2021
DOI: 10.1016/j.cbpa.2020.110861
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How cardiac output is regulated: August Krogh's proto-Guytonian understanding of the importance of venous return

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Cited by 15 publications
(7 citation statements)
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“…A second explanation for the increase in CO could be due to an increase in preload secondary to phenylephrine induced constriction of capillaries, peripheral veins, and central veins with a subsequent increase in stroke volume [ 37 ]. In a study in pigs that were experimentally treated to be adjusted on the Frank-Starling curve to make CO preload independent or preload dependent, phenylephrine increased CO in pigs on the preload dependent part of the curve but decreased CO in pigs on the preload independent part of the curve.…”
Section: Discussionmentioning
confidence: 99%
“…A second explanation for the increase in CO could be due to an increase in preload secondary to phenylephrine induced constriction of capillaries, peripheral veins, and central veins with a subsequent increase in stroke volume [ 37 ]. In a study in pigs that were experimentally treated to be adjusted on the Frank-Starling curve to make CO preload independent or preload dependent, phenylephrine increased CO in pigs on the preload dependent part of the curve but decreased CO in pigs on the preload independent part of the curve.…”
Section: Discussionmentioning
confidence: 99%
“…The most notable alterations in SV in reptiles and amphibians occur as decreases associated with apnea. The greatest decrease in SV seen in these animals is associated with the apnea required during their physical effort in the water [7,17,53,66,69,86,123].…”
Section: Adjustment Of the Sv To Exercise In Vertebratesmentioning
confidence: 99%
“…SV is determined by contractility and the characteristics of the ventricle, mainly regarding its filling capacity. Similarly, the control of the SV is accomplished by two different pathways, nervous and hormonal [7,17,69].…”
mentioning
confidence: 99%

Cardiovascular Response to Exercise in Vertebrates: Update

López-Román,
Gómez-Lucas,
Jiménez-Herranz
et al. 2024
Preprint
“…Increased adrenergic stimulation during exercise or stress (2,14) induces PKA phosphorylation of Ser23/24, thereby abolishing the TnI-TnC protein-protein interaction (11,15) and decreasing myofilament Ca 2+ affinity (16). Accordingly, this process accelerates dissociation of Ca 2+ during diastole and increases the rate of cardiomyocyte relaxation (13,17,18), which is essential for preserving adequate cardiac filling at elevated heart rates concomitantly driven by adrenergic stimulation (13,19,20). Deletion of the cTnI N-terminal extension in transgenic mice has been shown to mimic the effect of PKA phosphorylation (21)(22)(23) and benefit diastolic cardiac performance, particularly during aging (10) and deficient ß-adrenergic signaling (24).…”
Section: Main Textmentioning
confidence: 99%