Cardiac Relaxation
Cardiac Relaxation - Related Videos
07:51
Mechanical Control of Relaxation Using Intact Cardiac Trabeculae
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Cited by 2 •
2023
Rapid myocardial and cardiac relaxation is essential for normal physiology. Mechanical relaxation mechanisms are now known to be dependent on strain rate. This protocol provides an overview of the acquisition and analysis of experiments to further study the mechanical control of relaxation.
01:29
Relaxation of Skeletal Muscles
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2024
The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions. When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
11:37
Cardiac Magnetic Resonance Imaging
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2023
Source: Frederick W. Damen and Craig J. Goergen, Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana In this video, high field, small-bore magnetic resonance imaging (MRI) with physiological monitoring is demonstrated to acquire gated cine loops of the murine cardiovascular system. This procedure provides a basis for assessing left-ventricular function, visualizing vascular networks, and quantifying motion of organs due to respiration. Comparable small animal...
07:51
Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
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Cited by 37 •
2011
An automated myography method for force measurements in isolated mesenteric arteries is described. It employs a Mulvany-Halpern Auto Dual Wire Myograph 510A to determine responses to phenylephrine and extracellular calcium. The method allows consistent determination of isometric responses to agonists in small vessels of diameters of 60 - 300 μm, independently.
01:28
Classification of Skeletal Muscle Relaxants
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2023
Skeletal muscle relaxants are a group of drugs that can reduce muscle stiffness and induce temporary paralysis to relieve pain. These agents can act centrally to reduce muscle tone or spasms in painful conditions such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), or spinal injuries; they are called antispasmodics or spasmolytics. Peripherally acting skeletal muscle relaxants interfere with the neurotransmission at the neuromuscular end plate to induce paralysis during...
FAQs
Cardiac relaxation depends on a fall in cytosolic calcium rather than simply cessation of contraction. SERCA pumps return calcium to the sarcoplasmic reticulum, while the sodium-calcium exchanger extrudes it from the cell. These routes reduce calcium available to the contractile apparatus, initiating molecular changes that allow tension to decline and ventricular filling to proceed during diastole.
SERCA and the sodium-calcium exchanger contribute through different calcium-handling routes. SERCA promotes reuptake into the sarcoplasmic reticulum, whereas the exchanger supports calcium extrusion. Considering both mechanisms helps bioengineers interpret relaxation kinetics more precisely, because the timing and effectiveness of either route can influence how quickly engineered heart muscle releases tension and returns toward its resting state.
As cytosolic calcium declines, calcium disengages from troponin, and this promotes detachment of actin-myosin cross-bridges. The sequence connects intracellular calcium handling with mechanical relaxation: calcium removal is translated into reduced interaction within the contractile apparatus and consequently lower muscle tension. This link is central when interpreting relaxation as a functional property of cardiac muscle.
Researchers can examine the timing of tension release and return toward the resting state in engineered heart tissues. Relating these mechanical kinetics to the underlying calcium-removal processes provides a way to characterize contractile function. This analysis can reveal how a bioengineered tissue manages the transition from contraction to relaxation that supports ventricular filling, rather than treating contraction alone as a complete performance measure.
Measurements of relaxation kinetics provide functional information for representing and evaluating cardiac behavior. In computational cardiac models, they help characterize how contractile activity changes over time, while disease platforms use them to support studies of diastolic dysfunction. This shared readout connects model or tissue behavior with impaired relaxation, making it valuable for comparing normal and disease-related function.
Researchers can compare relaxation behavior when studying drug responses or evaluating biomaterials and therapies intended to improve cardiac performance. The timing of tension release offers a functional basis for determining whether an intervention changes cardiac relaxation, rather than relying only on treatment intent or material design. In this way, relaxation analysis links engineering choices to measurable contractile outcomes.