4 research outputs found

    Morphometric measurements.

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    <p>A: Lumen diameter (µm) in vessels divided in groups of non-muscularized-, partially- and fully-muscularized vessels. B: Wall/lumen ratio divided in groups of non-muscularized-, partially- and fully-muscularized vessels. C: Number of non-muscularized-, partially- and muscularized vessels in each experimental group. D: Wall area of the vessels divided in groups of vessel diameter. * P<0.05 vs. wild type and <sup>#</sup> P<0.05 vs. normoxia. Statistical interaction was observed in Figure (B) for non-muscularized vessels.</p

    Lung mRNA expression levels of A) eNOS, K<sub>Ca</sub>2.1, K<sub>Ca</sub>2.2, K<sub>Ca</sub>2.3, K<sub>Ca</sub>3.1, and K<sub>Ca</sub>1.1; B) α-Smooth muscle actin (α-SMA), collagen-1, and TGFβ.

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    <p>Data are given as means ±SEM, n = 7–8. Data were analyzed by two-way ANOVA and differences were considered significant when *P<0.05 from wild type, <sup>#</sup> P<0.05 from normoxia. Statistical interaction (£) was observed in K<sub>Ca</sub>2.3 expression (A). C–E) Genotyping: C:Gel electrophoresis shows that polymerase chain reacton (PCR) detected the K<sub>Ca</sub>2.3-wild type allele (wild type (+)) and the tTA allele (T) in K<sub>Ca</sub>2.3<sup>T/+</sup>, and K<sub>Ca</sub>2.3<sup>T/T</sup>. D and E: PCR detected the targeted allele in K<sub>Ca</sub>3.1<sup>−/+</sup> and in K<sub>Ca</sub>3.1<sup>−/−</sup> as well as the wild type allele in K<sub>Ca</sub>3.1<sup>+/−</sup> and K<sub>Ca</sub>3.1<sup>+/+</sup>. A DNA ladder was used to determine products sizes.</p

    Characteristics of the animals.

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    <p>Selected morphological and functional characteristics and hematocrit of the normoxic and hypoxic strains. Values are means ±SEM, n = 7–8. BPM =  beats per minute. BW =  body weight. *P<0.05 vs. wild type;</p>#<p>P<0.05 vs. normoxia; 2-way ANOVA (n = 7–8 per group).</p

    Right ventricular systolic blood pressure and hypertrophy.

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    <p>A) The effect of chronic hypoxia on right ventricular systolic blood pressure (RVSBP) in wild type and K<sub>Ca</sub>3.1<sup>−/−</sup>/K<sub>Ca</sub>2.3<sup>T/T(+Dox)</sup> mice. Values are means ±SEM, normoxic wild type (n = 8) and K<sub>Ca</sub>3.1<sup>−/−</sup>/K<sub>Ca</sub>2.3<sup>T/T(+Dox)</sup> mice (n = 7). B) Representative trace of right ventricular pressure measurements in normoxic wild type mice (top) and normoxic K<sub>Ca</sub>3.1<sup>−/−</sup>/K<sub>Ca</sub>2.3<sup>T/T(+Dox)</sup> mice (bottom). C) Hypoxia induced right ventricular hypertrophy as indicated by alterations of the weight ratio of right ventricle/left ventricle + septum, in wild type and K<sub>Ca</sub>3.1<sup>−/−</sup>/K<sub>Ca</sub>2.3<sup>T/T(+Dox)</sup> mice, n = 8. D) The effect of hypoxia on right ventricular wall thickness/heart weight (HW) in wild type and K<sub>Ca</sub>3.1<sup>−/−</sup>/K<sub>Ca</sub>2.3<sup>T/T(+Dox)</sup> mice. Values are mean ±SEM, n = 8. Data were analyzed by 2−way ANOVA and differences were considered significant when *P<0.05 vs. wild type, <sup>#</sup> P<0.05 vs. normoxia.</p
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