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Investigating the hemodynamic parameters involved in microvasculature O2 regulation in skeletal muscle of Zucker Diabetic Fatty rat exposed to surface hypoxia
Author(s) -
Dias Gemma Marie,
Milkovich Stephanie,
Goldman Daniel,
Ellis Christopher G
Publication year - 2010
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.24.1_supplement.973.13
Subject(s) - hypoxia (environmental) , medicine , endocrinology , skeletal muscle , diabetes mellitus , hemodynamics , hematocrit , oxygenation , microcirculation , chemistry , oxygen , organic chemistry
Pre‐diabetes is marked with elevated insulin levels that attenuate ATP release from red blood cells (RBCs) in response to hypoxia. In our lab using 7 week old Zucker Diabetic Fatty (ZDF) obese rats we have observed a significant reduction in RBC velocity (Vel), supply rate (SR) and O 2 saturation in skeletal muscle resulting in a decreased capillary O 2 supply compared to control animals (ZDF lean). To test whether pre‐diabetic animals can support the tissue metabolic demand, a custom O 2 exchange gas chamber was used to create a hypoxic (HX) challenge by altering pO 2 at the surface of exposed skeletal muscle from 55 to 15 mmHg for 2 minutes and back 55. Hemodynamic data for each capillary segment for each pO 2 was quantified with intravital video microscopy and a functional image analysis system. Previous analysis indicates that mean SR for each pO 2 significantly differed within the lean group (p=0.0011), but not within the obese group. The data was reanalyzed to determine whether Vel or hematocrit (Hct) contribute to the SR change. Hct but not Vel, significantly increased in response to the hypoxic challenge in the lean group (p=0.0003). In the obese group neither Vel or Hct responded to the hypoxia. This suggests that Hct contributes to O 2 regulation and that in pre‐diabetes the O 2 regulatory mechanisms of the microvasculature are impaired and unable to support a hypoxic challenge. (NIH R33 HL089094 ).