Negative Inotropic Agents
Negative Inotropic Agents - Related Videos
01:26
Heart Failure Drugs: Inotropic Agents
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2024
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
09:54
A Recovery Cardiopulmonary Bypass Model Without Transfusion or Inotropic Agents in Rats
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Cited by 2 •
2018
Here, we present a protocol to describe a simple recovery cardiopulmonary bypass model without transfusion or inotropic agents in a rat. This model allows the study of the long-term multiple organ sequelae of cardiopulmonary bypass.
10:19
Reducing Agents
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2023
Source: Vy M. Dong and Daniel Kim, Department of Chemistry, University of California, Irvine, CA Controlling the reactivity and selectivity during the synthesis of a molecule is very important criteria for chemists. This has led to the development of many reagents that allow chemists to pick and choose reagents suitable for a given task. Quite often, a balance between reactivity and selectivity needs to be achieved. This experiment will use IR spectroscopy to monitor the reaction and to...
11:27
Preparation and In Vitro Characterization of Dendrimer-based Contrast Agents for Magnetic Resonance Imaging
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Cited by 5 •
2016
This protocol describes the preparation and characterization of a dendrimeric magnetic resonance imaging (MRI) contrast agent that carries cyclen-based macrocyclic chelates coordinating paramagnetic gadolinium ions. In a series of MRI experiments in vitro, this agent produced an amplified MRI signal when compared to the commercially available monomeric analogue.
07:40
Introducing Experimental Agents into the Mouse
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2023
Many investigations performed in mice (Mus musculus) require the administration of an experimental agent to the animal. For example, it may be of interest to test the efficacy of a specific therapy, to induce a pathologic condition, or to administer anesthesia or palliative care. In order to ensure safe and efficient delivery, it is important to consider a variety of factors prior to the administration of the treatment. This video, which reviews agent administration in the mouse, begins by...
FAQs
Less calcium entering cardiomyocytes leaves less calcium available to activate the contractile machinery. This weakens the interaction responsible for myocardial contraction, so each heartbeat can generate less force. The resulting reduction in contractile workload also helps explain why these agents can lower myocardial oxygen demand while altering the heart’s pumping capacity.
The sarcoplasmic reticulum serves as an internal calcium source for cardiomyocytes. If its calcium release is limited, the concentration available during contraction falls even when calcium entry is not completely blocked. This provides a distinct cellular route for reducing force and connects intracellular calcium handling with the strength of cardiac pumping.
Weakening beta-adrenergic stimulation reduces an important signal that normally supports stronger cardiac contraction. In contrast, other negative inotropic agents act more directly by reducing calcium entry or sarcoplasmic-reticulum calcium release. These mechanisms converge on decreased contractile force, but they influence different points in the signaling pathway that controls cardiomyocyte activity.
Lowering contractile force can reduce myocardial workload, but excessive suppression may also diminish cardiac output. This creates a physiological tradeoff: reducing the heart’s demand for oxygen may benefit conditions such as angina, while too much reduction in pumping strength can impair whole-organ circulation. The balance depends on the extent of contractile inhibition.
Their established uses include hypertension, angina, and selected cardiac arrhythmias. The shared rationale is to reduce cardiac workload or modify activity that contributes to the condition, while avoiding an excessive fall in output. Different agents may be relevant because they reduce force through calcium-related pathways or by weakening beta-adrenergic stimulation.
A useful biological analysis follows several linked levels: the agent changes calcium handling or beta-adrenergic signaling in cardiomyocytes, contraction becomes weaker, myocardial workload and oxygen demand decrease, and cardiac output may also change. This cellular-to-organ framework helps explain both therapeutic effects and the consequences of excessive suppression.