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Histamine H3 activation depresses cardiac function in experimental sepsis
1Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3E OZ3.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 6, 1998
Summary
Blocking histamine H3 receptors improved cardiovascular function in canine sepsis models. This suggests H3 receptor activation contributes to sepsis-induced cardiovascular collapse.
Area of Science:
- Cardiovascular Physiology
- Neuropharmacology
- Sepsis Pathophysiology
Background:
- Histamine H3 receptors are primarily known as inhibitory presynaptic receptors.
- They can decrease norepinephrine release during heightened sympathetic activity.
- Their role in sepsis-induced cardiovascular dysfunction is not well understood.
Purpose of the Study:
- To investigate the potential role of histamine H3 receptor activation in sepsis.
- To determine if H3 receptor blockade can improve cardiovascular function during sepsis.
Main Methods:
- Utilized a canine model of Escherichia coli sepsis.
- Administered an H3 receptor blocker to septic canines.
- Measured cardiac output, systemic blood pressure, and left ventricular contractility.
- Analyzed plasma histamine concentrations.
- Performed in vitro experiments with septic plasma.
Main Results:
- H3 receptor blockade significantly increased cardiac output (3.6 to 5.3 l/min) and systemic blood pressure (mean 76 to 96 mmHg) in septic canines.
- Left ventricular contractility was also enhanced post-blockade.
- Plasma histamine levels were modestly elevated in the H3-blocker-sepsis group.
- Histamine H3 receptor activation was detected in vitro under septic plasma conditions.
Conclusions:
- Activation of histamine H3 receptors appears to contribute to cardiovascular collapse during sepsis.
- H3 receptor blockade demonstrates therapeutic potential for improving cardiovascular function in sepsis.