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Pulmonary Pressure (pulmonary + pressure)

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Medical Sciences	100%

Selected Abstracts

Endothelin receptors blockade blunts hypoxia-induced increase in PAP in humans

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2010
I. Pham
Eur J Clin Invest 2010; 40 (3): 195,202 Abstract Background, Activation of the endothelin-1 (ET-1) pathway may be involved in hypoxia-induced pulmonary vasoconstriction, increase in pulmonary pressure and high altitude pulmonary oedema. Thus, we investigated the effect of the ETA/ETB receptor antagonist, bosentan, on pulmonary artery systolic pressure (PASP) in healthy subjects (n = 10). Design, We used a double-blind, placebo-controlled, randomized, cross-over design to study the effects of a single oral dose of bosentan (250 mg) on PASP after 90-min-exposure to normobaric hypoxia (FiO2 = 0·12). We measured PASP and cardiac output by echocardiography, systolic arterial blood pressure, arterial O2 saturation (SaO2), and blood gases at rest and during a sub-maximal exercise. Results, PASP in normoxia at rest was 23·5 ± 2·7 and during exercise 39·8 ± 11·6 mmHg (P < 0·0001). During the placebo period, hypoxia induced a significant decrease in SaO2, PaO2 and PCO2 and increase in pH. PASP at rest increased significantly: 32·1 ± 3·5 mmHg (P < 0·001 vs. normoxia). Bosentan significantly blunted the hypoxia-induced increase in PASP: bosentan: 27·0 ± 3·3 mmHg, P = 0·002 vs. placebo at rest, but not during exercise: bosentan 39·8 ± 11·6 vs. placebo 43·0 ± 8·5 mmHg, ns. Bosentan had no effect on the hypoxia-induced changes in blood gases, or on cardiac output and systolic arterial blood pressure, which were not modified by hypoxia. Conclusion, A single oral dose of bosentan blunted an acute hypoxia-induced increase in PASP in healthy subjects, without altering cardiac output or systemic blood pressure. [source]

Haemodynamic effects of ,75 mmHg negative pressure therapy in a porcine sternotomy wound model

INTERNATIONAL WOUND JOURNAL, Issue 1 2009
Arash Mokhtari
Abstract Previous research has shown ,125 mmHg to be the optimal negative pressure for creating an environment that promotes wound healing, and this has therefore been adopted as a standard pressure for patients with deep sternal wound infection. However, it has not yet been clearly shown that ,125 mmHg is the optimal pressure from a haemodynamic point of view. Furthermore, there have been reports of cardiac rupture during ,125 mmHg negative pressure therapy. We therefore studied the effects of a lower pressure: ,75 mmHg. Twelve pigs were used. After median sternotomy, sealed negative pressure therapy of ,75 mmHg was applied. Baseline measurements were made and continuous recording of the cardiac output, end-tidal CO2 production, mean arterial pressure, mean pulmonary pressure (pulmonary artery pressure), systemic vascular resistance, pulmonary vascular resistance, left atrial pressure and central venous pressure was started. Six pigs served as controls. No statistically significant difference was observed in any of the haemodynamic parameters studied, compared with the controls. The present study shows that, with a suitable foam application technique, ,75 mmHg can be applied without compromising the central haemodynamics. [source]

Hemodynamic profile and tissular oxygenation in orthotopic liver transplantation: Influence of hepatic artery or portal vein revascularization of the graft

LIVER TRANSPLANTATION, Issue 11 2006
Carlos Moreno
We performed a prospective, randomized study of adult patients undergoing orthotopic liver transplantation, comparing hemodynamic and tissular oxygenation during reperfusion of the graft. In 30 patients, revascularization was started through the hepatic artery (i.e., initial arterial revascularization) and 10 minutes later the portal vein was unclamped; in 30 others, revascularization was started through the portal vein (i.e., initial portal revascularization) and 10 minutes later the hepatic artery was unclamped. The primary endpoints of the study were mean systemic arterial pressure and the gastric-end-tidal carbon dioxide partial pressure (PCO2) difference. The secondary endpoints were other hemodynamic and metabolic data. The pattern of the hemodynamic parameters and tissue oxygenation values during the dissection and anhepatic stages were similar in both groups At the first unclamping, initial portal revascularization produced higher values of mean pulmonary pressure (25 ± 7 mm of Hg vs. 17 ± 4 mm of Hg; P < 0.05) and wedge and central venous pressures. At the second unclamping, initial portal revascularization produced higher values of cardiac output and mean arterial pressure (87 ± 15 mm of Hg vs. 79 ± 15 mm of Hg; P < 0.05) and pulmonary blood pressure. Postreperfusion syndrome was present in 13 patients (42.5%) in the arterial group and in 11 patients (36%) in the portal group. During revascularization, the values of gastric and arterial pH decreased in both groups and recovered at the end of the procedure, but were more accentuated in the initial arterial revascularization group. In conclusion, we found that initial arterial revascularization of the graft increases pulmonary pressure less markedly, so it may be indicated for those patients with poor pulmonary and cardiac reserve. Nevertheless, for the remaining patients, initial portal revascularization offers more favorable hemodynamic and metabolic behavior, less inotropic drug use, and earlier normalization of lactate and pH values. Liver Transpl, 2006. © 2006 AASLD. [source]

Neuronal nitric oxide synthase does not contribute to the modulation of pulmonary vascular tone in fetal lambs with congenital diaphragmatic hernia (nNOS in CDH lambs),

