SYMPATHOMIMETIC DRUGS IN ACUTE VIRAL BRONCHIOLITIS

PEDIATRICS ◽  
1969 ◽  
Vol 44 (4) ◽  
pp. 493-497 ◽  
Author(s):  
P. D. Phelan ◽  
H. E. Williams

Mean pulmonary resistance and inspiratory and expiratory pulmonary resistance were measured in 10 infants with acute viral bronchiolitis before and after the administration of isoprenaline or orciprenaline by aerosol. No consistent change in any measurement of pulmonary resistance was recorded following the administration of the drugs.

1983 ◽  
Vol 55 (2) ◽  
pp. 558-561 ◽  
Author(s):  
J. Lindenfeld ◽  
J. T. Reeves ◽  
L. D. Horwitz

In resting conscious dogs, administration of cyclooxygenase inhibitors results in modest increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that vasodilator prostaglandins play a role in maintaining the low vascular resistance in the pulmonary bed. To assess the role of these vasodilator prostaglandins on pulmonary vascular resistance during exercise, we studied seven mongrel dogs at rest and during exercise before and after intravenous meclofenamate (5 mg/kg). Following meclofenamate, pulmonary vascular resistance rose both at rest (250 24 vs. 300 +/- 27 dyn . s . cm-5, P less than 0.01) and with exercise (190 +/- 9 vs. 210 +/- 12 dyn . s . cm-5, P less than 0.05). Systemic vascular resistance rose slightly following meclofenamate both at rest and during exercise. There were no changes in cardiac output. The effects of cyclooxygenase inhibition, although significant, were less during exercise than at rest. This suggests that the normal fall in pulmonary vascular resistance during exercise depends largely on factors other than vasodilator prostaglandins.


1981 ◽  
Vol 241 (5) ◽  
pp. H756-H759 ◽  
Author(s):  
C. W. Leffler ◽  
J. R. Hessler

Products of reactions catalyzed by prostaglandin cyclo-oxygenase [prostaglandins (PG), thromboxanes] were analyzed by gas chromatography with electron-capture detection in the venous effluents of in situ Krebs-perfused lungs of exteriorized fetal goats and sheep before and after ventilation with air. The major products were 6-keto-PGF1 alpha and 6,15-diketo[13,14-dihydro] PGI2 without blood components. After ventilation, which decreased pulmonary vascular resistance to 63% of the before-ventilation value, lung production of 6-keto-PGF1 alpha and metabolite increased 50 and 230%, respectively. These data, in addition to earlier findings of inhibition of ventilation-induced pulmonary vasodilation by indomethacin and increased net production of PG-like material after ventilation of blood-perfused fetal lungs, support the hypothesis that ventilation of fetal lungs with air at birth increases synthesis of PGI2 by or near pulmonary resistance vessels, resulting in high local concentrations of PGI2 near its site of production. PGI2 appears to be important in the pulmonary vascular resistance decrease that is necessary for successful perinatal transition.


1990 ◽  
Vol 69 (1) ◽  
pp. 245-250 ◽  
Author(s):  
J. M. Fouke ◽  
R. A. DeLemos ◽  
M. J. Dunn ◽  
E. R. McFadden

Short-term exposure to 0.5 parts per million (ppm) ozone has been shown to cause an increase in respiratory resistance in primates that can be diminished by 50% with pretreatment with cromolyn sodium. Because of the known membrane-stabilizing effects of cromolyn and the resultant inhibition of mediator production, we hypothesized a role for the products of arachidonic acid (AA) metabolism in these events. We exposed five adult male baboons to 0.5 ppm ozone on two occasions, once with cromolyn pretreatment and once without. Pulmonary resistance (RL) was monitored and bronchoalveolar lavage (BAL) was performed before and after each exposure. The BAL was analyzed for a stable hydrolysis product of prostacyclin, 6-keto-prostaglandin (PG) F1 alpha, PGE2, a stable hydrolysis product of thromboxane (Tx) A2, TxB2, and PGF2 alpha. RL increased after ozone exposure (1.62 +/- 0.23 to 3.77 +/- 0.51 cmH2O.l-1.s, difference 2.15; P less than 0.02), and this effect was partially blocked by cromolyn (1.93 +/- 0.09 to 3.18 +/- 0.40 cmH2O.l-1.s, difference 1.25; P less than 0.02). The base-line levels of the metabolites of AA in the BAL were as follows (in pg/ml): 6-keto-PGF1 alpha 72.78 +/- 12.6, PGE2 145.92 +/- 30.52, TxB2 52.52 +/- 9.56, and PGF2 alpha 22.28 +/- 5.42. Ozone exposure had no effect on the level of any of these prostanoids (P = NS). These studies quantify the magnitude of cyclooxygenase products of AA metabolism in BAL from baboon lungs and demonstrate that changes in the levels of these mediators in BAL are not prerequisites for ozone-induced increases in respiratory resistance.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 61 (2) ◽  
pp. 734-740 ◽  
Author(s):  
P. W. Catron ◽  
J. Bertoncini ◽  
R. P. Layton ◽  
M. E. Bradley ◽  
E. T. Flynn

