Histamine H3 activation depresses cardiac function in experimental sepsis
| Autor: | Gregg Eschun, J. Yang, Steven N. Mink, Deepak Bose, Hans Jacobs, Xing Li, R. B. Light |
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| Rok vydání: | 1998 |
| Předmět: |
Cardiac function curve
medicine.medical_specialty Physiology Adrenergic Blood Pressure Biology Inhibitory postsynaptic potential Histamine Agonists Norepinephrine (medication) Sepsis chemistry.chemical_compound Dogs Physiology (medical) Internal medicine medicine Animals Receptors Histamine H3 Cardiac Output Receptor Escherichia coli Infections Blood Volume Hemodynamics Heart medicine.disease Myocardial Contraction Endocrinology chemistry Heart Function Tests Circulatory system Vascular Resistance Histamine medicine.drug |
| Zdroj: | Journal of Applied Physiology. 85:1693-1701 |
| ISSN: | 1522-1601 8750-7587 |
| DOI: | 10.1152/jappl.1998.85.5.1693 |
| Popis: | In the heart, histamine (H3) receptors may function as inhibitory presynaptic receptors that decrease adrenergic norepinephrine release in conditions of enhanced sympathetic neural activity. We hypothesized that H3-receptor blockade might improve cardiovascular function in sepsis. In a canine model of Escherichia coli sepsis, we found that H3-receptor blockade increased cardiac output (3.6 to 5.3 l/min, P< 0.05), systemic blood pressure (mean 76 to 96 mmHg, P < 0.05), and left ventricular contractility compared with pretreatment values. Plasma histamine concentrations increased modestly in the H3-blocker–sepsis group compared with values obtained in a nonsepsis–time-control group. In an in vitro preparation, histamine H3 activation could be identified under conditions of septic plasma. We conclude that activation of H3 receptors may contribute to cardiovascular collapse in sepsis. |
| Databáze: | OpenAIRE |
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