra.

9 recordsLinked to original sources
PubMed1979

[Changes in the acid-base and water-electrolyte balance induced by salbutamol. "In vivo" studies in patients with chronic broncho-pulmonary disease and "in vitro" by tonometry of venous blood].

The Authors studied the effects of e.v. Salbutamol evaluating the acute "in vivo" variations of acid-base and hydro-electrolitic balance in 16 chronic obstructive lung patients undergoing e.v. drug administration, and also ionic variations "in vitro" of venous blood samples incubated and tonometrated with the drug. The results "in vivo" do not show variations of acid-base equilibrium (paO2, paCO2, pH, HCO3-); whereas diminution of haematocrit (Ht), rise of urinary osmolarity and variations of hydro-electrolitic balance (Na+, K+, Cl-) are demonstrated. The results "in vitro" do not show considerable variations on ionic assessment. These data, according to the other latest result, indicate the possible role of haemodilution. We think that the explanation of these phenomena could be a modification of renal water and electrolytes reabsorption, likely under the influence of antidiuretic hormone (ADH), stimulated in the hypothalamus and activated also by the beta-stimulant drug at tubular cell receptors.

Acid-Base Equilibrium↗
PubMed1979

[Comparative evaluation of the respiratory function and the acid-base equilibrium in patients with chronic bronchopulmonary disease after intravenous administration of 5 beta receptor agonists].

The Authors studied lung mechanics, acid-base balance parameters, arterial blood pressure and pulse rate in five different groups of chronic obstructive lung disease patients, undergoing e.v. different bronchodilators. The drug were: 1. group: 500 gamma of orciprenalina; 2. group: 500 gamma of idrossi-fenil-orciprenalina; 3. group: 200 gamma of salbutamolo; 4. group: 100 gamma of trimetochinolo; 5. group: 500 gamma of terbutalina. The comparative analysis of bronchodilators, their cardiovascular effects and on acid-base balance indicate that mainly salbutamol and trimetochinol have negligeable adverse effects.

Acid-Base Equilibrium↗
PubMed1977

Aspects of bronchial reactivity to prostaglandins and aspirin in asthmatic patients.

The behaviour of bronchial reactivity to PGF2alpha was studied in asthmatic patients under various experimental conditions. Premedication with aminophylline, i.v., and, to a lesser extent, with DSCG afforded a partial protection, while beclomethasone dipropionate was inactive under this point of view. Diftalone, a new non-steroid anti-inflammatory agent, was well tolerated in 9 aspirin-intolerant asthmatic patients, and did not modify the bronchial response to PGF2alpha which was found to be generally lower then that of other aspirin-tolerant asthmatic patients. PGE 1-2 and DSCG prevented the bronchospasm induced by inhalation or ingestion of acetylsalicylic acid in a small group of patients. Good protection was also reached with PGE1-2 in the exercise-induced bronchospasm.

Adolescent↗
PubMed1976

[Clinico-radiological and functional aspects of respiratory syndromes caused by collagen diseases].

The clinical and radiological features in 100 patients with collagen diseases (rheumatoid arthritis, lupus, sclerodermia, dermatomyositis, and panarteritis nodosa) were compared with respiratory performance. 56 patients were drawn from the series of Pende et Al. and 44 from a personal series. The results are set out in tables and graphs. It was found that lung lesions due to collagen disease have no special clinical and radiological features. Respiratory performance is that of a restrictive syndrome that gradually progresses from A.R. to E.S., S. and P.M., accompanied by obstruction of the large airways, as shown by hyperinsufflation in sclerodermia and reduced specific conductance in rheumatoid arthritis.

Adult↗
PubMed1976

Clinical, functional and pathogenetic aspects of bronchial reactivity to prostaglandins F2alpha, E1, and E2.

Based on our results and on those reported in literature, we may draw the following conclusions. As a rule, asthmatic patients are markedly more sensitive than normal subjects to the bronchoconstrictive action of PGF2alpha by aerosol. However, the individual response is quite variable, which predicts and justifies some exceptions. On this subject, we found a peculiar exception in a female patient with extrinsic asthma, who tolerated abnormally large amounts of PGF2alpha. In contrast, we found a normal subject, who developed a bronchial hypersensitivity to PGF2alpha of frankly asthmatic type, following a moderate postinfluenzal bronchitis. Intravenously PGF2alpha loses the most part of its bronchoconstrictive effect, probably because it is rapidly metabolized before it may reach the bronchial receptors involved in the bronchospastic response. On the contrary, the action on vascular smooth muscle of the pulmonary circulation is evident, just because it is reached before the above transformation, mainly performed by 15-PG-dehydrogenase. An important component of the PGF2alpha-induced bronchospasm, although varying individually, is surely nonspecific, as it is shown by the protection obtained with an atropine-like agent. The moderate but significant protection obtained with DSCG, may be interpreted in a way similar to the one exerted again by DSCG on other nonspecific stimuli. Since indoramine has no effect in preventing PGF2alpha-induced bronchospasm, the intervention of bronchial alpha-receptors in the pathogenesis of this type of bronchospasm may be excluded. Nonsteroid antiinflammatory agents do not seem to change in asthmatic patients bronchial reactivity to PGF2alpha, as was found recently with other specific and nonspecific stimuli. Our studies do not modify current thought regarding the poor present therapeutic value of PGE as bronchodilator agents. Prospects are no better with the stereoisomer of PGF2alpha, PGF2beta (41), with endoperoxides PGG2 and PGH2 (42) and with the analogues 15-methyl-PGE2, 15-epi-PGA2, and 8-iso-PGE1 (43). However, it is reassuring that, even in the absence of a demonstrable bronchodilator effect, both PGE1 and PGE2 are capable to prevent in a large degree the specifically and nonspecifically induced bronchospasm.

Adult↗