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing “silent” pulmonary bubble emboli do not alter lung mechanics.


1985 ◽  
Vol 59 (3) ◽  
pp. 884-889 ◽  
Author(s):  
H. Baier ◽  
L. Yerger ◽  
R. Moas ◽  
A. Wanner

The influence of lung inflation on lung elasticity and pulmonary resistance (RL) and on pulmonary and bronchial hemodynamics was examined in five anesthetized, mechanically ventilated adult sheep before and after treatment with the cyclooxygenase inhibitor indomethacin (2 mg/kg). Lung inflation was accomplished by increasing levels of positive end-expiratory pressure (PEEP). Measurements of pulmonary vascular resistance (PVR), bronchial blood flow (Qbr), and RL were obtained with a Swan-Ganz catheter, with an electromagnetic flow probe placed around the carinal artery, and by relating airflow to transpulmonary pressure (Ptp), respectively. Before indomethacin, increasing PEEP from 5 to 15 cmH2O increased mean lung volume (VL) to 135% (P less than 0.01), Ptp to 165% (P less than 0.005), and PVR to 132% (P less than 0.05) of base line and decreased mean Qbr (normalized for cardiac output) to 53% (P less than 0.05) of base line. Mean RL showed a tendency to decrease with a mean value of 67% of base line at 15 cmH2O PEEP. After indomethacin the corresponding values were 121% for VL, 155% for Ptp, 124% for PVR, 35% for Qbr, and 31% for RL. The PEEP-dependent changes were not different before and after indomethacin except for mean VL, which increased less (P less than 0.05) after indomethacin. The failure of indomethacin to modify PEEP-induced changes in RL, PVR, and Qbr was also present when these parameters were expressed as a function of Ptp. These findings suggest that the cyclooxygenase products elaborated during lung inflation reduce lung elasticity but fail to influence airflow resistance and pulmonary and bronchial hemodynamics.


Author(s):  
Aleksandar Puklavec ◽  
Ljubomir Antekolović ◽  
Pavle Mikulić

The aim of this study was to examine the acquisition of the long jump skill in elementary school children using augmented feedback of varying type and frequency. Eighty-eight boys and girls aged (mean ± SD) 11 ± 0.5 years, without any prior experience in the long jump skill acquisition,  were assigned to one of the four study groups: (1) the group receiving only verbal feedback on key errors, (2) the group receiving both verbal and video feedback on key errors, (3) the group receiving both verbal and video feedback on all errors, and (4) the group receiving no feedback. Before and after an 8-week training intervention, long jump distance and relevant kinematic variables were recorded. The results indicated that the group receiving both verbal and video feedback on all errors improved the most in terms of the long jump distance. Varying feedback influenced kinematic parameters differently, as there was no consistent change in the monitored kinematic variables across groups. It was concluded that, when learning a complex motor skill in a typical Physical Education setting, elementary school children are likely to benefit the most when receiving frequent feedback (both verbal and using video analysis, focusing on all errors) in comparison with the situation in which they receive feedback reduced in the type (only verbal) and the frequency (focusing only on key errors).Keywords: bandwidth feedback; kinematics; knowledge of performance; motor learning. --- Cilj ovoga rada bio je ispitati utjecaj različitih količina i vrsta povratnih informacija (PI) u procesu usvajanja tehnike skoka u dalj kod učenika osnovne škole. Osamdeset i osam učenika i učenica, starosti 11 (±0,5) godina, bez prethodnoga iskustva u treningu skoka u dalj, raspodijeljeno je u jednu od četiriju skupina ispitanika koje su dobivale PI: (1) verbalno samo na ključne greške, (2) verbalno i vizualno samo na ključne greške, (3) verbalno i vizualno na sve greške ili (4) nisu primale PI. Duljina skoka i relevantni kinematički parametri skoka u dalj izmjereni su prije i nakon 8-tjednog eksperimentalnoga tretmana. Rezultati istraživanja pokazali su kako je grupa koja je primala PI, na svaku grešku verbalnim i vizualnim putem najviše napredovala u smislu duljine skoka u dalj. Različite količine i vrste PI različito djelovale su na promatrane kinematičke parametre te nisu uočene konzistentne promjene između grupa. Zaključeno je kako djeca osnovnoškolske dobi prilikom usvajanja kompleksne motoričke vještine imaju više koristi od većih frekvencija PI (verbalnih i vizualnih na sve greške) u usporedbi s reduciranim PI prema vrsti (samo verbalne) ili frekvenciji (samo na ključne greške).Ključne riječi: kinematika; motoričko učenje; poznavanje izvedbe; reducirane povratne informacije.


