Influence of a lymphagogue, CLS 2210, on regional cardiac lymphatics and the electrocardiogram after coronary artery occlusion in the dog

L. Szlavy, I. Repa, A. De Courten

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Abstract

To examine the role of cardiac lymphatic drainage in myocardial infarction, we quantified the effect of a lymphagogue, CLS 2210, on the number and appearance of myocardial lymphatics as well as the electrocardiogram following coronary occlusion in the dog. Thirty minutes and six hours after intravenous administration of the benzenesulfonate compound, (CLS 2210) cardiac lymphatics in the distribution of the left anterior descending coronary artery (LAD) were determined and further delineated by postmortem cardiac lymphangiograms. The results were compared with treated and untreated dogs without and with descending coronary artery ligation including the noninfarcted zone; that is, myocardium within the distribution of left circumflex coronary (LCC) artery. After 30 minutes in dogs receiving CLS 2210 without LAD ligation, number of lymphatics (point count/cm2, see Methods) were respectively - LAD zone: 2.62 ± 0.11 or 10.9% of left ventricular (LV) surface; LCC zone: 2.87 ± 0.10, whereas after six hours - LAD zone 8.04 ± 0.03 or 32.3% LV surface; LCC zone - 8.13 ± 0.06 compared with uncreated controls - LAD zone 1.71 ± 0.11 or 6.6% of LV surface; LCC zone 1.65 ± 0.12 ( p <0.0001). At similar intervals in dogs with LAD ligation, the findings were at 30 minutes LAD zone 0.78 ± 0.07 or 3.1% of LV surface and at 360 minutes was 0.80 ± 0.08 or 3.3% of LV surface. In conjunction with CLS 2210 administration, however, LAD zone showed at 30 minutes 2.50 ± 0.12 or 10% of LV surface (p <.01) and at 360 minutes was 10.34 ± 0.03 or 35.1% of LV surface. Moreover, in dogs with LAD ligation and CLS 2210 adminstration, electrocardiograma at six hours showed diminished ST-segment elevation. The data suggest that CLS 2210 facilitates preservation of myocardial lymphatics and hence cardiac lymph transport and with its other 'angioprotective' affects (antagonizes platelets and lowers blood viscosity) limits myocardial infarct size following coronary artery occlusion.

Original languageEnglish
Pages (from-to)15-20
Number of pages6
JournalLymphology
Volume19
Issue number1
Publication statusPublished - 1986

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Coronary Occlusion
Coronary Vessels
Electrocardiography
Dogs
Ligation
Myocardial Infarction
Blood Viscosity
Lymph
Intravenous Administration
CLS 2210
Drainage
Myocardium
Blood Platelets

ASJC Scopus subject areas

  • Immunology

Cite this

Influence of a lymphagogue, CLS 2210, on regional cardiac lymphatics and the electrocardiogram after coronary artery occlusion in the dog. / Szlavy, L.; Repa, I.; De Courten, A.

In: Lymphology, Vol. 19, No. 1, 1986, p. 15-20.

