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Impaired Blood Pressure Compensation after Hemorrhage in Obesity
Author(s) -
Xiang Lusha,
Clemmer John,
Lu Silu,
Lee Lynn,
Hester Robert
Publication year - 2012
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.26.1_supplement.684.23
Subject(s) - hematocrit , blood pressure , medicine , blood volume , basal (medicine) , vasoconstriction , endocrinology , heart rate , chemistry , anesthesia , cardiology , insulin
Increased morbidity and mortality following severe hemorrhage have been shown in obese humans and animals, whereas the mechanisms are unknown. The compensatory mechanisms following hemorrhage involve an increase in total peripheral vascular resistance (TPR) along with capillary fluid shifts. We hypothesize that the cardiovascular response and capillary fluid shifts following hemorrhage are impaired in obese Zucker rats (OZ), an animal model of obesity. Blood pressure (BP), heart rate (HR), arteriolar and venous blood gas, and oxygen consumption (VO 2 ) were measured in lean Zucker rats (LZ) and OZ (11–12 wk) before and 1 hour after 35% total blood volume loss. Cardiac output (CO) was estimated using the Fick principle. The basal BP, CO, HR, TPR, and HCT were not different between LZ and OZ. After the 1 hour recovery period, both LZ and OZ exhibited decreased BP, CO, VO 2 , and hematocrit (HCT) along with increased TPR. The BP recovery was impaired in OZ (64% ± 3% recovery from basal) as compared with LZ (79% ± 2% recovery from basal). The HR was restored in the LZ but was decreased in the OZ (Table). Additionally, OZ exhibited a lower TPR and a higher HCT than LZ (Table). These results suggest impaired blood pressure compensation in OZ following severe hemorrhage due to an attenuated vasoconstriction and capillary fluid shift. (Supported by NIH HL‐51971 and HL‐89581)