Simultaneous recording of his bundle electrogram, electrocardiogram, and systolic tension from intact modified Langendorff rat heart preparations I: Effects of perfusion time, cadmium, and lead

Kopp, Stephen J.; Baker, James C.; D'Agrosa, Louis S.; Hawley, Philip L.

doi:10.1016/0041-008x(78)90093-5

Cited by 24 publications

(5 citation statements)

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“…Additionally, chronic and acute lead poisoning causes cardiac and vascular damage with potentially lethal consequences (8,9). Lead also has other effects on the cardiovascular system, www.bjournal.com.br Braz J Med Biol Res 43 (5) 2010 including endothelial dysfunction (10) and inhibition of the sarcolemmal sodium potassium ATPase (11).…”

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confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentrationresponse curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E + ), lead acetate increased maximal response (E max ) (control: 364.4 ± 36, Pb 2+ : 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD 2 ; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E -) lead had no effect but increased baseline perfusion pressure (E + : 79.5 ± 2.4, E -: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on E max and pD 2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenasederived vasoconstrictors and involving reactive oxygen species.

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confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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“…Acute and chronic Pb ++ exposure can cause potentially lethal consequences [9,10], because it acts in different places into the cardiovascular system, including endothelial dysfunction [11], direct effects on cardiac excitability and contractility [10], tissue damage by free radicals [12], cardiotoxicity and heart failure [13] and increasing blood pressure [14]. A study in 62 people exposed to Pb ++ [7] showed a positive correlation between increasing inhibition of nitric oxide with increasing blood lead levels, which involves an association between Pb ++ exposure and an increasing cardiovascular risk.…”

Section: Discussionmentioning

confidence: 99%

“…In general, more than 143000 people died every year from Pb-related diseases, developing countries have the highest mortality rates [6]. Experimental and epidemiologic studies have reported Pb ++ effects on cardiac system [7][8][9][10][11][12][13][14]. An experimental study shows that Pb ++ blocks the L-type Ca ++ channels [15].…”

Section: Introductionmentioning

confidence: 99%

Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study

Tobón

Pachajoa

Ugarte

et al. 2017

VII Latin American Congress on Biomedical Engineering CLAIB 2016, Bucaramanga, Santander, Colombia, October 26th -28th, 2016

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“…KCl-arrested hearts and the CdC12-arrested hearts result in diastolic papillary muscles within 90-95 % of optimum muscle length. Some observations suggest that the cadmium may be interfering with the excitatory effects of calcium; e.g., the rapidity of action of the low concentration of CdC12 (5raM) in 0.9 % NaC1, the divalent nature of this cation, and the transmission blockade within the ventricles as measured by the electrocardiogram (10,11).…”

Section: Discussionmentioning

confidence: 99%

The pattern of sarcomere lengths through the left ventricular free wall: differences between open and closed-chest rats

1983

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Sarcomere lengths were measured with an optical microscope at five sites through the free wall of the open-chest rat left ventricle. After pentobarbital anesthesia the hearts were arrested with 5 mM cadmium chloride and 0.9% saline and fixed with formaldehyde solution. Serial sections (250 microns thick) were cut from endocardium to epicardium with a freezing microtome. Selected sections were sonified, mixed with a gelatin-water solution, and placed on a glass slide. There was a progressive increase in mean sarcomere lengths with increasing intraventricular pressures though the sarcomeres did not significantly exceed their optimum length. There was a distinct and statistically significant difference in the pattern of sarcomere lengths through the ventricular wall between our previous closed-chest study and the present open-chest study. In this open-chest animals, there was an almost linear pattern of increasing sarcomere lengths from endocardium to epicardium over the range of semiphysiologic diastolic intraventricular pressures (6, 12, and 24 cm H2O -- 0.59, 1.18, 2.35 kPa). These results appear to caution against extrapolations on ventricular function derived from open chest studies to the normal physiologic conditions.

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Simultaneous recording of his bundle electrogram, electrocardiogram, and systolic tension from intact modified Langendorff rat heart preparations I: Effects of perfusion time, cadmium, and lead

Cited by 24 publications

References 13 publications

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study

The pattern of sarcomere lengths through the left ventricular free wall: differences between open and closed-chest rats

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