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Triolein‐induced renal arterial vasoconstriction and its reversal in a rat model
Author(s) -
Patel Sapna,
Adler F.,
McIff T.,
Poisner A.,
Herndon B.,
Quinn T.,
Molteni A.
Publication year - 2009
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.23.1_supplement.lb148
Subject(s) - triolein , losartan , captopril , vasoconstriction , medicine , angiotensin ii , endocrinology , chemistry , receptor , blood pressure , biochemistry , lipase , enzyme
Fat embolism syndrome (FES) is a respiratory process that may occur after bone fractures and is manifested by severe pulmonary vasoconstriction. It can be modeled in the rat by intravenous (iv) triolein. Our past work has shown the benefits of an ACE‐ inhibitor (captopril) or A2‐type 1 receptor blocker (losartan) on triolein treated pulmonary vessels. To investigate renal vascular effects of FES, we studied the histopathological changes in small arteries with and without treatment by these drugs (n=5/group). Rats received 0.2 ml triolein with necropsy at 24, 48, 96, or 264 hrs. Others received triolein and 50 mg/kg captopril or 10 mg/kg losartan with necropsy at 48 hrs (n=5/group). Saline controls were necropsied at 24 and 264 hrs (4‐5/group). At 400x, 3 vessels per high power field were digitally captured. The diameters of the lumen and medial wall were measured and statistically analyzed. Triolein vs control produced renal vasoconstriction up to 96 hr, p=0.03. Luminal dilation occurred at 48 hr in rats that received treatment with captopril or losartan. Lipid droplets were seen in the glomeruli at all times with the largest at 24 hr, progressively diminishing in size with time. Adventitial edema was evident in triolein‐dosed rats compared to controls (trend, p=0.09). This FES model produces renal vessel constriction that clears independently by 264 hrs. Treatment with captopril or losartan preserves vessel patency. This suggests the reversibility of FES‐related renal vascular changes, and, that the renin‐angiotensin system plays a role in its pathogenesis. Funding: MA & EJ Asher Orthopedic Research Endowment.