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Effect of vasopressin on left ventricular performance
C P Cheng1, Y Igarashi, H S Klopfenstein
1Section of Cardiology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157.
The American Journal of Physiology
|January 1, 1993
Summary
Arginine vasopressin (AVP) impairs left ventricular (LV) performance by decreasing contractility and altering pressure-volume relationships. Unlike methoxamine, AVP depresses cardiac function despite increasing arterial elastance.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Arginine vasopressin (AVP) is a hormone with known vasoconstrictive properties.
- The direct effects of AVP on left ventricular (LV) performance, particularly in the context of intact reflexes, require detailed investigation.
Purpose of the Study:
- To evaluate the impact of arginine vasopressin (AVP) infusion on the left ventricular (LV) performance in conscious dogs.
- To differentiate the effects of AVP from other agents that increase arterial elastance (Ea).
Main Methods:
- Conscious dogs underwent AVP infusion (6 mcg/kg/min for 2 min).
- Measurements included LV pressures, volumes, heart rate, stroke volume, and coronary sinus blood flow.
- LV pressure-volume relations and derived parameters (dP/dtmax, stroke work) were analyzed.
Main Results:
- AVP significantly increased plasma AVP levels, LV end-systolic pressure, end-systolic volume, total systemic resistance, and arterial elastance (Ea).
- Heart rate and stroke volume decreased significantly following AVP infusion.
- AVP depressed LV performance, evidenced by decreased slopes in LV end-systolic P-V, dP/dtmax-VED, and stroke work-VED relations.
- Coronary sinus blood flow remained unchanged.
- A similar increase in Ea induced by methoxamine did not depress LV performance.
Conclusions:
- Arginine vasopressin (AVP) administration leads to a depression of left ventricular (LV) performance in conscious dogs.
- The observed cardiac depression by AVP is distinct from the effects of methoxamine, suggesting a specific negative inotropic effect of AVP.
- These findings highlight the complex cardiovascular actions of AVP beyond simple afterload augmentation.