Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia

T. Tonnessen, A. Giaid, D. Saleh, P. A. Naess, Masashi Yanagisawa, G. Christensen

Research output: Contribution to journalArticle

119 Citations (Scopus)

Abstract

Circulating levels of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1) are increased in association with myocardial ischemia and infarction. The present study investigates whether ET-1 is synthesized and produced locally in the ischemic heart. Sixteen pigs were divided into three groups. In the first group, the left anterior descending coronary artery was occluded for 90 minutes, followed by 150 minutes of reperfusion (group A, n=8). Two additional groups were subjected to 90 minutes (group B, n=4) or 240 minutes (group C, n=4) of ischemia without reperfusion. Biopsies from the nonischemic and ischemic myocardium were rapidly obtained from the beating heart and subsequently examined by Northern blot, in situ hybridization, and immunohistochemistry. Arterial plasma ET-1 was measured before ischemia and at the end of the experiments. Northern blot revealed a twofold increase in ET-1 mRNA in the ischemic myocardium compared with the nonischemic myocardium. In situ hybridization showed a considerable increase in ET-1 mRNA over the ischemic cardiomyocytes. Substantial ET-1-like immunoreactivity (ET- 1-ir) was detected in cardiomyocytes in the ischemic region. In contrast, little or no ET-1-ir or mRNA was detected in nonischemic cardiomyocytes. Both in the ischemic and nonischemic regions, little ET-1-ir was detected in vascular endothelial cells or vascular smooth muscle cells. There was no difference in the intensity and distribution of ET-1 mRNA expression or ET- 1-ir among experimental groups A, B, and C. Arterial plasma ET-1 was increased only in group A, the reperfused group. In conclusion, these findings provide a definitive evidence for a de novo synthesis of ET-1 by cardiomyocytes subjected to ischemia in vivo.

Original languageEnglish (US)
Pages (from-to)767-772
Number of pages6
JournalCirculation Research
Volume76
Issue number5
StatePublished - 1995

Fingerprint

Endothelin-1
Cardiac Myocytes
Swine
Ischemia
Myocardium
Messenger RNA
Northern Blotting
Reperfusion
In Situ Hybridization
Vasoconstrictor Agents
Vascular Smooth Muscle
Smooth Muscle Myocytes
Endothelium
Myocardial Ischemia
Coronary Vessels
Endothelial Cells
Immunohistochemistry
Myocardial Infarction
Biopsy
Peptides

Keywords

  • endothelin-1
  • immunohistochemistry
  • in situ hybridization
  • myocardial ischemia
  • Northern blot

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Tonnessen, T., Giaid, A., Saleh, D., Naess, P. A., Yanagisawa, M., & Christensen, G. (1995). Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia. Circulation Research, 76(5), 767-772.

Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia. / Tonnessen, T.; Giaid, A.; Saleh, D.; Naess, P. A.; Yanagisawa, Masashi; Christensen, G.

In: Circulation Research, Vol. 76, No. 5, 1995, p. 767-772.

Research output: Contribution to journalArticle

Tonnessen, T, Giaid, A, Saleh, D, Naess, PA, Yanagisawa, M & Christensen, G 1995, 'Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia', Circulation Research, vol. 76, no. 5, pp. 767-772.
Tonnessen, T. ; Giaid, A. ; Saleh, D. ; Naess, P. A. ; Yanagisawa, Masashi ; Christensen, G. / Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia. In: Circulation Research. 1995 ; Vol. 76, No. 5. pp. 767-772.
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AU - Christensen, G.

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AB - Circulating levels of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1) are increased in association with myocardial ischemia and infarction. The present study investigates whether ET-1 is synthesized and produced locally in the ischemic heart. Sixteen pigs were divided into three groups. In the first group, the left anterior descending coronary artery was occluded for 90 minutes, followed by 150 minutes of reperfusion (group A, n=8). Two additional groups were subjected to 90 minutes (group B, n=4) or 240 minutes (group C, n=4) of ischemia without reperfusion. Biopsies from the nonischemic and ischemic myocardium were rapidly obtained from the beating heart and subsequently examined by Northern blot, in situ hybridization, and immunohistochemistry. Arterial plasma ET-1 was measured before ischemia and at the end of the experiments. Northern blot revealed a twofold increase in ET-1 mRNA in the ischemic myocardium compared with the nonischemic myocardium. In situ hybridization showed a considerable increase in ET-1 mRNA over the ischemic cardiomyocytes. Substantial ET-1-like immunoreactivity (ET- 1-ir) was detected in cardiomyocytes in the ischemic region. In contrast, little or no ET-1-ir or mRNA was detected in nonischemic cardiomyocytes. Both in the ischemic and nonischemic regions, little ET-1-ir was detected in vascular endothelial cells or vascular smooth muscle cells. There was no difference in the intensity and distribution of ET-1 mRNA expression or ET- 1-ir among experimental groups A, B, and C. Arterial plasma ET-1 was increased only in group A, the reperfused group. In conclusion, these findings provide a definitive evidence for a de novo synthesis of ET-1 by cardiomyocytes subjected to ischemia in vivo.

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