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Related Concept Videos

Cardiac Output II: Effect of Stroke Volume on Cardiac Output01:22

Cardiac Output II: Effect of Stroke Volume on Cardiac Output

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Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
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Cardiac Output and Stroke Volume01:11

Cardiac Output and Stroke Volume

4.9K
Cardiac output (CO) is an integral aspect of human physiology, reflecting the heart's efficiency and responsiveness to the body's needs. It represents the volume of blood that the left or right ventricle ejects into the aorta or pulmonary trunk each minute. The CO is calculated by multiplying the heart rate (HR)—the number of heartbeats per minute—by the stroke volume (SV)—the amount of blood pumped out with each heartbeat.
In an average resting adult male, the typical cardiac...
4.9K
Series R—L Circuit Transients01:22

Series R—L Circuit Transients

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In a series resistor-inductor (R-L) circuit, closing the switch at the start of the time period simulates a three-phase short circuit, a fault condition where all three phases of an unloaded synchronous machine are short-circuited. When there is no fault impedance and no initial current, the initial voltage is determined by the phase angle of the source voltage.
Using Kirchhoff's Voltage Law (KVL) to analyze this circuit helps determine the total asymmetrical fault current, which consists...
397
Transient and Steady-state Response01:24

Transient and Steady-state Response

566
In control systems, test signals are essential for evaluating performance under various conditions. The ramp function is effective for systems undergoing gradual changes, while the step function is suitable for assessing systems facing sudden disturbances. For systems subjected to shock inputs, the impulse function is the most appropriate test signal.
These test signals are integral in designing control systems to exhibit two key performance aspects: transient response and steady-state...
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Regulation of Stroke Volume01:27

Regulation of Stroke Volume

5.2K
The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
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Cardiac Output I:Effect of Heart Rate on Cardiac Output01:19

Cardiac Output I:Effect of Heart Rate on Cardiac Output

2.6K
Cardiac Output
Cardiac output (CO) refers to the total amount of blood ejected by one of the ventricles in liters per minute (L/min). In a resting adult, CO ranges from 5 to 6 L/min, adjusting according to the body's metabolic requirements.
Effect of Heart Rate on Cardiac Output
Cardiac output adapts to metabolic demands during stress, physical activity, or illness. The autonomic nervous system regulates heart rate via the sinoatrial node. The parasympathetic nervous system decreases heart...
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Related Experiment Video

Updated: Feb 3, 2026

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
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Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes

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Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction.

Roland Veltkamp1,2, Stefan Uhlmann2, Marilena Marinescu1,2

  • 1Division of Brain Sciences, Imperial College London, London, UK.

Journal of Cachexia, Sarcopenia and Muscle
|November 1, 2018
PubMed
Summary

Experimental stroke in mice caused early cardiac dysfunction and atrophy, involving molecular changes like increased atrogin-1 and altered norepinephrine levels. Peroxisome proliferator-activated receptor gamma was identified as a key mediator in stroke-induced cardiac transcriptional dysregulation.

Keywords:
AtrophyCardiac dysfunctionCardiomyocytesIschaemic strokeLeft ventricular contractility

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Author Spotlight: Assessing Ischemic Stroke Damage Through Middle Cerebral Artery Occlusion Model
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Modeling Stroke in Mice: Transient Middle Cerebral Artery Occlusion via the External Carotid Artery
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Area of Science:

  • Cardiovascular Science
  • Neuroscience
  • Molecular Biology

Background:

  • Stroke is known to impact cardiac function, but the underlying mechanisms remain unclear.
  • Understanding the brain-heart interaction post-stroke is crucial for patient outcomes.

Purpose of the Study:

  • To investigate the effects of experimental stroke on cardiac function in mice.
  • To explore the molecular signaling pathways in the heart following ischemic brain injury.

Main Methods:

  • Mice underwent filament-induced middle cerebral artery occlusion or sham surgery.
  • Cardiac function was assessed using micro-echocardiography and troponin measurements.
  • Cardiac tissue analysis included heart weight, cardiomyocyte size, gene expression (atrogin-1, murf-1), and transcriptome analysis.

Main Results:

  • Stroke led to early (24-72h) but transient reduction in left ventricular contractility.
  • Cardiac dysfunction was associated with increased high-sensitive cardiac troponin and cardiomyocyte atrophy.
  • Molecular changes included increased atrogin-1 and murf-1, altered norepinephrine levels, and peroxisome proliferator-activated receptor gamma dysregulation.

Conclusions:

  • Stroke triggers a complex molecular response in the heart.
  • This response includes immediate, transient cardiac atrophy and dysfunction.
  • Peroxisome proliferator-activated receptor gamma may mediate stroke-induced cardiac transcriptional changes.