Comparisons of the release of vasodilator substances from left and right cardiac chambers of the isolated perfused rabbit heart: Implications for intraventricular thrombus formation

Berent Discigil, Yeow L. Chua, Paul J. Pearson, Paulo R B Evora, Andrea C. Celotto, Hartzell V Schaff

Research output: Contribution to journalArticle

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Abstract

Prostacyclin (PgI2) and endothelium-derived nitric oxide (EDNO) are produced by the arterial and venous endothelium. In addition to their vasodilator action on vascular smooth muscle, both act together to inhibit platelet aggregation and promote platelet disaggregation. EDNO also inhibits platelet adhesion to the endothelium. EDNO and PgI2 have been shown to be released from the cultured endocardial cells. In this study, we examined the release of vasoactive substances from the intact endocardium by using isolated rabbit hearts perfused with physiological salt solution (95% O2/5% CO2, T = 37 °C). The right and left cardiac chambers were perfused through separate constant-flow perfusion loops (physiological salt solution, 8 ml min-1). Effluent from left and right cardiac, separately, was bioassayed on canine coronary artery smooth muscle, which had been contracted with prostaglandin F2α_(2 × 10-6 M) and no change in tension was exhibit. However, addition of calcium ionophore A23187 (10-6 M) to the cardiac chambers' perfusion line induced vasodilation of the bioassay coronary ring, 61.4 ± 7.4% versus 70.49 ± 6.1% of initial prostaglandin F contraction for the left and right cardiac chambers perfusate, respectively (mean ± SEM, n = 10, p > 0.05). Production of vasodilator was blocked totally in the left heart but, only partially blocked in the right heart by adding indomethacin (10-5 M) to the perfusate, respectively, 95.2 ± 2.2% versus 41.5 ± 4.8% (mean ± SEM, n = 10, p < 0.05). 6-Keto prostaglandin F, measured in the endocardial superfusion effluent was also higher for the left cardiac chambers than for the right at the time of stimulation with the A23187, respectively, 25385.88 ± 5495 pg/ml (n = 8) versus 13,132.45 ± 1839.82 pg/ml (n = 8), (p < 0.05). These results showed that cyclooxygenase pathway plays major role in generating vasoactive substances for the left cardiac chamber endocardium; while it is not the main pathway for the right ventricular endocardium at which EDNO and PgI2 could act together and potentiate their antithrombogenic activities in isolated perfused rabbit heart. This may be an explanation for the intraventricular thrombus mostly seen in left ventricle rather than in right ventricle as a complication of myocardial infarction.

Original languageEnglish (US)
Pages (from-to)259-263
Number of pages5
JournalNitric Oxide - Biology and Chemistry
Volume20
Issue number4
DOIs
StatePublished - Jun 1 2009

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Vasodilator Agents
Endocardium
Nitric Oxide
Thrombosis
Platelets
Rabbits
Dinoprost
Calcimycin
Heart Ventricles
Endothelium
Muscle
Effluents
Blood Platelets
Perfusion
Salts
Scanning electron microscopy
Calcium Ionophores
Bioassay
Epoprostenol
Prostaglandin-Endoperoxide Synthases

Keywords

  • Endocardium
  • Endothelium
  • Heart ventricles
  • Nitric oxide
  • Prostacyclin

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Cancer Research
  • Physiology

Cite this

Comparisons of the release of vasodilator substances from left and right cardiac chambers of the isolated perfused rabbit heart : Implications for intraventricular thrombus formation. / Discigil, Berent; Chua, Yeow L.; Pearson, Paul J.; Evora, Paulo R B; Celotto, Andrea C.; Schaff, Hartzell V.

In: Nitric Oxide - Biology and Chemistry, Vol. 20, No. 4, 01.06.2009, p. 259-263.

