31 research outputs found

    Basal measurements from the right ventricle strips.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on the basal conditions of isometric force (A), time to peak tension (B), relaxation time to 90% (C), +dF/dt (D) and −dF/dt (E) of rat right ventricular strips from the Control, MI and HgCl<sub>2</sub>-MI groups. The results are reported as the means ± SEM for 10–12 animals per group. MI = myocardial infarction; dF/dt = time derivatives of right ventricular force development. *P<0.05 <i>vs</i> Control and HgCl<sub>2</sub>-MI; # P<0.05 <i>vs</i> Control (one-way ANOVA followed by Tukey's <i>post hoc</i> tests).</p

    Response to β-adrenergic stimuli.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on isoproterenol (ISO, 10<sup>−4</sup> M) conditions compared to steady-state condition of isometric force. The results are reported as the means ± SEM for 10–12 animals per group. MI = myocardial infarction; # P<0.05 <i>vs</i> Control (one-way repeated measures ANOVA followed by the Tukey's <i>post hoc</i> test).</p

    Tetanic contractions.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on relative tetanic peak force (A) and relative tetanic plateau force (B) in rat right ventricular strips from the Control, MI and HgCl<sub>2</sub>-MI groups. The results are reported as the means ± SEM for 10–12 animals per group. MI = myocardial infarction; * P<0.05 <i>vs</i> Control and HgCl<sub>2</sub>-MI (one-way ANOVA followed by the Tukey's <i>post hoc</i> test).</p

    Chronic Exposure to Low Doses of HgCl<sub>2</sub> Avoids Calcium Handling Impairment in the Right Ventricle after Myocardial Infarction in Rats

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    <div><p>Right ventricle systolic dysfunction is a major risk factor for death and heart failure after myocardial infarction (MI). Heavy metal exposure has been associated with the development of several cardiovascular diseases, such as MI. The aim of this study was to investigate whether chronic exposure to low doses of mercury chloride (HgCl<sub>2</sub>) enhances the functional deterioration of right ventricle strips after MI. Male Wistar rats were divided into four groups: Control (vehicle); HgCl<sub>2</sub> (exposure during 4 weeks- 1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m. to cover daily loss); MI surgery induced and HgCl<sub>2</sub>-MI groups. One week after MI, the morphological and hemodynamic measurements and isometric tension of right ventricle strips were investigated. The chronic HgCl<sub>2</sub> exposure did not worsen the injury compared with MI alone in the morphological or hemodynamic parameters evaluated. At basal conditions, despite similar maximum isometric force at L-max, relaxation time was increased in the MI group but unaffected in the HgCl<sub>2</sub>-MI compared to the Control group. Impairment of the sarcoplasmic reticulum (SR) function and reduction in the sarcolemmal calcium influx were observed in MI group associated with SERCA2a reduction and increased PLB protein expression. Induction of MI in chronic HgCl<sub>2</sub> exposed rats did not cause any alteration in the developed force at L-max, lusitropic function or −dF/dt except for a tendency of a reduction SR function. These findings could be partially explained by the normalization in the sarcolemmal calcium influx and the increase in NCX protein expression observed only in this group. These results suggest that chronic exposure to low doses of HgCl<sub>2</sub> prevents the impaired SR function and the reduced sarcolemmal calcium influx observed in MI likely by acting on NCX, PLB and SERCA2a protein expression.</p></div

    Measurements of sarcolemmal calcium influx.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on relative potentiation (ratio of post-rest contraction and steady-state contractions) of isometric contractions obtained after a 15 min pause in rat right ventricular strips from the Control, MI and HgCl<sub>2</sub>-MI groups. The results are reported as the means ± SEM for 10–12 animals per group. MI = myocardial infarction.*P<0.05 <i>vs</i> Control and HgCl<sub>2</sub>-MI; & P<0.05 <i>vs</i> Control and MI (one-way ANOVA followed by Tukey's <i>post hoc</i> tests).</p

    Functional assessment of sarcoplasmic reticulum.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on relative potentiation (ratio of post-rest contractions and steady-state contractions) of isometric contractions obtained after a 15, 30, and 60 s pause in rat right ventricular strips from the Control, MI and HgCl<sub>2</sub>-MI groups. The results are reported as the means ± SEM for 10–12 animals per group. MI = myocardial infarction. # P<0.05 <i>vs</i> Control in the same time pause (one-way ANOVA followed by Tukey's <i>post hoc</i> tests).</p

    Right ventricle proteins levels.

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    <p>The effect of myocardial infarction in rats with continuous exposure to HgCl<sub>2</sub> on the densitometry analysis of the Western blot for SERCA2a (A), PLB (B), PLB phosphorylated at serine 16 (C), SERCA/PLB ratio (D), NCX (E) in rat right ventricular strips from Control, MI and HgCl<sub>2</sub>-MI groups. The results are reported as the means ± SEM for 5–6 animals per group. MI = myocardial infarction; * P<0.05 <i>vs</i> Control and HgCl<sub>2</sub>-MI; # P<0.05 <i>vs</i> Control; & P<0.05 <i>vs</i> Control and MI (one-way ANOVA followed by the Tukey's <i>post hoc</i> test).</p

    The Legacy Of El Salvador\u27s Murdered Jesuits

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    <p>Effects of the specific NAD(P)H oxidase inhibitor, apocynin (0.3 mM), on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.</p

    Protein expression levels of the ventricular α-1 Na<sup>+</sup>, K<sup>+</sup>-ATPase subunit.

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    <p>Bands that are representative of the Western blots of the expression of α-1 Na<sup>+</sup>, K<sup>+</sup>-ATPase subunit and GAPDH (Glyceraldehyde 3-phosphate dehydrogenase) are presented at the top of the figure. Results are expressed as the ratio between the area and density of α-1 Na<sup>+</sup>, K<sup>+</sup>-ATPase subunit and GAPDH in the control (Ct) and lead treated (Pb) groups. Number of animals = 7 for each group. <i>p</i>>0.05, Ct vs Pb, Student t<i>-</i>test.</p

    Effects of the TEA in aortic segments from both untreated and lead-treated rats (A).

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    <p>Effects of the nonselective K<sup>+</sup> channel blocker, TEA (2 mM) on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. The inset shows differences in dAUC in the presence and absence of TEA. Effects of the co-incubation of catalase/TEA in aortic segments from untreated and lead-treated rats (B). Effects of the co-incubation of catalase (1000 U/mL) with TEA (2 mM) on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.</p
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