Leukotriene-mediated coronary vasoconstriction and loss of myocardial contractility evoked by low doses of Escherichia coli hemolysin in perfused rat hearts
hemolysin has been implicated as an important pathogenic factor in extraintestinal infections including sepsis. We investigated the effects of coronary administration of hemolysin on cardiac function in isolated rat hearts perfused at constant flow. Prospective, experimental study. Research laborato...
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Published in | Critical care medicine Vol. 31; no. 3; p. 683 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
01.03.2003
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Abstract | hemolysin has been implicated as an important pathogenic factor in extraintestinal infections including sepsis. We investigated the effects of coronary administration of hemolysin on cardiac function in isolated rat hearts perfused at constant flow.
Prospective, experimental study.
Research laboratory at a university hospital.
Isolated hearts from male Wistar rats.
Isolated hearts were perfused with purified hemolysin for 60 min.
Low concentrations of the toxin in the perfusate (0.1-0.2 hemolytic units/mL) caused a dose-dependent coronary vasoconstriction with a marked increase in coronary perfusion pressure, which was paralleled by a decrease in left ventricular developed pressure (and the maximum rate of left ventricular pressure increase). Moreover, 0.2 hemolytic units/mL hemolysin evoked ventricular fibrillation within 10 mins of toxin application. These events were accompanied by the liberation of leukotrienes (LTC4, LTD4, LTE4, and LTB4), thromboxane A2, prostaglandin I2, and the cell necrosis markers lactate dehydrogenase and creatine kinase into the recirculating perfusate. The lipoxygenase inhibitor MK-886 fully blocked the toxin-induced coronary vasoconstrictor response and the loss of myocardial contractility and reduced the release of lactate dehydrogenase and creatine kinase. In contrast to this, the cyclooxygenase inhibitor indomethacin was entirely ineffective. In addition, hemolysin elicited an increase in heart weight and left ventricular end-diastolic pressure, the latter again being suppressed by MK-886.
Low doses of hemolysin cause strong coronary vasoconstriction, linked with loss of myocardial performance, release of cell injury enzymes, and electrical instability, with all events being largely attributable to toxin-elicited leukotriene generation in the coronary vasculature. Bacterial exotoxins such as hemolysin thus may be implicated in the cardiac abnormalities encountered in septic shock. |
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AbstractList | hemolysin has been implicated as an important pathogenic factor in extraintestinal infections including sepsis. We investigated the effects of coronary administration of hemolysin on cardiac function in isolated rat hearts perfused at constant flow.
Prospective, experimental study.
Research laboratory at a university hospital.
Isolated hearts from male Wistar rats.
Isolated hearts were perfused with purified hemolysin for 60 min.
Low concentrations of the toxin in the perfusate (0.1-0.2 hemolytic units/mL) caused a dose-dependent coronary vasoconstriction with a marked increase in coronary perfusion pressure, which was paralleled by a decrease in left ventricular developed pressure (and the maximum rate of left ventricular pressure increase). Moreover, 0.2 hemolytic units/mL hemolysin evoked ventricular fibrillation within 10 mins of toxin application. These events were accompanied by the liberation of leukotrienes (LTC4, LTD4, LTE4, and LTB4), thromboxane A2, prostaglandin I2, and the cell necrosis markers lactate dehydrogenase and creatine kinase into the recirculating perfusate. The lipoxygenase inhibitor MK-886 fully blocked the toxin-induced coronary vasoconstrictor response and the loss of myocardial contractility and reduced the release of lactate dehydrogenase and creatine kinase. In contrast to this, the cyclooxygenase inhibitor indomethacin was entirely ineffective. In addition, hemolysin elicited an increase in heart weight and left ventricular end-diastolic pressure, the latter again being suppressed by MK-886.
Low doses of hemolysin cause strong coronary vasoconstriction, linked with loss of myocardial performance, release of cell injury enzymes, and electrical instability, with all events being largely attributable to toxin-elicited leukotriene generation in the coronary vasculature. Bacterial exotoxins such as hemolysin thus may be implicated in the cardiac abnormalities encountered in septic shock. |
Author | Seeger, Werner Klingenberger, Pascal Bournelis, Emmanoyil Buerke, Michael Sibelius, Ulf Heep, Martina Grandel, Ulrich Kiss, Ladislau Grimminger, Friedrich |
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Snippet | hemolysin has been implicated as an important pathogenic factor in extraintestinal infections including sepsis. We investigated the effects of coronary... |
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SubjectTerms | Animals Coronary Circulation Coronary Vessels - physiopathology Disease Models, Animal Dose-Response Relationship, Drug Escherichia coli Escherichia coli Infections - complications Exotoxins - adverse effects Heart Failure - immunology Heart Failure - microbiology Heart Failure - physiopathology Hemolysin Proteins - adverse effects In Vitro Techniques Indoles - pharmacology Leukotrienes - physiology Lipoxygenase Inhibitors - pharmacology Male Myocardial Contraction Prospective Studies Rats Shock, Septic - immunology Shock, Septic - microbiology Shock, Septic - physiopathology Vasoconstriction Ventricular Dysfunction, Left - immunology Ventricular Dysfunction, Left - microbiology Ventricular Dysfunction, Left - physiopathology Ventricular Fibrillation - immunology Ventricular Fibrillation - microbiology Ventricular Fibrillation - physiopathology Ventricular Pressure |
Title | Leukotriene-mediated coronary vasoconstriction and loss of myocardial contractility evoked by low doses of Escherichia coli hemolysin in perfused rat hearts |
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