Early recognition of collapsing hemodynamics in pulmonary embolism is necessary to avoid cardiac arrest using aggressive medical therapy or mechanical cardiac support. The aim of the study was to identify the maximal acute hemodynamic compensatory steady state. Overall, 40 dynamic obstructions of pulmonary artery were performe d and hemodynamic data were collected. Occlusion of only left or right pulmonary artery did not lead to the hemodynamic collapse. When gradually obstructing the bifurcation, the right ventri cle end-diastolic area expanded proportionally to pulmonary artery mean pressure from 11.6 (10.1, 14.1) to 17.8 (16.1, 18.8) cm 2 (p<0.0001) and pulmonary artery mean pressure increased from 22 (20, 24) to 44 (41, 47) mmHg (p<0.0001) at the poin t of maximal hemodynamic compensatory steady state. Sim ilarly, mean arte rial pressure decreased from 96 (87, 101) to 60 (53, 78) mmHg (p<0.0001), central venous pressure increased from 4 (4, 5) to 7 (6, 8) mmHg (p<0.0001), heart rate increased from 92 (88, 97) to 147 (122, 165) /min (p<0.0001), contin uous cardiac output dropped from 5.2 (4.7, 5.8) to 4.3 (3.7, 5.0) l/min (p=0.0023), modified shock index increased from 0.99 (0.81, 1.10) to 2.31 (1.99, 2.72), p<0.0001. In conclusion, in stead of continuous cardiac output all of the analyzed parameters can sensitively determine the individual maximal compensatory response to obstructive shock. We assume their monitoring can be used to predict the critical phase of the hemodynamic status in routine practice., J. Kudlička ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Two mechanisms contribute in the development of pulmonary hypertension in pulmonary embolism (PE) - obstruction of pulmonary blood vessels and vasoconstriction. We hypothesize that hypoxia, increased shear stress and/or activation of gathered leukocytes in the PE may cause a release of reactive oxygen species (ROS). Therefore our aim was to determine the influence of the ROS scavenger Tempol on pulmonary hypertension and to d escribe NO synthase activity and production of NO oxidative products (NOx) after PE. In general anesthesia sephadex microspheres suspended in PSS were applied in right jugular vein as the pulmonary microembolism. Than we measured in isolated salt solution -perfused lungs the changes in perfusion pressure, activity of NO synthase and NOx plasma concentration in 7 groups of rats: C: control group (n=5), CN: C + sodium nitroprusside (SN) (n=5), EN: PE + SN (n=5), ETN: Tempol + PE + SN (n=5), CL : C + L -NAME (n=5 ), EL: PE + L-NAME (n=5), ETL: Tempol + PE + L -NAME (n=5). Tempol was applied intraperitoneally before PE. Animals that received Tempol (groups TN, TL) had significantly lower basal perfusion pressure than those which did not rec eive Tempol (EN, EL). Overa ll we measured a higher decrease of perfusion pressure than in the control group (C) after applica tion of SN. Administration of L-NAME after PE (EL) increased the pressure more than in the control group (NL). NOx concentration was higher after PE. We found that preventive administration of Tempol decreases the increase in perfusion pressure after PE. PE increased NO release and concentration of NOx., R. Mizera, D. Hodyc, J. Herget., and Obsahuje bibliografii