Pulmonary Resistance

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Peter D Pare - One of the best experts on this subject based on the ideXlab platform.

  • chronic fenoterol exposure increases in vivo and in vitro airway responses in guinea pigs
    American Journal of Respiratory and Critical Care Medicine, 1994
    Co-Authors: Zhonglin Wang, A M Bramley, A Mcnamara, Peter D Pare, Tony R Bai
    Abstract:

    We tested the hypothesis that the regular inhalation of a beta 2-adrenergic receptor (beta 2AR) agonist increases airway responsiveness in guinea pigs. A potent beta 2AR agonist, fenoterol hydrobromide, in sublaryngeal doses equivalent to maximal doses used in the treatment of asthma on a weight basis (5.28 micrograms/kg), was administered by nebulizer three times a day for 6 weeks to normal adolescent guinea pigs (FEN, n = 10) and to ovalbuminsensitized guinea pigs challenged twice weekly with ovalbumin (OA + FEN, n = 20), although not in the 12 h prior to or 4 h after antigen challenge. Controls included saline-treated normal animals (CON, n = 10) and ovalbumin-sensitized animals treated with repeated antigen challenge and saline (OA, n = 20). At 72 h after the last administration of saline, fenoterol, and ovalbumin, the dose-response relationship between Pulmonary Resistance (RL) and nebulized acetylcholine (ACh) was measured. RLmax increased 2-fold and the ACh concentration causing a 10-fold increase ...

  • limitation of airway smooth muscle shortening by cartilage stiffness and lung elastic recoil in rabbits
    Journal of Applied Physiology, 1993
    Co-Authors: R H Moreno, James C Hogg, C Lisboa, Peter D Pare
    Abstract:

    Airway smooth muscle can contract to 20% of its starting length when stimulated maximally and allowed to contract isotonically in vitro. In vivo airway smooth muscle contraction of this degree would result in widespread airway closure. We hypothesized that elastic loads related to cartilage stiffness and lung parenchyma-airway interdependence limit in vivo airway smooth muscle shortening. We measured Pulmonary Resistance in anesthetized tracheostomized New Zealand White rabbits before and after intravenous treatment with papain in a concentration that produced generalized cartilage softening. Papain treatment caused a significant increase in Pulmonary Resistance that was completely reversed by application of 4 cmH2O positive end-expiratory pressure and that was partially reversed by vagotomy. Papain pretreatment also resulted in a substantial alteration in the Pulmonary Resistance-dose relationship to intravenously administered acetylcholine. In addition, maximal Resistance after the highest concentration of acetylcholine was greater in papain-treated animals than in the control animals, but the position of the dose-response relationship was not shifted (i.e., there was no change in the effective dose causing 50% maximal response). Application of 4 cmH2O positive end-expiratory pressure in untreated animals resulted in a marked decrease in the bronchoconstriction produced by an effective dose of acetylcholine causing 50% of maximal response, whereas application of 4 cmH2O negative end-expiratory pressure resulted in a marked enhancement of the bronchoconstrictor response to the same intravenous dose of acetylcholine. We conclude that cartilage elasticity and lung recoil are important determinants of the ability of airway smooth muscle to shorten and produce airway narrowing in vivo.

  • effect of vagal stimulation and parenteral acetylcholine on canine trachealis muscle shortening
    Journal of Applied Physiology, 1992
    Co-Authors: Mitsushi Okazawa, Peter D Pare, Y Wakai, S Osborne, Jeremy Road
    Abstract:

    Canine trachealis smooth muscle shortening (TMS) in response to vagal nerve stimulation is approximately 30%, far less than the 70% predicted from in vitro studies. We hypothesized that in vivo airway smooth muscle activation during vagal stimulation may be submaximal, and in this study we wished to determine TMS during maximal activation. TMS was studied in 12 alpha-chloralose-anesthetized dogs during vagal stimulation, systemic acetylcholine injection, and local acetylcholine injection. Bilateral vagal stimulation produced TMS of 26 +/- 5% (SE) length at functional residual capacity (LFRC). Maximal TMS during systemic injection of acetylcholine was 28 +/- 12% LFRC but may have been limited by delivery of acetylcholine to the muscle because asystole occurred at higher concentrations. TMS was greatest during local injection of acetylcholine (48 +/- 7% LFRC). There was a greater increase in Pulmonary Resistance and decrease in dynamic compliance during systemic acetylcholine injection than during vagal stimulation. We conclude that bilateral vagal nerve stimulation does not maximally activate trachealis smooth muscle but that the maximal shortening achieved with local injection of acetylcholine is still less than isotonic shortening in vitro. These data suggest that maximal shortening in vivo is limited by the afterload provided by the tracheal cartilaginous rings.