PEDIATRIC PULMONOLOGY, Issue 4 2008
Anthony S. de Buys Roessingh MD
Abstract Aim The aim of this study was to determine the presence of the neuronal nitric oxide synthase (nNOS) in near full-term lambs with congenital diaphragmatic hernia (CDH) and its role in the modulation of pulmonary vascular basal tone. Methods We surgically created diaphragmatic hernia on the 85th day of gestation. On the 135th, catheters were used to measure pulmonary pressure and blood flow. We tested the effects of 7-nitroindazole (7-NINA), a specific nNOS antagonist and of N -nitro- l -arginine (l -NNA), a nonspecific nitric oxide synthase antagonist. In vitro, we tested the effects of the same drugs on isolated pulmonary vessels. The presence of nNOS protein in the lungs was detected by Western blot analysis. Results Neither 7-NINA nor l -NNA modified pulmonary vascular basal tone in vivo. After l -NNA injection, acetylcholine (ACh) did not decrease significantly pulmonary vascular resistance (PVR). In vitro, l -NNA increased the cholinergic contractile-response elicited by electric field stimulation (EFS) of vascular rings from lambs with diaphragmatic hernia. Conclusion We conclude that nNOS protein is present in the lungs and pulmonary artery of near full-term lamb fetuses with diaphragmatic hernia, but that it does not contribute to the reduction of pulmonary vascular tone at birth. Pediatr Pulmonol. 2008; 43:313,321. © 2008 Wiley-Liss, Inc. [source]

Right ventricular myocardial isovolumic relaxation time and pulmonary pressure

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2006
Pulsed Doppler tissue imaging in resurrection of Burstin's nomogram
Summary Aims:, Non-invasive assessment of pulmonary artery systolic pressure (PASP) has several limitations. As previously described by Burstin, the right ventricular (RV) isovolumic relaxation time (IVRt) is sensitive to changes in PASP. We therefore compared RV myocardial IVRt, derived by Doppler tissue imaging (DTI), with simultaneously measured invasive PASP. Methods and results:, Twenty-six consecutive patients (18 males, mean age 52 ± 12 years, range 23,75) underwent a simultaneous Doppler echocardiography, including DTI, and cardiac catheterization examination for measurement of PASP and right atrial mean pressures. IVRt was measured using the myocardial velocities by pulsed DTI at both basal and mid cavity segments of the RV free wall. As diastolic time intervals are influenced by heart rate IVRt was corrected for heart rate (IVRt/RR%). A significant correlation was found between PASP and regional IVRt/RR% at both the basal (r = 0·42, P<0·05) and mid cavity segment (r = 0·71, P<0·001). Furthermore, when only patients with normal right atrial pressures (<7 mmHg) were taken into account, the correlation coefficient improved at both basal and mid cavity segments (r = 0·74, P<0·05 and r = 0·83, P<0·01). Conclusion:, Pulsed Doppler-derived IVRt correlates well with PASP. The use of pulsed DTI for measurement of IVRt is simple, reproducible and easy to obtain. We propose this method as an additional non-invasive tool in the assessment of PASP. [source]

Rest and exercise hemodynamics before and after valve replacement-A combined doppler/catheter study

CLINICAL CARDIOLOGY, Issue 1 2000
G. Inselmann M.D.
Abstract Background: Hemodynamic improvement is a common finding following valve replacement. However, despite a normally functioning prosthesis and normal left ventricular ejection fraction, some patients may show an abnormal hemodynamic response to exercise. Methods: In a combined catheter/Doppler study, rest and exercise hemodynamics were evaluated in 23 patients following aortic (n = 12) (Group 1) or mitral valve (n = 11) (Group 2) replacement and compared with preoperative findings. Patient selection was based on absence of coronary artery disease and left ventricular failure as shown by preoperative angiography. Cardiac output, pulmonary artery pressure, pulmonary capillary pressure, and pulmonary resistance were measured by right heart catheterization, whereas the gradient across the valve prosthesis was determined by Doppler echocardiography. Postoperative evaluation was done at rest and during exercise. The mean follow-up was 8.2 ± 2.2 years in Group 1 and 4.2 ± 1 years in Group 2. Results: With exercise, there was a significant rise in cardiac output in both groups. In Group 1, mean pulmonary pressure/capillary pressure decreased from 24 ± 9/18 ± 9 mmHg preoperatively to 18 ± 2/12 ± 4 mmHg postoperatively (p < 0.05), and increased to 43 ± 12/30 ± 8 mmHg with exercise (p < 0.05). The corresponding values for Group 2 were 36 ± 12/24 ± 6 mmHg preoperatively, 24 ± 7/17 ± 6 mmHg postoperatively (p < 0.05), and 51 ± 2/38 ± 4 mmHg with exercise (p < 0.05). Pulmonary vascular resistance was 109 ± 56 dyne·s·cm -5 preoperatively, 70 ± 39 dyne·s·cm -5 postoperatively (p < 0.05), and 70 ± 36 dyne·s·cm -5 with exercise in Group 1. The corresponding values for Group 2 were 241 ± 155 dyne·s·cm -5, 116 ± 39 dyne·s·cm -5 (p < 0.05), and 104 ± 47 dyne·s·cm -5. There was a significant increase in the gradients across the valve prosthesis in both groups, showing a significant correlation between the gradient at rest and exercise. No correlation was found between valve prosthesis gradient and pulmonary pressures. Conclusion: Exercise-induced pulmonary hypertension and abnormal left ventricular filling pressures seem to be a frequent finding following aortic or mitral valve replacement. Both hemodynamic abnormalities seem not to be determined by obstruction to flow across the valve prosthesis and may be concealed, showing nearly normal values at rest but a pathologic response to physical stress. [source]