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Neither hemodilution changes nor autoregulatory or non‐autoregulatory renal medullary blood flow changes explain the amplification of RIHP during saline volume expansion in the rat
Author(s) -
MoralesLoredo Juan Humberto,
BritoOrta María Dolores,
LópezRodríguez Juan Francisco,
RodríguezMartínez Manuel
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.1059.18
Subject(s) - saline , chemistry , medullary cavity , perfusion , blood flow , medicine , anesthesia
To assess the determinants of Renal Interstitial Hydrostatic Pressure (RIHP) amplification during saline volume expansion (E), [Pr]p, Ht, renal perfusion pressure (RPP), renal medullary blood flow (RMBF) and RIHP were measured in two groups of anesthetized, left renal denervated, hormonally clamped and RPP controlled rats, with or without medullary interstitial infusion of L‐NAME (LNA group or VHC group, respectively ) during both hydropenia (H) and E (0.58 ml/min, i.v., 2.5% of bw). RMBF was measured by laser‐Doppler flowmetry and RIHP by sub‐capsular catheter. Under RPP control (100 mmHg), LNA group showed a decrease in %ΔRMBF (−24.7 ± 7 %) vs VHC group (−8 ± 4%, p=0.05) during H, however, during E both group rose similarly their %ΔRMBF (49.8 ± 13% LNA group vs 33.7 ± 5% VHC group). Delta (Δ= E ‐ H) of [Pr]p was of −1.7 ± 0.08 g/dl in LNA group vs −1.6 ± 0.07 g/dl in VHC group (ns). ΔHt was of −10.3 ± 0.6% in LNA group vs −8.0 ± 0.7% in VHC group (p=0.03). ΔRIHP was of 4.2 ± 0.7 mmHg in LNA group vs 3.6 ± 0.4 mmHg in VHC group (ns). Both groups showed a similar upper shift of %ΔRMBF/RPP relationship from H to E, however, whereas LNA group showed autoregulation of %ΔRMBF during E, VHC group did not. Both groups showed similar flat ΔRIHP/RPP relationships during H, which were amplified similarly during E. Conclusion: Data modeling indicated that RIHP amplification during E in the rat is independent of hemodilution and autoregulatory and non‐autoregulatory changes in RMBF. Supported by: C07‐FAI‐11‐14.50.