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

<p>Bands that are representative of the Western blots of the expression of α-1 Na⁺, K⁺-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⁺, K⁺-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

Basal measurements from the right ventricle strips.

<p>The effect of myocardial infarction in rats with continuous exposure to HgCl₂ 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 HgCl₂-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 HgCl₂-MI; # P<0.05 <i>vs</i> Control (one-way ANOVA followed by Tukey's <i>post hoc</i> tests).</p

Measurements of sarcolemmal calcium influx.

<p>The effect of myocardial infarction in rats with continuous exposure to HgCl₂ 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 HgCl₂-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 HgCl₂-MI; & P<0.05 <i>vs</i> Control and MI (one-way ANOVA followed by Tukey's <i>post hoc</i> tests).</p

(A, B) The effect of indomethacin (Indo, 10 µM), on the concentration-response curves for phenylephrine in aortic rings in control (CT) conditions or HgCl2.

<p>Results (mean±SEM) are expressed as a percentage of the response to 75 mmol/l KCl. *<i>P</i><0.05 by ANOVA. Number of animals used in parentheses. (C) Differences in the area under the concentration-response curve (dAUC) in aortic rings cultured in the presence of indomethacin (10 µM) under control (CT) conditions and after acute incubation with mercury HgCl₂. *<i>P</i><0.05 by Student’s <i>t</i>-test.</p

Tissue lead concentrations after 30 days of lead treatment (100 ppm).

<p>Means ± SEM. Number of animals = 7 each group.</p><p>*<i>p</i><0.05, as assessed using Student’s t<i>-</i>test.</p

Peak and plateau of the isometric force in isolated left ventricular papillary after tetanic stimulation in the absence and presence of verapamil (Ver) of control (Ct), lead treated (Pb), control+verapamil (Ct Ver), lead treatred+verapamil (Pb Ver).

<p>Each column represents the means ± SEM. Number of animals = 6 for each group. *<i>p</i><0.05, Pb <i>vs.</i> control, one-way ANOVA, followed by Tukey’s test.</p

Protein expression levels of the ventricular calcium pump SR (SERCA 2), phospholamban (PLB), phospho-Tre¹⁷-PLB, phospho-Ser¹⁶-PLB, as well as the ratios phospho-Tre¹⁷-PLB/PLB and phospho-Ser¹⁶-PLB/PLB from controls (Ct) and lead treated (Pb) groups.

<p>Bands are representative of the Western blots of the expression of SERCA-2, PLB, phospho-Tre¹⁷-PLB, phospho-Ser¹⁶-PLB and GAPDH (Glyceraldehyde 3-phosphate dehydrogenase) are presented at the top of the figure. The results are expressed as the ratio between the area and density of SERCA-2 or PLB and GAPDH in the Ct- and Pb-groups. Number of animals = 7 for each group.*<i>p</i><0.05, Ct vs Pb, Student t<i>-</i>test.</p

Tetanic contractions.

<p>The effect of myocardial infarction in rats with continuous exposure to HgCl₂ on relative tetanic peak force (A) and relative tetanic plateau force (B) in rat right ventricular strips from the Control, MI and HgCl₂-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 HgCl₂-MI (one-way ANOVA followed by the Tukey's <i>post hoc</i> test).</p

Effects of lead exposure on haemodynamic arterial and ventricular parameters in anaesthetised rats.

<p>Systolic Arterial Pressure (SAP); Diastolic Arterial Pressure (DAP); Mean Arterial Pressure (MAP); Left Ventricular Systolic Pressure (LVSP); End Left Ventricular Diastolic Pressure (LVDP); Right Ventricular Systolic Pressure (RVSP); End Right Ventricular Diastolic Pressure (RVDP); Left Ventricular Positive (dP/dt+LV) and Negative (dP/dt – LV) Derivates; Right Ventricular Positive (dP/dt+RV) and Negative (dP/dt – RV) Derivates; and Heart Rate (HR). Means ± SEM. Animal number range = 9–12.</p><p>*<i>p</i><0.05, as assessed using Unpaired Student’s t-test.</p

Chronic Exposure to Low Doses of HgCl₂ Avoids Calcium Handling Impairment in the Right Ventricle after Myocardial Infarction in Rats

<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 (HgCl₂) enhances the functional deterioration of right ventricle strips after MI. Male Wistar rats were divided into four groups: Control (vehicle); HgCl₂ (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 HgCl₂-MI groups. One week after MI, the morphological and hemodynamic measurements and isometric tension of right ventricle strips were investigated. The chronic HgCl₂ 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 HgCl₂-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 HgCl₂ 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 HgCl₂ 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