Research output: Contribution to journalArticle

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abstract = "Prostacyclin (PgI2) and endothelium-derived nitric oxide (EDNO) are produced by the arterial and venous endothelium. In addition to their vasodilator action on vascular smooth muscle, both act together to inhibit platelet aggregation and promote platelet disaggregation. EDNO also inhibits platelet adhesion to the endothelium. EDNO and PgI2 have been shown to be released from the cultured endocardial cells. In this study, we examined the release of vasoactive substances from the intact endocardium by using isolated rabbit hearts perfused with physiological salt solution (95{\%} O2/5{\%} CO2, T = 37 °C). The right and left cardiac chambers were perfused through separate constant-flow perfusion loops (physiological salt solution, 8 ml min-1). Effluent from left and right cardiac, separately, was bioassayed on canine coronary artery smooth muscle, which had been contracted with prostaglandin F2α_(2 × 10-6 M) and no change in tension was exhibit. However, addition of calcium ionophore A23187 (10-6 M) to the cardiac chambers' perfusion line induced vasodilation of the bioassay coronary ring, 61.4 ± 7.4{\%} versus 70.49 ± 6.1{\%} of initial prostaglandin F2α contraction for the left and right cardiac chambers perfusate, respectively (mean ± SEM, n = 10, p > 0.05). Production of vasodilator was blocked totally in the left heart but, only partially blocked in the right heart by adding indomethacin (10-5 M) to the perfusate, respectively, 95.2 ± 2.2{\%} versus 41.5 ± 4.8{\%} (mean ± SEM, n = 10, p < 0.05). 6-Keto prostaglandin F1α, measured in the endocardial superfusion effluent was also higher for the left cardiac chambers than for the right at the time of stimulation with the A23187, respectively, 25385.88 ± 5495 pg/ml (n = 8) versus 13,132.45 ± 1839.82 pg/ml (n = 8), (p < 0.05). These results showed that cyclooxygenase pathway plays major role in generating vasoactive substances for the left cardiac chamber endocardium; while it is not the main pathway for the right ventricular endocardium at which EDNO and PgI2 could act together and potentiate their antithrombogenic activities in isolated perfused rabbit heart. This may be an explanation for the intraventricular thrombus mostly seen in left ventricle rather than in right ventricle as a complication of myocardial infarction.",
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AU - Pearson, Paul J.

AU - Evora, Paulo R B

AU - Celotto, Andrea C.

AU - Schaff, Hartzell V

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AB - Prostacyclin (PgI2) and endothelium-derived nitric oxide (EDNO) are produced by the arterial and venous endothelium. In addition to their vasodilator action on vascular smooth muscle, both act together to inhibit platelet aggregation and promote platelet disaggregation. EDNO also inhibits platelet adhesion to the endothelium. EDNO and PgI2 have been shown to be released from the cultured endocardial cells. In this study, we examined the release of vasoactive substances from the intact endocardium by using isolated rabbit hearts perfused with physiological salt solution (95% O2/5% CO2, T = 37 °C). The right and left cardiac chambers were perfused through separate constant-flow perfusion loops (physiological salt solution, 8 ml min-1). Effluent from left and right cardiac, separately, was bioassayed on canine coronary artery smooth muscle, which had been contracted with prostaglandin F2α_(2 × 10-6 M) and no change in tension was exhibit. However, addition of calcium ionophore A23187 (10-6 M) to the cardiac chambers' perfusion line induced vasodilation of the bioassay coronary ring, 61.4 ± 7.4% versus 70.49 ± 6.1% of initial prostaglandin F2α contraction for the left and right cardiac chambers perfusate, respectively (mean ± SEM, n = 10, p > 0.05). Production of vasodilator was blocked totally in the left heart but, only partially blocked in the right heart by adding indomethacin (10-5 M) to the perfusate, respectively, 95.2 ± 2.2% versus 41.5 ± 4.8% (mean ± SEM, n = 10, p < 0.05). 6-Keto prostaglandin F1α, measured in the endocardial superfusion effluent was also higher for the left cardiac chambers than for the right at the time of stimulation with the A23187, respectively, 25385.88 ± 5495 pg/ml (n = 8) versus 13,132.45 ± 1839.82 pg/ml (n = 8), (p < 0.05). These results showed that cyclooxygenase pathway plays major role in generating vasoactive substances for the left cardiac chamber endocardium; while it is not the main pathway for the right ventricular endocardium at which EDNO and PgI2 could act together and potentiate their antithrombogenic activities in isolated perfused rabbit heart. This may be an explanation for the intraventricular thrombus mostly seen in left ventricle rather than in right ventricle as a complication of myocardial infarction.

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KW - Endothelium

KW - Heart ventricles

KW - Nitric oxide

KW - Prostacyclin

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