Journal article
Hemodynamic sequelae of regression of experimental atherosclerosis
The Journal of clinical investigation, Vol.71(1), pp.104-113
01/1983
DOI: 10.1172/JCI110738
PMID: 6848553
Abstract
Regression of experimental atherosclerosis is characterized by decreased intimal thickness and luminal enlargement, but intimal fibrosis becomes more dense. We tested the hypothesis that fibrosis of arteries during regression might limit vasodilator capacity and restrict hemodynamic improvement despite luminal improvement. We studied limb, coronary, and cerebral hemodynamics in 11 normal cynomolgus monkeys, 10 monkeys given an atherogenic diet for 20 mo and 8 monkeys given a regression diet for an additional 18 mo. The atherogenic diet induced lesions of moderate severity (50-60% stenosis); owing to characteristic vessel growth during the atherogenic period, luminal size did not decrease correspondingly. Regression monkeys showed typical changes of regression with luminal enlargement but increased fibrosis. The iliac artery was perfused at constant blood flow and maximal vasodilatation was produced with papaverine. Blood flow was measured with microspheres during maximal vasodilatation in the coronary bed (adenosine) and cerebral bed (hypercapnia). In normal monkeys, minimal vascular resistances were 1.95 +/- 0.19 mm Hg/ml/min X 100 g (mean +/- SE) (limb), 0.13 +/- 0.01 (coronary), and 0.44 +/- 0.02 (cerebral). In atherosclerotic monkeys minimal resistance increased (P less than 0.05) 108, 62, and 166% in the limb, coronary, and cerebral beds, respectively. In regression monkeys, minimal resistance increased from values found in atherosclerotic animals in the limb (+22%), decreased inconsistently in the coronary bed (-19%), and decreased significantly in the cerebral bed (-44%, P less than 0.05). Thus morphologic regression was accompanied by significant hemodynamic improvement during maximal dilatation only in cerebral vessels. We conclude that increases in luminal size during regression of atherosclerotic lesions may not be associated with increases in vasodilator capacity, as intimal fibrosis may limit physiologically important hemodynamic improvement.
Details
- Title: Subtitle
- Hemodynamic sequelae of regression of experimental atherosclerosis
- Creators
- Mark L ArmstrongDonald D HeistadMelvin L MarcusDonald J PiegorsFrancois M Abboud
- Resource Type
- Journal article
- Publication Details
- The Journal of clinical investigation, Vol.71(1), pp.104-113
- Publisher
- American Society for Clinical Investigation
- DOI
- 10.1172/JCI110738
- PMID
- 6848553
- ISSN
- 0021-9738
- eISSN
- 1558-8238
- Grant note
- HL 14230 / NHLBI NIH HHS\nHL 14388 / NHLBI NIH HHS\nHL 16066 / NHLBI NIH HHS
- Language
- English
- Date published
- 01/1983
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984025409002771
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