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Biomedical subjects

M Miniati

Publications and source records attributed to M Miniati.

At least 37 records · Page 2Linked to original sources

[Clinical and therapeutic aspects of alcohol withdrawal syndrome].

In this review the authors describe the symptomatology, and the etiopathogenetic hypothesis of alcohol withdrawal syndrome. Many drugs are used in the treatment of alcohol withdrawal syndrome: carbamazepine, clonidine, chlormethiazole, phenytoin and other compounds; actually benzodiazepines are the most important drugs for symptomatic relief to prevent major withdrawal syndrome. Particularly attention is recommended to the period of suspension with the aim of reducing alcohol consumption and correcting alcohol-related psychosocial problems.

Alcohol Drinking↗

The value of portable chest roentgenography in adult respiratory distress syndrome. Comparison with computed tomography.

In 17 patients with adult respiratory distress syndrome, we used data derived from computed tomographic (CT) scan densitometric analysis to validate the value of portable chest roentgenograms in objectively estimating the amount of pulmonary edema. Chest roentgenograms and CT scans were taken in the same ventilatory conditions (apnea at 10 cm H2O of positive end-expiratory pressure [PEEP]); blood gas samples and hemodynamic parameters were collected at the same time. Roentgenographic analysis was undertaken by independent observers using two standardized scoring systems proposed in the literature. CT scan analysis was performed using the CT number frequency distribution and the gas lung volume (measured by helium dilution technique) to estimate quantitatively the lung density, the lung weight, and the percentage of normally aerated and nonaerated tissue. Knowing the mean CT number of the pulmonary parenchyma in a group of normal subjects, we also inferred the ideal lung weight expected in the study population and computed the excess tissue mass as the difference between actual and ideal lung weight. Both the roentgenographic scoring systems showed direct correlation with the pulmonary impairment as detected by CT scan densitometric analysis (CT number, percentage of nonaerated tissue, lung weight, and excess tissue mass; p less than 0.01) and inverse relation with the percentage of normally aerated tissue (p less than 0.01). We also found a relationship between roentgenographic scores and the impairment in gas exchange as detected by shunt fraction (p less than 0.05). We conclude that standardized reading of portable chest roentgenograms by means of scoring tables is a valuable tool in estimating the amount of pulmonary edema in a patient with adult respiratory distress syndrome.

Absorptiometry, Photon↗

Nuclear medicine in ARDS: clinical applications.

ARDS is still characterized by an exceedingly high mortality rate. Methods are then needed to detect ARDS at the earliest clinical stage. Over the last decade, radioisotopic techniques have developed, aimed at demonstrating an abnormal neutrophil sequestration in the lung or detecting functional alterations of the pulmonary alveolar-capillary barrier, which likely precede the onset of respiratory distress. Preliminary application of these techniques in patients with ARDS yielded conflicting results in terms of sensitivity and specificity. On the contrary, lung vascular abnormalities have been consistently observed in patients with ARDS studied by perfusion lung scanning. They consist of focal, non segmental perfusion defects, mostly peripheral and dorsal, with redistribution of blood flow to non-dependent lung regions. This scintigraphic pattern may be considered typical of ARDS since it is not observed in other acute lung disorders. Perfusion abnormalities on lung scans are detectable from the very early stage of ARDS and correlate with the severity of the syndrome as reflected by gas exchange, central hemodynamics, and chest radiography. Perfusion lung scanning may then be used in the early detection and evaluation of vascular injury in ARDS.

Endothelium, Vascular↗

Lung tissue binding of iodobenzyl-propanediamine: involvement of beta-adrenergic receptors.

The basic compound N-N-N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3- propanediamine (HIPDM) accumulates in human and rabbit lungs, where it forms a slowly effluxable pool. In isolated perfused rat lung, HIPDM is taken up by a saturable, energy-independent mechanism, which is competitively inhibited by imipramine, chlorpromazine and propranolol. To ascertain whether beta-adrenergic receptors are involved in the binding process of HIPDM to lung tissue, the ability of unlabelled HIPDM to displace the beta-adrenergic receptor ligand [125I]iodocyanopindolol (ICYP) from rabbit lung beta-receptors was examined. Lung microsomal membrane fractions (75 micrograms ml-1) were incubated at 37 degrees C for 3 h with 68 pM ICYP (with or without 1 microM of (+/-)-propranolol) in the presence of HIPDM (10(-10)-10(-3) M). Bound and free radioactivity were separated through glass-fibre filters and the retained radioactivity was counted in a gamma-spectrometer. HIPDM competed with ICYP for beta-adrenoceptors (13% displacement at 10(-5) M. 50% at 5 x 10(-5) M, and 90% at 2 x 10(-4) M). The inhibition curve of ICYP binding by HIPDM was similar to that observed for (-)-noradrenaline. Although the results of the in vitro studies cannot be extrapolated to in vivo conditions, they suggest that beta-adrenergic receptors may be involved in the observed lung uptake of the basic amine HIPDM.