2014 ◽  
Vol 7 (1) ◽  
pp. 3
Author(s):  
Rodrigo A S Gonçalves ◽  
Sérgio Feitosa ◽  
Cláudia de Castro Selestrin ◽  
Vitor E Valenti ◽  
Fernando H de Sousa ◽  
...  

Perception ◽  
1979 ◽  
Vol 8 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Claes von Hofsten

Adaption to convergence-altering prism spectacles was studied. The subjects were trained for 8 min with either convergence-increasing or convergence-decreasing prisms. Before and after training they estimated the distance to a binocular dot varying in the stimulus it provided to convergence. Both the preadaptation and postadaptation estimates showed that the reciprocal of estimated target distance is linearly related to convergence. Further there was a consistent change in the direction of adaptation expected from the preadaptation to the postadaptation test. This change was accounted for in terms of a recalibration of the effective absolute convergence level.


1998 ◽  
Vol 85 (5) ◽  
pp. 1982-1988 ◽  
Author(s):  
Todd M. Officer ◽  
Riccardo Pellegrino ◽  
Vito Brusasco ◽  
Joseph R. Rodarte

We compared four algorithms by using least squares regression for determination of pulmonary resistance and dynamic elastance in subjects with emphysema, normal subjects, and subjects with asthma before and after bronchoconstriction. The four methods evaluated include 1) a single resistance and elastance, 2) separate resistances and elastances for each half breath, 3) separate inspiratory and expiratory resistances with a single elastance, and 4) separate inspiratory and expiratory resistances, an expiratory volume interaction term, and a single elastance. All methods gave comparable results in normal and asthmatic subjects. We found expiratory resistance was larger than inspiratory resistance in normal and asthmatic subjects during control conditions, but inspiratory resistance was higher than expiratory resistance in subjects who experienced severe bronchoconstriction in response to methacholine. In subjects who are flow limited, method 2 gives a higher inspiratory resistance than would be computed by assuming that the elastic pressure-volume curve passes through the zero-flow points. Methods 1 and 3 overestimate dynamic elastance and inspiratory resistance. Method 4appears to identify flow limitation and dynamic hyperinflation and gives a good measure of inspiratory resistance and dynamic elastance.


1975 ◽  
Vol 39 (1) ◽  
pp. 41-46 ◽  
Author(s):  
S. E. Levy ◽  
D. H. Simmons

Mongrel dogs (29) were anesthetized, paralyzed, and ventilated at a constant minute volume. AaD02 breathing air and 100% O2, venous admixture breathing air (Qva/Qt) and 100% O2 (Qs/Qt), single-breath diffusing capacity for CO (DLCO), and total pulmonary resistance (RL) and pulmonary compliance (CL) were measured before and after pulmonary embolization with autologus in vivo venous thrombi. Nine dogs were heparinized before embolization. In the 20 nonheparinized dogs AaDo2 breathing air increased from 11 to 26 mmHg, Qva/Qt from 4 to 22%, and Qs/At from 5 to 8%. DLCO decreased 24%, RL increased 43%, and CL fell 30%. In the nine heparinized dogs AaDo2 breathing air increased from 8 to 13 mmHg and Qva/Qt from 3 to 8%; Qs/Qt did not change. DLCO decreased 31%; RL and CL did not change significantly. The increase in Qva/Qt of 5% in the heparinized dogs was significantly less (P smaller than 0.001) than the increase of 18% in the nonheparinized dogs. These findings suggest that arterial hypoxemia following thromboembolism is due to ventilation-perfusion inequality caused by changes in lung mechanics.


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