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Biomedical subjects

J Cerrina

Publications and source records attributed to J Cerrina.

88 records · Page 5Linked to original sources
PubMed1984

Effects of a single bolus of urokinase in patients with life-threatening pulmonary emboli: a descriptive trial.

To evaluate hemodynamic, angiographic, and biological effects of a single bolus of urokinase, an open descriptive trial was conducted in a homogeneous group of 14 patients with acute life-threatening pulmonary emboli and without prior cardiopulmonary disease. For every patient the efficacy of the treatment was evaluated by comparing control and posttherapeutic values after the bolus injection of 15,000 IU/kg body weight urokinase (urinary source) administered in 10 min in the right atrium, followed by continuous intravenous full-dose heparin therapy. In two patients clinical status, hemodynamics, vascular obstruction, and biological (fibrinogen and plasminogen levels) parameters remained unchanged. One of these two patients died, making the mortality rate for the whole group 7%. Twelve of 14 patients showed rapid clinical improvement. Evaluation at 12 hr demonstrated significant decreases in pulmonary vascular obstruction (Miller index, 34%), total pulmonary vascular resistances (37%), and fibrinogen and plasminogen levels (41% and 40%, respectively), without any significant change in cardiac index. The hemodynamic sequential measurements performed (1,3, 6, and 12 hr) in seven of the 12 improved patients showed that the greatest percentage of the total hemodynamic improvement occurred within the first 3 hr after bolus administration of urokinase. No severe hemorrhagic complications were observed. Because of its rapid efficacy and its low cost, the bolus technique appeared particularly useful in the treatment of patients with acute life-threatening pulmonary emboli.

Aged↗
PubMed1983

Effects of diltiazem and other Ca2+ antagonists on guinea-pig tracheal muscle.

The effects of diltiazem and 3 other Ca2+ antagonists (verapamil, nicardipine, bepridil) were studied on isolated guinea-pig tracheal preparations which were contracted with several agonists. Assessment of the contractile agonists was performed under physiological conditions as well as in Ca2+-depleted solutions. The order of potency of the contractile agonists was LTD4 greater than ACh greater than 5-HT greater than Hist greater than BaCl2 greater than TEA greater than KCl. The efficacy of the physiological agonists ACh, Hist and LTD4 was moderately depressed in Ca2+-free solutions while the responses to non-specific agonists and 5-HT were markedly reduced. Diltiazem and verapamil reduced basal tone at concentrations greater than or equal to 10(-4) M. Diltiazem displaced all agonist concentration-effect curves to the right. The four Ca2+ antagonists studied had a marked effect on non-physiological agonists as compared to that on physiological agents. Increasing Ca2+ concentration only partially reversed the inhibitory effect of diltiazem.

Airway Resistance↗
PubMed1983

Effect of the Ca2+ antagonist nifedipine on the release of platelet-activating factor (PAF-acether), slow-reacting substance and beta-glucuronidase from human neutrophils.

Ca2+ antagonists such as nifedipine (Nif) inhibit processes that depend on extracellular Ca2+ in many muscular and secretory cells. The effect of Nif on mediator release and Ca2+ uptake by human polymorphonuclear neutrophils (PMN) has been investigated. Nif caused a concentration-dependent inhibition of the Ca2+ ionophore-induced release of platelet-activating factor (PAF-acether), slow-reacting substance (SRS) and to a lesser degree beta-glucuronidase (beta-glu). Nif inhibited the synthesis of PAF-acether rather than its release. Increasing Ca2+ concentration in the bathing medium from 1.3 to 2.8 mM completely reversed the effect of Nif on PAF-acether secretion. Nif at 1 and 5 microM reduced PMN45Ca2+ uptake induced by the Ca2+ ionophore A 23187. These results indicate that the inhibition by Nif of mediator release depends probably on the Ca2+-antagonistic property of the drug. A preliminary ex vivo study suggests that this inhibitory effect on neutrophil functions exists during therapeutic use.

Autacoids↗
PubMed1983

Sodium cromoglycate, verapamil and nicardipine antagonism to leukotriene D4 bronchoconstriction.

1--The effects of nicardipine, verapamil and sodium cromoglycate (SCG) on the increase in pulmonary airway resistance(RAw) and decrease in pulmonary dynamic compliance (CDyn) induced by leukotriene D4 (LTD4) 0.5 micrograms kg-1 and acetylcholine (ACh) 3 micrograms kg-1 were investigated in anaesthetized guinea-pigs. The effects of these three agents on the contractile effects of LTD4 and ACh were tested on isolated tracheal preparations of the guinea-pig. 2--Nicardipine and verapamil (0.3 and 1 mg kg-1), as well as SCG (3 and 10 mg kg-1), partially but significantly inhibited the effects of LTD4 on RAw. Partial inhibition of the effect of LTD4 on CDyn was only observed with verapamil (0.3 and 1 mg kg-1). Nicardipine and verapamil had no effect on ACh-induced bronchoconstriction in vivo. 3--In concentrations higher than 10(-5) M, nicardipine and verapamil inhibited the contractile effects of LTD4 and ACh on guinea-pig isolated trachea. SCG had no effect on this preparation. 4--These results suggest that nicardipine, verapamil and SCG partially reduce the component of bronchoconstriction associated with stimulation of irritant receptors by LTD4. However, the site and mechanism of action of Ca2+-entry antagonists remain uncertain.

Airway Resistance↗
PubMed1982

PEEP-induced airspace overdistension complicating paraquat lung.

