Balloon dilatation of porcine pulmonary arteries decreases endothelium-dependent relaxations and increases vasoconstriction to aggregating platelets

Susan J. Razzuk, Thomas M. Zellers

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Background: Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. Methods and Results: We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n=20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+ group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4±8% of constriction to 80 mmol/L KCl) and E- groups (24±5%), which were inhibited by pyrilamine, a histamine blocker (11±4%; P<.05), and an intact endothelium (8±5%; P<.05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70±6% relaxation), which were significantly (P<.05) inhibited in the BD group (20±7%), by L-nitro-arginine (EDNO blocker, 17±7%) and in the E-group (21±9%). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. Conclusions: Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.

Original languageEnglish (US)
Pages (from-to)1221-1228
Number of pages8
JournalCirculation
Volume91
Issue number4
StatePublished - Feb 15 1995

Fingerprint

Vasoconstriction
Pulmonary Artery
Endothelium
Dilatation
Swine
Blood Platelets
Constriction
Nitric Oxide
Histamine
Pyrilamine
Lung
Calcium Ionophores
Calcimycin
Nitroprusside
Epoprostenol
Platelet Aggregation
Vasodilation
Thrombin
Acetylcholine
Smooth Muscle

Keywords

  • Angioplasty
  • Endothelium-derived factors

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Balloon dilatation of porcine pulmonary arteries decreases endothelium-dependent relaxations and increases vasoconstriction to aggregating platelets",
abstract = "Background: Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. Methods and Results: We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n=20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+ group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4±8{\%} of constriction to 80 mmol/L KCl) and E- groups (24±5{\%}), which were inhibited by pyrilamine, a histamine blocker (11±4{\%}; P<.05), and an intact endothelium (8±5{\%}; P<.05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70±6{\%} relaxation), which were significantly (P<.05) inhibited in the BD group (20±7{\%}), by L-nitro-arginine (EDNO blocker, 17±7{\%}) and in the E-group (21±9{\%}). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. Conclusions: Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.",
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T1 - Balloon dilatation of porcine pulmonary arteries decreases endothelium-dependent relaxations and increases vasoconstriction to aggregating platelets

AU - Razzuk, Susan J.

AU - Zellers, Thomas M.

PY - 1995/2/15

Y1 - 1995/2/15

N2 - Background: Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. Methods and Results: We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n=20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+ group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4±8% of constriction to 80 mmol/L KCl) and E- groups (24±5%), which were inhibited by pyrilamine, a histamine blocker (11±4%; P<.05), and an intact endothelium (8±5%; P<.05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70±6% relaxation), which were significantly (P<.05) inhibited in the BD group (20±7%), by L-nitro-arginine (EDNO blocker, 17±7%) and in the E-group (21±9%). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. Conclusions: Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.

AB - Background: Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. Methods and Results: We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n=20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+ group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4±8% of constriction to 80 mmol/L KCl) and E- groups (24±5%), which were inhibited by pyrilamine, a histamine blocker (11±4%; P<.05), and an intact endothelium (8±5%; P<.05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70±6% relaxation), which were significantly (P<.05) inhibited in the BD group (20±7%), by L-nitro-arginine (EDNO blocker, 17±7%) and in the E-group (21±9%). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. Conclusions: Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.

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KW - Endothelium-derived factors

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