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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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A decreasing function describes a relationship where the output consistently declines as the input increases. This means that for any two input values, if one is greater than the other, the corresponding output is smaller. Mathematically, a function f is decreasing on an interval I if for every x1 < x2​ in I, f (x1) > f (x2). This type of behavior is visually identified on a graph that slopes downward from left to right.The nature of a function can be analyzed by calculating...
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Updated: Feb 5, 2026

The Mouse Stroke Unit Protocol with Standardized Neurological Scoring for Translational Mouse Stroke Studies
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Clopidogrel may decrease the risk of post-stroke infection after ischaemic stroke.

T J Kim1, J S Lee2, M-K Kang1

  • 1Department of Neurology, Seoul National University Hospital, Seoul, Korea.

European Journal of Neurology
|September 1, 2018
PubMed
Summary
This summary is machine-generated.

Clopidogrel use was associated with a reduced risk of post-stroke infection in patients experiencing ischaemic stroke. This finding suggests clopidogrel may help prevent infections following stroke.

Keywords:
P2Y12 receptor antagonistclopidogrelpost-stroke infection

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Area of Science:

  • Neurology
  • Pharmacology
  • Infectious Diseases

Background:

  • The P2Y12 receptor is implicated in platelet activation, thrombosis, and systemic inflammation.
  • Clopidogrel, a P2Y12 receptor antagonist, is known to reduce inflammation and systemic infection.
  • Post-stroke infections are a significant complication following ischaemic stroke.

Purpose of the Study:

  • To investigate the potential protective effect of clopidogrel against post-stroke infections.
  • To evaluate the association between clopidogrel use and the incidence of infection after ischaemic stroke.

Main Methods:

  • A cohort of 1643 patients with acute ischaemic stroke was analyzed.
  • Patients were divided into clopidogrel users and non-users.
  • Inverse probability of treatment weighting (IPTW) was used to adjust for baseline differences.

Main Results:

  • Post-stroke infection occurred in 6.7% of clopidogrel users versus 12.2% of non-users (P ≤ 0.001).
  • Clopidogrel users had a significantly lower risk of post-stroke infection (OR 0.56; 95% CI 0.42-0.75) after IPTW adjustment.
  • Clopidogrel use was also linked to reduced intensive care unit admission.

Conclusions:

  • Clopidogrel use is associated with a decreased risk of infection after ischaemic stroke.
  • The findings suggest clopidogrel may mitigate infection severity and incidence in stroke patients.
  • Further prospective research is warranted to confirm these results.