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Characterization of cardiovascular performance during ischemia‐reperfusion injury in obese vs. lean Ossabaw swine (1150.4)
Author(s) -
Sassoon Daniel,
Goodwill Adam,
Conteh Abass,
Noblet Jillian,
Mather Kieren,
Tune Johnathan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1150.4
Subject(s) - medicine , cardiology , blood pressure , ischemia , diastole , heart rate , reperfusion injury , cardiac output
This study examined the effects of obesity/metabolic syndrome (MetS) on left ventricular pressure‐volume relations at baseline and in response to ischemia‐reperfusion injury. Measurements were obtained in lean and obese Ossabaw swine at rest, following 30 min occlusion of the left circumflex artery, and 2 hours after the release of the occlusion. Baseline end‐diastolic volume (83±5 ml vs. 74±5 ml) and cardiac output (2215±389 ml/min vs. 2511±389 ml/min) were not significantly different in lean vs. MetS swine. However, mean arterial pressure was ~40% higher in MetS swine at rest and during reperfusion, while heart rate increased ~15‐20 beats/min with ischemia‐reperfusion in both groups. Assessment of inotropic status revealed that both cardiac output and blood pressure were augmented relative to end‐diastolic filling volumes in MetS vs. lean swine under all conditions (p<0.001). These apparent differences in cardiac function were associated with a marked reduction in the time to ischemia‐induced ventricular fibrillation in lean (17.5±7 min; n = 3 of 6) vs. MetS (3.3±1 min; n = 4 of 6) swine. These findings suggest that increases in blood pressure and cardiac function in MetS, at rest and following ischemia‐reperfusion injury, are independent of changes in filling volume and could contribute to increased susceptibility to fatal ventricular arrhythmias. Grant Funding Source : Supported by HL117620; This publication was made possible in part by Grant Number TL1 TR000162 (A. S