FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W173663682> ?p ?o ?g. }

• W173663682 endingPage "41" @default.
• W173663682 startingPage "27" @default.
• W173663682 abstract "Early reports have attributed cardiac failure during acute and chronic models of shock to peripheral vascular dysfunction and decreased venous return. More recently interest has focused on the heart as a primary target responsible for cardiovascular changes associated with acute endotoxin or hemorrhagic shock. At present, it remains controversial whether the heart fails early following the induction of experimental hypodynamic shock. Data from our laboratory have shown that myocardial contractility was increased early following acute endotoxin and splanchnic artery occlusion shock, and it was not until the agonal or terminal phase that contractility was depressed. We have used the slope of the left ventricular pressure-dimension relationship (Ees) as our index of contractile function. This technique is preferential since it is not affected by changes in the loading conditions on the heart. Unlike most reports that have used LV dP/dt as an index of contractility in the intact animal, we have shown that Ees and LV dP/dt do not uniformly reflect changes in contractility. LV dP/dt and related measures do, however, reflect the overall global changes in myocardial performance, which are affected by changes in preload, afterload, heart rate, and contractility. The reductions in LV dP/dt therefore mainly reflect the changes in arterial blood pressure associated with acute hypodynamic shock. The increase in contractility reported during endotoxin shock were shown to be induced by stimulation of beta-adrenergic receptors--when the beta-blocking drug, propranolol, was given to animals during shock, contractility decreased. The mechanism(s) responsible for the failure of the heart during the late or agonal periods of shock is (are) unknown. We have shown in dogs who die as a result of endotoxin shock that the hearts exhibit a progressive energy deficit, whereas animals surviving the experimental protocol maintained levels of ATP and creatine phosphate. It is unclear if the changes in high-energy phosphates during endotoxin shock cause irreversibility. Other potential mediators of cardiac failure have included ischemia/hypoxia, toxic myocardial depressant factors, deterioration of sympathetic influences on the heart, electrophysiologic and ionic disturbances, etc. The relationship between these factors and failure of the heart in vivo during various shock paradigms remains to be elucidated." @default.
• W173663682 created "2016-06-24" @default.
• W173663682 creator A5018484035 @default.
• W173663682 date "1990-01-01" @default.
• W173663682 modified "2023-09-23" @default.
• W173663682 title "When does the heart fail during shock?" @default.
• W173663682 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/2137382" @default.
• W173663682 hasPublicationYear "1990" @default.
• W173663682 type Work @default.
• W173663682 sameAs 173663682 @default.
• W173663682 citedByCount "12" @default.
• W173663682 countsByYear W1736636822015 @default.
• W173663682 countsByYear W1736636822018 @default.
• W173663682 countsByYear W1736636822020 @default.
• W173663682 crossrefType "journal-article" @default.
• W173663682 hasAuthorship W173663682A5018484035 @default.
• W173663682 hasConcept C123576724 @default.
• W173663682 hasConcept C126322002 @default.
• W173663682 hasConcept C164705383 @default.
• W173663682 hasConcept C178853913 @default.
• W173663682 hasConcept C2777953023 @default.
• W173663682 hasConcept C2778151854 @default.
• W173663682 hasConcept C2778198053 @default.
• W173663682 hasConcept C2781300812 @default.
• W173663682 hasConcept C39133596 @default.
• W173663682 hasConcept C48277249 @default.
• W173663682 hasConcept C500558357 @default.
• W173663682 hasConcept C71924100 @default.
• W173663682 hasConcept C84393581 @default.
• W173663682 hasConceptScore W173663682C123576724 @default.
• W173663682 hasConceptScore W173663682C126322002 @default.
• W173663682 hasConceptScore W173663682C164705383 @default.
• W173663682 hasConceptScore W173663682C178853913 @default.
• W173663682 hasConceptScore W173663682C2777953023 @default.
• W173663682 hasConceptScore W173663682C2778151854 @default.
• W173663682 hasConceptScore W173663682C2778198053 @default.
• W173663682 hasConceptScore W173663682C2781300812 @default.
• W173663682 hasConceptScore W173663682C39133596 @default.
• W173663682 hasConceptScore W173663682C48277249 @default.
• W173663682 hasConceptScore W173663682C500558357 @default.
• W173663682 hasConceptScore W173663682C71924100 @default.
• W173663682 hasConceptScore W173663682C84393581 @default.
• W173663682 hasIssue "1" @default.
• W173663682 hasLocation W1736636821 @default.
• W173663682 hasOpenAccess W173663682 @default.
• W173663682 hasPrimaryLocation W1736636821 @default.
• W173663682 hasRelatedWork W1975104654 @default.
• W173663682 hasRelatedWork W2022089943 @default.
• W173663682 hasRelatedWork W2032964067 @default.
• W173663682 hasRelatedWork W2074671498 @default.
• W173663682 hasRelatedWork W2110084174 @default.
• W173663682 hasRelatedWork W2169190460 @default.
• W173663682 hasRelatedWork W2278145879 @default.
• W173663682 hasRelatedWork W2339902912 @default.
• W173663682 hasRelatedWork W2409320320 @default.
• W173663682 hasRelatedWork W2770178563 @default.
• W173663682 hasVolume "30" @default.
• W173663682 isParatext "false" @default.
• W173663682 isRetracted "false" @default.
• W173663682 magId "173663682" @default.
• W173663682 workType "article" @default.