Ry (Bio 1D software; Viber Lourmat, Marne La VAllee, France). Relative quantification was systematically ?performed by normalization with b-actin (Sigma-Aldrich, St Louis, MO, USA) on each blots. Samples from sham and shunted pigs were randomly tested in each Western Blot and one randomly chosen reference sample was deposited on all different blots to allow the comparison and the quantification of all different blots together.MorphometryPulmonary arterial morphometry was performed as previously described [5?]. Only the smallest pulmonary resistive arterioles with an external diameter (ED) of ,75 mm and a complete muscular coat were measured. Medial thickness (MT) was related to arterial size with the following formula: MT = (2xMT/ED)Statistical Pentagastrin AnalysisValues are reported as mean 6 standard error of the mean (SEM). Statistical analyses were performed using StatView 5.0 Software. The hemodynamic and biological data of 16574785 6-month shunt and 6-month sham groups were compared by performing one-way analysis of variance (one-way ANOVA). When the F ratio of thisInflammation and HO-1 in Right Ventricular FailureTable 1. Primers used for RTQ-PCR in porcine lung and myocardial tissue.Genes HO-1 Sense Antisense HO-2 Sense Antisense TNF-a Sense Antisense ICAM-1 Sense Antisense ICAM-2 Sense Antisense VCAM-1 Sense Antisense IL-33 Sense Antisense ST2 Sense Antisense IL-19 Sense Antisense STAT3 Sense AntisensePrimer Sequences59-ATGTGAATGCAACCCTGTGA-39 39-GGAAGCCAGTCAAGAGACCA-59-CGCAGCAGTTCAAGCAGTT-39 39-CCTCCTCCACGATCTTCTCTT-59-TCTGGACTTTGCTGAATCTGG-39 39-TGAGGGGGTCTGAAGGAGTAA-partially reported elsewhere [8], the mPpa/Q relationships were shifted to higher pressures with an increase in slope hellosham (3.460.4 mmHg.L21.min.m22) vs shunt (7.260.6 mmHg.L21.min.m22), p = 0.0003] (8). There was a marked decrease in Ees/Ea ratio (sham (1.5160.06) vs shunt (0.6860.07), p = 0.000001) [8], indicating a RV-arterial uncoupling in the 6-month shunted compared with the 6-month shamoperated pigs. Cardiac index (Q) (sham (3.560.3 L.min21.m22) vs shunt (1.960.1 L.min21.m22), p = 0.0002) [8] and stroke volume decreased (sham (4265 mL.Beat21) vs shunt (2765 mL.Beat21), p = 0.003) and right atrial pressure (Pra) tended to increase (sham (6.160.3 mmHg) vs shunt (7.160.5 mmHg), p = 0.09). Six-month aorta-pulmonary shunting was associated with increased Z0 and ZC impedance (Figure 1). After 6-month systemic-to-pulmonary shunting, pulmonary arterial thickness increased, mostly in the smallest pulmonary arteries (,75 mm) (Figure 2).59-GCTATCTTGGGCAGTGTTGG-39 39-AGGCTGGTGTGCTAAGTTTCA-59-GCCCACTTTTGTGACCGTAG-39 39-GGTGATGGTGAGGGTTTCA-Pulmonary Hypertensive Disease – Pulmonary Expressions of Heme Oxygenases and Cell Adhesion MoleculesSystemic-to-pulmonary shunting was associated with a non significant but strong tendency to the decreased gene (p = 0.06) and protein (p = 0.07) expressions of inducible HO-1 isoenzyme in lung tissue (Figure 3A and 3B), while pulmonary gene expression of constitutive HO-2 isoenzyme did not change (Figure 3A). As illustrated in Figure 3A, pulmonary gene expressions of cell surface glycoproteins mediating inflammatory cell adhesion, such as ICAM-1 and ICAM-2 increased, while pulmonary expression of VCAM-1 did not change.59-GAGTTAATCCGGTTGGGACA-39 39-TTCACAGAACTGCCCTCCTC-59-CCGGCAAAGTCTCGATAAAA-39 39-ATGATAAGGCCAGAGCGAAG-59-CCTGGAGTTCATTCCCTCTG-39 39-GGAGATTGTTGGTGCTCCTT-Pulmonary Hypertensive Disease – Pulmonary Expressions of Tumor Necrosis Factor(TNF.
