Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 85: 1693-1701, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 5, 1693-1701, November 1998

Histamine H3 activation depresses cardiac function in experimental sepsis

X. Li1,3, G. Eschun1, D. Bose1,2,4, H. Jacobs5, J. J. Yang1, R. B. Light1, and S. N. Mink1,3

Departments of 1 Medicine, 2 Anesthesiology, 3 Physiology, 4 Pharmacology and Therapeutics, and 5 Biochemistry and Molecular Biology, University of Manitoba, Winnipeg, Manitoba, Canada R3E OZ3

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.

cardiac depression; septic shock; sympathetic response


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