Research output: Contribution to journalArticle

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abstract = "To examine the role of cardiac lymphatic drainage in myocardial infarction, we quantified the effect of a lymphagogue, CLS 2210, on the number and appearance of myocardial lymphatics as well as the electrocardiogram following coronary occlusion in the dog. Thirty minutes and six hours after intravenous administration of the benzenesulfonate compound, (CLS 2210) cardiac lymphatics in the distribution of the left anterior descending coronary artery (LAD) were determined and further delineated by postmortem cardiac lymphangiograms. The results were compared with treated and untreated dogs without and with descending coronary artery ligation including the noninfarcted zone; that is, myocardium within the distribution of left circumflex coronary (LCC) artery. After 30 minutes in dogs receiving CLS 2210 without LAD ligation, number of lymphatics (point count/cm2, see Methods) were respectively - LAD zone: 2.62 ± 0.11 or 10.9{\%} of left ventricular (LV) surface; LCC zone: 2.87 ± 0.10, whereas after six hours - LAD zone 8.04 ± 0.03 or 32.3{\%} LV surface; LCC zone - 8.13 ± 0.06 compared with uncreated controls - LAD zone 1.71 ± 0.11 or 6.6{\%} of LV surface; LCC zone 1.65 ± 0.12 ( p <0.0001). At similar intervals in dogs with LAD ligation, the findings were at 30 minutes LAD zone 0.78 ± 0.07 or 3.1{\%} of LV surface and at 360 minutes was 0.80 ± 0.08 or 3.3{\%} of LV surface. In conjunction with CLS 2210 administration, however, LAD zone showed at 30 minutes 2.50 ± 0.12 or 10{\%} of LV surface (p <.01) and at 360 minutes was 10.34 ± 0.03 or 35.1{\%} of LV surface. Moreover, in dogs with LAD ligation and CLS 2210 adminstration, electrocardiograma at six hours showed diminished ST-segment elevation. The data suggest that CLS 2210 facilitates preservation of myocardial lymphatics and hence cardiac lymph transport and with its other 'angioprotective' affects (antagonizes platelets and lowers blood viscosity) limits myocardial infarct size following coronary artery occlusion.",
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N2 - To examine the role of cardiac lymphatic drainage in myocardial infarction, we quantified the effect of a lymphagogue, CLS 2210, on the number and appearance of myocardial lymphatics as well as the electrocardiogram following coronary occlusion in the dog. Thirty minutes and six hours after intravenous administration of the benzenesulfonate compound, (CLS 2210) cardiac lymphatics in the distribution of the left anterior descending coronary artery (LAD) were determined and further delineated by postmortem cardiac lymphangiograms. The results were compared with treated and untreated dogs without and with descending coronary artery ligation including the noninfarcted zone; that is, myocardium within the distribution of left circumflex coronary (LCC) artery. After 30 minutes in dogs receiving CLS 2210 without LAD ligation, number of lymphatics (point count/cm2, see Methods) were respectively - LAD zone: 2.62 ± 0.11 or 10.9% of left ventricular (LV) surface; LCC zone: 2.87 ± 0.10, whereas after six hours - LAD zone 8.04 ± 0.03 or 32.3% LV surface; LCC zone - 8.13 ± 0.06 compared with uncreated controls - LAD zone 1.71 ± 0.11 or 6.6% of LV surface; LCC zone 1.65 ± 0.12 ( p <0.0001). At similar intervals in dogs with LAD ligation, the findings were at 30 minutes LAD zone 0.78 ± 0.07 or 3.1% of LV surface and at 360 minutes was 0.80 ± 0.08 or 3.3% of LV surface. In conjunction with CLS 2210 administration, however, LAD zone showed at 30 minutes 2.50 ± 0.12 or 10% of LV surface (p <.01) and at 360 minutes was 10.34 ± 0.03 or 35.1% of LV surface. Moreover, in dogs with LAD ligation and CLS 2210 adminstration, electrocardiograma at six hours showed diminished ST-segment elevation. The data suggest that CLS 2210 facilitates preservation of myocardial lymphatics and hence cardiac lymph transport and with its other 'angioprotective' affects (antagonizes platelets and lowers blood viscosity) limits myocardial infarct size following coronary artery occlusion.

AB - To examine the role of cardiac lymphatic drainage in myocardial infarction, we quantified the effect of a lymphagogue, CLS 2210, on the number and appearance of myocardial lymphatics as well as the electrocardiogram following coronary occlusion in the dog. Thirty minutes and six hours after intravenous administration of the benzenesulfonate compound, (CLS 2210) cardiac lymphatics in the distribution of the left anterior descending coronary artery (LAD) were determined and further delineated by postmortem cardiac lymphangiograms. The results were compared with treated and untreated dogs without and with descending coronary artery ligation including the noninfarcted zone; that is, myocardium within the distribution of left circumflex coronary (LCC) artery. After 30 minutes in dogs receiving CLS 2210 without LAD ligation, number of lymphatics (point count/cm2, see Methods) were respectively - LAD zone: 2.62 ± 0.11 or 10.9% of left ventricular (LV) surface; LCC zone: 2.87 ± 0.10, whereas after six hours - LAD zone 8.04 ± 0.03 or 32.3% LV surface; LCC zone - 8.13 ± 0.06 compared with uncreated controls - LAD zone 1.71 ± 0.11 or 6.6% of LV surface; LCC zone 1.65 ± 0.12 ( p <0.0001). At similar intervals in dogs with LAD ligation, the findings were at 30 minutes LAD zone 0.78 ± 0.07 or 3.1% of LV surface and at 360 minutes was 0.80 ± 0.08 or 3.3% of LV surface. In conjunction with CLS 2210 administration, however, LAD zone showed at 30 minutes 2.50 ± 0.12 or 10% of LV surface (p <.01) and at 360 minutes was 10.34 ± 0.03 or 35.1% of LV surface. Moreover, in dogs with LAD ligation and CLS 2210 adminstration, electrocardiograma at six hours showed diminished ST-segment elevation. The data suggest that CLS 2210 facilitates preservation of myocardial lymphatics and hence cardiac lymph transport and with its other 'angioprotective' affects (antagonizes platelets and lowers blood viscosity) limits myocardial infarct size following coronary artery occlusion.

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