This report describes a case of paraquat poisoning, treated with continuous positive airway pressure. After an initial phase of acute respiratory failure with diffuse pulmonary edema, we observed radiologically a complete clearing of both lungs, associated with an aspect of overdistension. Surprisingly, FRC was above normal, as was total quasi static compliance. The patient died on the 15th day, with intractable hypoxemia. Pathologic analysis revealed large zones of parenchyma with overdistended airspaces, explaining the emphysematous-like aspect of the lungs. We propose that the attempts to increase lung volume with CPAP, at an early phase of diffuse epithelial disorganization, may have, partially at least, dilated the remaining distal airspaces.

Adult↗
PubMed1981

Inhibition of exercise-induced asthma by a calcium antagonist, nifedipine.

Contraction of bronchial smooth muscle and release of mediators by mast cells are involved in asthmatic attacks and are calcium dependent. Therefore, we investigated the effects of a calcium antagonist, nifedipine, in asthma. Ten patients with asthma and documented exercise-induced bronchoconstriction exercised on 2 separate days after single-blind sublingual administration of 20 mg of placebo or nifedipine. The exercise-induced decreases in forced vital capacity, peak expiratory flow, and maximal expiratory flow after exhalation of 50 and 75% of the forced vital capacity were not modified on placebo but were prevented by nifedipine. Ten other asymptomatic patients with asthma and documented exercise-induced bronchoconstriction were studied at rest before and 45 min after nifedipine. The forced vital capacity, peak expiratory flow, and maximal expiratory flows were initially reduced and did not increase after nifedipine. Thus, nifedipine does not modify the basal bronchial tone of patients with asthma but does prevent exercise-induced asthma.

Adolescent↗
PubMed1978

[Results of the surgical treatment of congenital mitral insufficiency].

The authors report 21 cases of congenital mitral incompetence undergoing surgery between 1972 and 1977. There were 3 operative deaths and 2 late deaths. Of the survivors, 10 had a good result and 5 a fair result. The factors influencing the results have been associated lesions (aortic stenosis and ventricular septal defects are more serious than atrial septal defects and abnormalities of origin of the left coronary artery), the type of repair (which is better if it seeks to correct the frequently complex valvular abnormality at all levels), and especially the degree of dilatation of the left ventricle. By contrast, age had no influence either on the operative risk or on the quality of the results.

Adolescent↗
PubMedDate not supplied

[Effect of verapamil, nicardipine and disodium cromoglycate on the bronchoconstrictor effects of histamine].

The effects of nicardipine, verapamil and sodium cromoglycate (SCG) on the increase in pulmonary airway resistance (Raw) and decrease in pulmonary dynamic compliance (C.Dyn.) induced by histamine (Hist) (3 and 30 micrograms x kg-1, i.v.) and acetylcholine (ACh) (3 and 30 micrograms x kg-1, i.v.) were investigated in anaesthetized guinea-pigs. The effects of these three agents on the contractile effects of Hist and ACh were tested on isolated tracheal preparations of the guinea pig. Nicardipine (0.3 and 1 mg . kg-1, i.v.) and verapamil (1 mg . kg-1, i.v.) as well as SCG (3 and 10 mg . kg-1, i.v.) partially but significantly inhibited the effects of Hist on Raw. These substances had no effect on Hist-induced decrease in C.Dyn. Nicardipine and verapamil had no effect on ACh-induced bronchoconstriction in vivo. SCG partially but significantly inhibited the effects of ACh (30 micrograms . kg-1) on Raw. In concentrations higher than 3 x 10(-6) M, nicardipine and verapamil inhibited the contractile effects of Hist and ACh on guinea-pig isolated trachea. SCG had no effect on this preparation. The results suggest that nicardipine, verapamil and SCG partially reduce the component of bronchoconstriction associated with stimulation of irritant receptor by Hist. However, the site and mechanism of action of Ca++-entry antagonists remain uncertain.

Acetylcholine↗
PubMedDate not supplied

Bronchial response to hyperventilation of dry air at room temperature in normals and asthmatics.

The bronchial effects of three levels (25, 40 and 60 1 X min-1) of voluntary isocapnic hyperventilation of dry air at room temperature (20-22 degrees C) have been studied in 18 normal, non-atopic subjects and in 25 nonperennial asthmatics who were asymptomatic and whose airway obstruction at the time of the study was mild, with a peak expiratory flow rate of 6.1 +/- 1.5 (SD) 1 X s-1 vs a predicted 8.4 +/- 1.3 1 X s-1. The bronchial response was assessed by use of maximal expiratory flow-volume curves obtained before and 1, 5, 10 and 15 min after the 5 min hyperventilation challenge. In normal subjects, there was a minimal though significant (p less than 0.001; two-way analysis of variance) fall in maximal expiratory flows which did not increase with the level of hyperventilation and was not accompanied by a fall in forced vital capacity. The bronchial response of asthmatics differed from that in normal: the fall in maximal expiratory flows was significantly greater, associated with a significant fall in forced vital capacity and increased with the level of hyperventilation. Results in 10 asthmatics studied on two different study days were highly reproducible. Sensitivity and specificity are excellent (approximately equal to 1) for the 40 1 X min-1 hyperventilation challenge. Our results suggest that isocapnic voluntary hyperventilation of dry air at room temperature (20-22 degrees C) is a highly satisfactory screening test to detect bronchial hyperreactivity.

Adolescent↗