L Goossens - One of the best experts on this subject based on the ideXlab platform.

  • the airway response of horses with recurrent airway obstruction heaves to aerosol administration of ipratropium bromide
    Equine Veterinary Journal, 1993
    Co-Authors: N E Robinson, Cédric Berney, F J Derksen, L Goossens
    Abstract:

    The airway response to aerosol administration of the anticholinergic agent ipratropium bromide was determined in 8 horses with recurrent airway obstruction (heaves). The reversibility of airway obstruction was confirmed by measuring lung function before and during stabling; and by determining the response to atropine administration (0.02 mg/kg bwt intravenously). The dose-response to ipratropium bromide was determined using a Williams square design experiment in which 25, 50 or 75 micrograms ipratropium bromide/ml (4 ml/100 kg bwt) or the same volume of vehicle was administered to each horse by nebulisation. Lung function was measured before and 1 and 4 h after nebulisation. Vehicle had no effect on lung function. Ipratropium decreased the maximal change in pleural pressure during tidal breathing (delta Pplmax) and Pulmonary Resistance (RL) and increased dynamic compliance (Cdyn). At the 1 h measurement period, the effect on RL and Cdyn was dose-dependent. A separate experiment demonstrated that the duration of action of ipratropium was between 4 and 6 h.

Bernard Charbonnier - One of the best experts on this subject based on the ideXlab platform.

  • rapid haemodynamic improvement following saruplase in recent massive Pulmonary embolism
    Thrombosis and Haemostasis, 1998
    Co-Authors: Gerard Pacouret, Gwyn Hopkins, Sarah J Barnes, Bernard Charbonnier
    Abstract:

    In a single centre pilot study, saruplase (20 mg bolus plus 60 mg infusion over 1 h) was administered to twenty patients with an angiographically documented recent massive Pulmonary embolism: Miller index of at least 20 and mean Pulmonary artery pressure of at least 20 mmHg. The lytic ability of saruplase to cause normalization of haemodynamic parameters over the first 12 h and reperfusion of Pulmonary arteries at 24 h was assessed. A decrease of 25 ± 10% in total Pulmonary Resistance was evident at 30 min. Haemodynamic parameters continued to improve with total Pulmonary Resistance decreasing by 29 ± 8% and 40 ± 11% at 1 and 12 h respectively. Relative improvement in Miller index 24 ± 6 h after saruplase treatment was 38 ± 9%. Two patients suffered recurrent Pulmonary embolism, two severe bleeding events were observed. One patient died following a haemorrhagic stroke.

  • effects of intravenous urokinase versus alteplase on total Pulmonary Resistance in acute massive Pulmonary embolism a european multicenter double blind trial
    Journal of the American College of Cardiology, 1992
    Co-Authors: Guy Meyer, Herve Sors, Bernard Charbonnier, Wolfgang Kasper, Jeanpierre Bassand, Ian H Kerr, Emmanuel Lesaffre, Philippe Vanhove, Marc Verstraete
    Abstract:

    Twelve centers participated in a double-blind study in which 63 patients with angiographically documented acute massive Pulmonary embolism were randomly assigned to treatment with either urokinase (4,400 U/kg as an intravenous bolus infusion, then 4,400 U/kg per h over 12 h; n = 29) or alteplase (10 mg as an intravenous bolus infusion, then 90 mg over 2 h) followed by heparin (n = 34). The primary objective was to compare the resolution of Pulmonary embolism as judged by the change in total Pulmonary Resistance over the initial 2 h. Further objectives were to evaluate the changes in total Pulmonary Resistance over the next 10 h and the degree of angiographic resolution at 12 to 18 h. At 2 h, total Pulmonary Resistance decreased by 18 +/- 22% in the urokinase group and by 36 +/- 17% in the alteplase group (p = 0.0009). Continuous monitoring of Pulmonary artery mean pressure, cardiac index and total Pulmonary Resistance revealed that these variables improved faster in the alteplase group, with consistently significant intergroup differences from 30 min up to 3 to 4 h. After 12 h, the decrease in total Pulmonary Resistance was 53 +/- 19% in the urokinase group compared with 48 +/- 17% in the alteplase group and the reduction in the angiographic severity score was 30 +/- 25% compared with 24 +/- 18%, respectively, with no significant intergroup differences. Bleeding was equally frequent in the two treatment groups, except that more urokinase-treated patients experienced hematomas at puncture sites.