Animals↗

Objective radiographic criteria to differentiate cardiac, renal, and injury lung edema.

To assess the value of the chest radiograph in differentiating various types of pulmonary edema, we retrospectively analyzed 119 films of patients with pulmonary edema caused by left heart decompensation (group 1;N = 56), renal failure (group 2; N = 19), and lung microvascular injury (group 3; N = 44). Chest radiographs were examined independently by two trained observers, unaware of the clinical diagnosis, according to a standardized reading table. The two observers assigned chest films to the corresponding group with an accuracy of 86% and 90%, respectively. To test the observers' objectivity, we used radiographic findings as input variables for discriminant analysis. Computer-generated numerical functions identified pulmonary edema etiology with an accuracy of 88% when considering the three groups together. When groups were compared as pairs, percentages of correct classification were 91% (group 1 vs. group 2), 93% (group 1 vs. group 3), and 100% (group 2 vs. group 3). Thus, a standardized reading of chest radiographs may be considered a reliable clinical method for identifying pulmonary edema etiology.

Heart Failure↗

Theoretical and practical considerations of measuring extravascular lung water.

The volume of extravascular lung water is currently measured in vivo from the difference in mean transit times of the extrapolated first-pass dilution curves of two indicators, one diffusible and the other confined to the intravascular space. To overcome the limitations of this method, one can prolong the measurement interval, introduce a highly diffusible indicator, or both. In the first case, recirculating indicators are measured and included in the computation by deconvolution of the mean transit time through the lung. In the second case, heat is used as the water indicator. In the third case, not yet explored, recirculating heat would be measured and long thermal transit times uncovered. In view of the complexity of the deconvolution method and the pitfalls of the thermal dilution method, a radiographic score of pulmonary edema may be more useful clinically to assess the volume of extravascular lung water in patients with heart disease or adult respiratory distress syndrome.

Animals↗

Factors affecting regional pulmonary blood flow in chronic ischemic heart disease.

To assess the effect of left heart disease on pulmonary blood flow distribution, we measured mean pulmonary arterial and wedge pressures, cardiac output, pulmonary vascular resistance, pulmonary blood volume, and arterial oxygen tension before and after treatment in 13 patients with longstanding ischemic heart failure and pulmonary edema. Pulmonary edema was evaluated by a radiographic score, and regional lung perfusion was quantified on a lung scan by the upper to lower third ratio (U:L ratio) of pulmonary blood flow per unit of lung volume. In all cases, redistribution of lung perfusion toward the apical regions was observed; this pattern was not affected by treatment. After treatment, pulmonary vascular pressures, resistance, and edema were reduced, while pulmonary blood volume did not change. At this time, pulmonary vascular resistance showed a positive correlation with the U:L ratio (r = 0.78; P less than 0.01), whereas no correlation was observed between U:L ratio and wedge pressure, pulmonary edema, or arterial oxygen tension. Hence, redistribution of pulmonary blood flow, in these patients, reflects chronic structural vascular changes prevailing in the dependent lung regions.

Blood Volume↗

Reabsorption kinetics of albumin from pleural space of dogs.

The reabsorption of albumin from the pleural space was measured in eight dogs receiving 0.5 ml intrapleural injection of 131I-labeled albumin and a simultaneous intravenous injection of 125I-labeled albumin. Plasma curves for both tracers were obtained over 24 h. The 125I-albumin curve served as input function of albumin for interstitial spaces, including pleura, whereas the 131I-albumin curve represented the output function from pleural space. The frequency function of albumin transit times from pleural space to plasma was obtained by deconvolution of input-output plasma curves. Plasma recovery of 131I-albumin was complete by 24 h, and the mean transit time from pleura to plasma averaged 7.95 +/- 1.57 (SD) h. Albumin reabsorption occurred mainly via lymphatics as indicated by experiments in 16 additional dogs in which their right lymph ducts or thoracic ducts were ligated before intrapleural injection. A pleural lymph flow of 0.020 +/- 0.003 (SD) ml.kg-1.h-1 was estimated, which is balanced by a comparable filtration of fluid into the pleural space. This suggests that, under physiological conditions, the subpleural lymphatics represent an important control mechanism of pleural liquid pressure.

