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Biomedical subjects

R Duranti

Publications and source records attributed to R Duranti.

78 records · Page 5Linked to original sources

Respiratory muscle overloading and dyspnoea during bronchoconstriction in asthma: protective effects of fenoterol.

Whether, and to what extent, beta 2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 micrograms of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VT was expressed both in actual values and as % of IC. Changes in VT (%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplsw was expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw (%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1 of > or = 40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1 was similar after placebo and fenoterol, while increase in RL was lower after fenoterol (P < 0.005); (ii) VT(%IC) increased less after fenoterol (P < 0.027); (iii) increases in Pplsw (%Pplsn) was lower after fenoterol (P < 0.001); (iv) delta Borg (from saline) was lower (P < 0.01) after fenoterol; (v) differences in delta Borg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2 = 0.67). In conclusion, at UDB 100 micrograms of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1 alone.

Adrenergic beta-Agonists↗

Intrathecal cholecystokinin interacts with morphine but not substance P in modulating the nociceptive flexion reflex in the rat.

The effect of intrathecal (IT) cholecystokinin (CCK), substance P (SP) and morphine (MO) on spinal cord excitability was studied in decerebrate, spinalized rats. CCK had a weaker facilitatory effect on the nociceptive flexion reflex than SP. The possible functional significance of the coexistence of CCK and SP in neurons projecting to the spinal cord was tested by coadministration of the two peptides. At the doses tested no synergistic interaction on the reflex was found with CCK and SP. IT MO caused a brief enhancement followed by a prolonged depression of the reflex. A high dose of CCK injected prior to MO increased the facilitatory effect and decreased the depressive effect of the opiate on the reflex. The effect of desulfated (D) CCK was similar to CCK but at a higher dose. Naloxone (NAL) had a similar effect as CCK when administered prior to MO. The MO-induced depression of the reflex was readily reversed by NAL, but not by CCK. The results indicate that CCK may prevent the inhibitory effect of MO on spinal cord excitability to nociceptive stimulation, but does not reverse it. CCK may alter the balance of excitation-inhibition between various types of dorsal horn interneurons that are involved in the transmission of nociceptive information.

Animals↗

Control of breathing in normal subjects and in patients with chronic airflow obstruction.

In order to assess ventilatory control in patients with chronic airflow obstruction (CAO), the present study was carried out in nine patients with chronic obstructive pulmonary disease (COPD), eight asthmatics and nine normal subjects. We analysed the components of the respiratory control system at three levels: neural, assessed by diaphragmatic electromyography (EMGd), muscular, assessed by mouth occlusion pressure (P0.1), and ventilatory, assessed by mean inspiratory flow (VT/TI). EMGd was recorded by surface electrodes. During a CO2 rebreathing test, patients showed a normal or greater EMGd response slope (EMGdS), while for a given degree of EMGdS, P0.1 response slope (P0.1S) was found to be significantly reduced; in contrast, for a given degree of P0.1S, VT/TI response slope (VT/TIS) was found to be significantly reduced in COPD patients only. These data show that, compared to normal subjects, patients with CAO have a normal or increased neural component of the respiratory activity (EMGdS) and a relatively lower neuromuscular coupling (P0.1S/EMGdS). Probably due to different parenchymal and airway involvement, musculoventilatory transfer (VT/TIS/P0.1S) was found to be reduced in COPD patients but not in asthmatics. A complementary study, showing a good agreement between surface and oesophageal EMGd seems to confirm that surface EMGd is a useful and promising tool for clinical investigation.

Asthma↗