Jose Lopezsendon - One of the best experts on this subject based on the ideXlab platform.

  • atrial septal defect with severe Pulmonary hypertension in elderly patients usefulness of transient balloon occlusion
    Revista Espanola De Cardiologia, 2010
    Co-Authors: Angel Sanchezrecalde, Jose M Oliver, Guillermo Galeote, Ana Gonzalez, Luis Calvo, Santiago Jimenezvalero, Raul Moreno, Jose Lopezsendon
    Abstract:

    In patients with an atrial septal defect and severe Pulmonary hypertension, it is important to determine whether the latter is reversible before percutaneous or surgical closure. In addition to determining Pulmonary Resistance, one simple technique is to transiently occlude the septal defect using a balloon catheter and to evaluate the hemodynamic response. We defined a positive response as a ≥25% reduction in mean Pulmonary artery pressure during occlusion relative to the basal level, without a fall in systemic pressure or an increase in ventricular end-diastolic pressure. The study included five patients aged over 60 years with an atrial septal defect and severe Pulmonary hypertension who were referred for percutaneous closure. In one patient, the test gave a negative result and closure of the atrial septal defect was not performed. In the remaining four, closure was indicated. In three patients, closure was performed percutaneously, while the fourth underwent surgery. The drop in Pulmonary pressure observed during the test was maintained over the long term at a mean follow-up time of 22 months.

Jeanfrancois Viel - One of the best experts on this subject based on the ideXlab platform.

  • comparative efficacy of a two hour regimen of streptokinase versus alteplase in acute massive Pulmonary embolism immediate clinical and hemodynamic outcome and one year follow up
    Journal of the American College of Cardiology, 1998
    Co-Authors: Nicolas Meneveau, Francois Schiele, Damien Metz, Benoit Valette, Pierre Attali, Alain Vuillemenot, Gilles Grollier, Jacques Elaerts, Jeanmarie Mossard, Jeanfrancois Viel
    Abstract:

    Abstract Objectives. This study sought to compare the efficacy of 2-h regimens of alteplase and streptokinase in acute massive Pulmonary embolism. The primary end point was immediate hemodynamic improvement, and secondary end points included early clinical efficacy and safety, as well as 1-year clinical outcome. Background. Several thrombolytic regimens have been compared for the past 10 years in randomized studies, showing that 2-h infusion regimens of alteplase or urokinase lead to faster hemodynamic improvement than former 12- to 24-h administration protocols in acute massive Pulmonary embolism. Many trials have focused on immediate hemodynamic and angiographic outcomes, but none has addressed long-term follow-up after thrombolysis. Methods. Sixty-six patients with acute massive Pulmonary embolism (Miller score >17 and mean Pulmonary artery pressure >20 mm Hg) were randomly assigned to receive either a 100-mg 2-h infusion of alteplase (n = 23) or 1.5 million IU of streptokinase over 2 h (n = 43). In both groups, heparin infusion was started at the end of thrombolytic infusion and adapted thereafter. Total Pulmonary Resistance was monitored over a 12-h period. Pulmonary vascular obstruction was assessed 36 to 48 h after thrombolytic therapy. One-year follow-up information included death, cause of death, recurrent Pulmonary embolism, chronic thromboembolic Pulmonary hypertension, stroke and bleeding. Results. Both groups had similar baseline angiographic and hemodynamic characteristics of severity, with maintained cardiac output in 64 (97%) of 66 patients. The results (mean ± SD) demonstrated that despite a faster total Pulmonary Resistance improvement observed at 1 h in the alteplase group compared with the streptokinase group (33 ± 16% vs. 19 ± 16%, p = 0.006), a similar hemodynamic efficacy was obtained at 2 h when both thrombolytic regimens were completed (38 ± 18% vs. 31 ± 19%). There was no significant difference in either Pulmonary vascular obstruction at 36 to 48 h or bleeding complication rates. One-year event-free survival was similar in both groups, as most events were related to concomitant diseases. Conclusions. These results suggest that a 2-h regimen of streptokinase can be routinely used in patients with massive Pulmonary embolism and maintained cardiac output without obviously compromising efficacy or safety.