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Nitric oxide does not modulate the increases in blood flow, O2 consumption, or contractility during CaCl2
1Department of Anesthesiology, Illinois Masonic Medical Center, Chicago 60657, USA.
Insights
Calcium chloride (CaCl2) increases heart muscle contraction and oxygen demand. However, it also constricts coronary arteries, hindering blood flow and not affecting endothelium-derived nitric oxide (EDNO) pathways.
Area of Science:
- Cardiovascular Physiology
- Cardiac Metabolism
- Nitric Oxide Biology
Background:
- Endothelium-derived nitric oxide (EDNO) plays a crucial role in regulating vascular, metabolic, and contractile functions of the heart.
- Understanding the interplay between cardiac stimulation and NO-mediated regulation is vital for cardiovascular health.
Purpose of the Study:
- To investigate the cardiac effects of intracoronary calcium chloride (CaCl2) administration in dogs.
- To evaluate the role of EDNO in modulating these effects.
Main Methods:
- Anesthetized, open-chest dogs underwent left anterior descending coronary artery perfusion.
- Coronary blood flow (CBF), segmental shortening (SS), myocardial oxygen consumption (MVO2), and oxygen extraction (EO2) were measured.
- Responses to CaCl2 infusions were assessed before and after NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor.
Main Results:
- CaCl2 induced dose-dependent increases in SS and MVO2.
- CBF increased less proportionally than MVO2, leading to increased EO2, indicating vasoconstriction.
- L-NAME administration did not alter the cardiac effects of CaCl2.
Conclusions:
- CaCl2 exerts direct inotropic and coronary vasoconstricting effects.
- The vasoconstriction by CaCl2 impairs the matching of coronary blood flow to increased metabolic demand.
- EDNO does not appear to modulate the cardiac responses to CaCl2 in this model.
Objective:
Endothelium-derived nitric oxide (EDNO) has been shown to have vascular, metabolic, and contractile effects in the heart. We evaluated these effects during intracoronary (i.c.) administration of CaCl2 in dogs.
Methods:
The left anterior descending coronary artery of nine anesthetized, open-chest dogs was perfused at controlled pressure (80 mm Hg) with arterial blood. Coronary blood flow (CBF) was measured with a Doppler transducer and segmental shortening (SS) with ultrasonic crystals. Myocardial oxygen consumption (MVO2) and oxygen extraction (EO2) were calculated. Responses were assessed during i.c. infusions of CaCl2 (5, 10, 15 mg min-1) before and after administration of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 300 micrograms min-1 for 15 min, i.c.).
Results:
Before L-NAME, CaCl2 caused dose-dependent, proportional increases in SS and MVO2. Although CBF also increased, these responses were less than proportional to those in MVO2, and thus EO2 increased. L-NAME did not alter the cardiac effects of CaCl2.
Conclusions:
(1) CaCl2 had direct inotropic and coronary vasoconstricting effects. (2) The vasoconstricting effect impaired coupling of CBF to the augmented metabolic demands by local vasodilating mechanisms. (3) EDNO did not modulate the increases in CBF, MVO2, or SS during administration of CaCl2.