Absorption↗

Pulmonary retention of iodobenzyl-propanediamine in humans. Effect of cigarette smoking.

N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propanediamine (HIPDM), a synthetic basic compound with high affinity for lung tissue of various animal species, was labeled with 123I and injected into normal smokers (n = 9) and into asymptomatic smokers (n = 9). Time/activity curves were recorded for 90 min by gamma camera. HIPDM lung clearance was described by two exponential components. In smokers, the mean time of the first component, 10 +/- 1.4 min (mean +/- SEM), did not significantly differ from that of nonsmokers (9.7 +/- 0.9 min), whereas the mean time of the second component (12.9 +/- 0.6 h) was longer than that of nonsmokers (6.7 +/- 0.2 h). The intercept to the ordinate of the second exponential component was significantly higher in smokers (90.3 +/- 1.5%) than in nonsmokers (80.7 +/- 1.9%). Control studies in rabbits showed that, 2 min after intravenous injection, 95% of HIPDM is taken up by the lung; time/activity curves were similar to those obtained in humans. The longer pulmonary persistence of HIPDM in smokers may reflect an increased number of cellular binding sites or may be the expression of hindered HIPDM biotransformation. The rabbit can be used as a model to further investigate HIPDM kinetics in relation to lung dysfunction.

Adolescent↗

Extravascular lung water.

Extravascular lung water (idQw1) is measured in vivo from the difference in mean transit times, computed by extrapolating the dilution curves, of two indicators, one freely diffusible, the other confined to the intravascular space. Using 3H2O it has been shown that idQw1 is smaller than the amount of extravascular water obtained from the difference between wet and dry lung weight (Qw1). Extrapolation allows one to use dilution curves for a short time, i.e., up to onset of obvious recirculation. Clearing the dilution curves or recirculation by deconvolution extends the observation time, which then becomes limited by sampling duration rather than onset of recirculation. This procedure entails recording recirculating tracers in the pulmonary artery (PA). Dilutions of tracers at input in PA and output in a systemic artery must be related to each other as continuous time functions. This is accomplished by means of a convolution integral. Deconvolution yields the frequency function of water molecule transit time in the extravascular lung space, l(t). In dogs and men, in both normal and edematous lungs, l(t) exhibits a knee and a fairly long tail. Extravascular lung water computed from l(t), idcQw1, agrees with Qw1 and correlates with data on the extravascular thermal volume of the lung and with radiographic findings of lung edema. A radiographic score of pulmonary edema may be used clinically to assess extravascular lung water in cardiac patients and in patients with adult respiratory distress syndrome.

Capillary Permeability↗

Interstitial distribution of charged macromolecules in the dog lung: a kinetic model.

A mathematic model was constructed to investigate conflicting physiologic data concerning the charge effect of continuous capillaries to macromolecules in the lung. We simulated the equilibration kinetics of lactate dehydrogenase (MR 4.2 nM) isozymes LDH 1 (pI = 5.0) and LDH 5 (pI = 7.9) between plasma and lymph using previously measured permeability coefficients, lung tissue distribution volumes (VA) and plasma concentrations (CP) in lung tissue. Our hypothesis is that the fixed anionic charges in interstitium, basement membrane, and cell surfaces determine equilibration rather than charged membrane effects at the capillary barrier, so the same capillary permeability coefficients were used for both isozymes. Capillary filtration rates and protein fluxes were calculated using conventional flux equations. Initial conditions at baseline and increased left atrial pressures (PLA) were those measured in animal studies. Simulated equilibration of isozymes over 30 h in the model at baseline capillary pressures accurately predicted the observed differences in lymph/plasma concentration ratios (CL/CP) between isotopes at 4 h and equilibration of these ratios at 24 h. Quantitative prediction of isozyme CL/CP ratios was also obtained at increased PLA. However, an additional cation selective compartment representing the surface glycocalyx was required to accurately simulate the initial higher transcapillary clearances of cationic LDH 5. Thus experimental data supporting the negative barrier, positive barrier, and no charge barrier hypotheses were accurately reproduced by the model using only the observed differences in interstitial partitioning of isozymes without differences in capillary selectivity.

Animals↗