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Related Concept Videos

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Regulation of Stroke Volume

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

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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
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The loudness of a sound source is related to how energetically the source is vibrating, consequently making the molecules of the propagation medium vibrate. To measure the loudness of a source, the physical quantity of interest is the intensity. This is defined as the energy emitted per unit of time per unit of area perpendicular to the sound wave's propagation direction. Since the total energy is greater if the source vibrates for a longer duration and over a larger area, dividing the...
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Related Experiment Video

Updated: Feb 13, 2026

PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
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Temporal Imaging Dynamics in ischemic Stroke: Intensity- vs. volume-based metrics.

Horst Urbach1, Alexander Rau2, Ömer Bagcilar2

  • 1From the Dept. of Neuroradiology, Medical Center - University of Freiburg, Faculty of Medicine (H.U., A.R., Ö.B., E.K.), University of Freiburg; Center for Stroke Research Berlin (I.G., J.F.), Charite - Universitätsmedizin Berlin; and Dept. of Medical Physics, Medical Center, University of Freiburg, Faculty of Medicine (M.R., E.K.), University of Freiburg. horst.urbach@uniklinik-freiburg.de.

AJNR. American Journal of Neuroradiology
|February 11, 2026
PubMed
Summary

Tissue signal intensities in acute ischemic stroke change more with time than volumetric measures. This suggests infarct evolution is progressive tissue injury, not just expansion, with intensity metrics better reflecting this change.

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Area of Science:

  • Neurology
  • Radiology
  • Biomedical Imaging

Background:

  • The progression of ischemic tissue damage after a thromboembolic occlusion is influenced by hypoperfusion and reperfusion timing.
  • Temporal dynamics of hypoperfusion and tissue damage in acute ischemic stroke remain incompletely understood.

Purpose of the Study:

  • To compare the association between onset-to-imaging time and volumetric versus intensity-based imaging markers in acute ischemic stroke.
  • To investigate how different imaging modalities (CT and MRI) and metrics reflect tissue damage over time.

Main Methods:

  • Retrospective analysis of 288 CT and 275 MR acute stroke examinations.
  • Estimation of hypoperfusion and infarct core volumes using VEOcore software with standard thresholds.
  • Quantification of tissue damage using ASPECTS and normalized signal intensities (NCCT, ADC, DWI, CBF, Tmax).
  • Multivariable linear regression was used to assess associations with onset-to-imaging time, adjusting for covariates.

Main Results:

  • Volumetric measures showed limited time-dependence: ASPECTS decreased by -0.33 points/h and ADC-core volume increased by +1.8 mL/h.
  • Perfusion-related volumetric measures (CBF < 30%, Tmax > 6s) did not significantly change with time.
  • Intensity measures demonstrated significant time-dependence: NCCT intensity decreased by -1.1%/h, ADC intensity by -0.69%/h, while DWI-b0 and DWI-b1000 increased by +2.3%/h and +4.9%/h, respectively.

Conclusions:

  • Tissue signal intensities in acute ischemic stroke exhibit a stronger time-dependence compared to volumetric measures.
  • Infarct evolution appears to reflect progressive tissue injury rather than solely volumetric expansion.
  • Intensity-based metrics from NCCT and DWI may be more suitable for assessing "infarct growth rate" than perfusion-based metrics.