Related Experiment Videos
Effects of histamine H1-receptor stimulation on coronary hemodynamics in man
Insights
Selective H1-receptor stimulation causes coronary artery dilation in humans. Histamine infusion, even in patients with coronary artery disease (CAD) and vasospastic angina, is unlikely to provoke coronary spasm after cimetidine pretreatment.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Histamine affects cardiovascular function via H1 and H2 receptors.
- Understanding selective H1-receptor effects on coronary hemodynamics is crucial.
Purpose of the Study:
- To investigate the impact of selective H1-receptor stimulation on human coronary hemodynamics.
- To assess the potential for histamine to induce coronary spasm in patients with coronary artery disease (CAD).
Main Methods:
- Ten patients underwent cardiac catheterization with coronary sinus pacing.
- Histamine infusion (0.5 µg/kg/min) was administered after cimetidine pretreatment.
- Measurements included mean aortic pressure, coronary sinus blood flow, coronary vascular resistance, and myocardial oxygen consumption.
Main Results:
- H1-receptor stimulation led to a significant decrease in mean aortic pressure and coronary vascular resistance.
- Coronary sinus blood flow and myocardial oxygen consumption remained unchanged.
- One patient with CAD experienced angina, ST elevation, reduced blood flow, and increased resistance.
Conclusions:
- Selective H1-receptor stimulation induces significant coronary vasodilation in humans.
- Histamine infusion post-cimetidine pretreatment appears unlikely to trigger coronary spasm, even in susceptible patients.
Abstract:
Exogenous histamine in man induces significant cardiovascular effects mediated by activation of H1 and H2-receptors present on human heart and on coronary arteries. We studied the effects of selective H1-receptor stimulation on human coronary hemodynamics in 10 patients undergoing cardiac catheterization. All patients were pretreated with cimetidine before the histamine infusion (0.5 micrograms/kg/min i.v. for 5 min). Six of these patients had normal coronary arteries and four had single vessel coronary artery disease (CAD) and vasospastic angina. During the study heart rate was held constant (100 beats/min) by coronary sinus pacing. We measured mean aortic pressure (MAP), coronary sinus blood flow (CSBF), coronary vascular resistance (CVR) and myocardial oxygen consumption (MVO2) at rest, during histamine infusion, and 10 min after the end of the infusion. During infusion, MAP decreased from 103 +/- 5 to 85 +/- 6 mmHg (p less than 0.02) and CVR from 1.00 +/- 0.16 to 0.81 +/- 0.14 mmHg/ml/min (p less than 0.05); CSBF and MVO2 did not significantly change. All parameters returned to baseline at the end of the infusion. The response was similar in patients with normal coronary arteries and in 3 patients with CAD. Only one patient with CAD developed angina with ST segment elevation in D3, reduction in CSBF and an increase in CVR. These results indicate that H1-receptor stimulation in man induces significant coronary dilatation and that histamine infusion after cimetidine pretreatment is unlikely to provoke coronary spasm in patients with vasospastic angina.