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Histamine decreases left ventricular contractility in normal human subjects
D J Cooper1, C R Thompson, K R Walley
1University of British Columbia, Division of Cardiology, St. Paul's Hospital, Vancouver, Canada.
Insights
Histamine reduces human heart contractility by affecting left ventricular function. This effect is mediated, in part, by H1 receptors, as shown by studies on healthy volunteers.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Histamine is a key mediator in allergic reactions and inflammation.
- Its direct effects on human cardiac contractility remain incompletely understood.
- Understanding histamine's cardiac impact is crucial for managing cardiovascular conditions.
Purpose of the Study:
- To investigate the impact of histamine on human left ventricular contractility.
- To determine the role of H1 receptors in histamine's cardiac effects.
Main Methods:
- Healthy volunteers underwent measurements of heart rate, arterial pressure, and left ventricular dimensions via echocardiogram.
- Baseline contractility was assessed using pressure-dimension and wall stress-velocity relationships.
- Histamine infusions were administered before and after H1 receptor antagonist (diphenhydramine) pretreatment.
Main Results:
- Histamine decreased end-systolic pressure but not end-systolic dimension or fractional shortening.
- Histamine reduced velocity of circumferential fiber shortening at consistent end-systolic wall stress.
- H1 receptor antagonist pretreatment inhibited these observed effects of histamine.
Conclusions:
- Histamine's primary effect on the human heart is a reduction in left ventricular contractility.
- This negative inotropic effect is significantly mediated by H1 receptor activation.
Abstract:
To determine whether histamine alters human left ventricular contractility we measured heart rate, calibrated carotid arterial pressure, and left ventricular dimensions (echocardiogram) in nine healthy volunteers. We assessed baseline contractility using the end-systolic pressure-dimension relationship and the end-systolic meridional wall stress-rate-corrected velocity of circumferential fiber shortening relationship determined over a wide range of afterloads using phenylephrine and nitroprusside infusions. We then infused histamine for 3-5 min at a dose predetermined to decrease mean arterial pressure by 20%, both before and after H1 receptor antagonist pretreatment (diphenhydramine 50 mg i.v.). Histamine decreased end-systolic pressure but, unlike an equally hypotensive infusion of nitroprusside, did not decrease end-systolic dimension or increase fractional shortening. Histamine also decreased velocity of circumferential fiber shortening at the same end-systolic meridional wall stress as controls (P < 0.05). These effects of histamine were inhibited by H1 antagonist pretreatment. We conclude that the dominant effect of histamine on the human heart is to decrease left ventricular contractility and that this decrease in contractility is dependent, at least partially, on H1-receptor activation.