title: Dynamic synchrotron imaging of diabetic rat coronary microcirculation in vivo.
abstract: OBJECTIVE
  In diabetes, long-term micro- and macrovascular damage often underlies the functional decline in the cardiovascular system. However, it remains unclear whether early-stage diabetes is associated with in vivo functional impairment in the coronary microvasculature. Synchrotron imaging allows us to detect and quantify regional differences in resistance microvessel caliber in vivo, even under conditions of high heart rate.
  
  
  RESULTS
  Synchrotron cine-angiograms of the coronary vasculature were recorded using anesthetized Sprague-Dawley rats 3 weeks after treatment with vehicle or streptozotocin (diabetic). In the early diabetic state, in the presence of nitric oxide and prostacyclin, vessel diameters were smaller (P<0.01) and endothelium-dependent vessel recruitment was already depressed (P<0.05). Endothelium-dependent and -independent vasodilatory responses in individual coronary vessels were not different in vivo. Inhibition of NO and PGI(2) production in diabetes uncovered early localized impairment in dilation. Diabetic animals displayed focal stenoses and segmental constrictions during nitric oxide synthase/cyclooxygenase blockade, which persisted during acetylcholine infusion (P<0.05), and a strong trend toward loss of visible microvessels.
  
  
  CONCLUSIONS
  Synchrotron imaging provides a novel method to investigate coronary microvascular function in vivo at all levels of the arterial tree. Furthermore, we have shown that early-stage diabetes is associated with localized coronary microvascular endothelial dysfunction.
authors.affiliation: Department of Cardiac Physiology, National Cerebral & Cardiovascular Research Center Research Institute, 5-7-1 Fujishirodai, Suita-shi, Osaka 565-8565, Japan. shirai@ri.ncvc.go.jp
authors.forename: Mathew J
authors.initials: MJ
authors.lastname: Jenkins
authors.forename: Amanda J
authors.initials: AJ
authors.lastname: Edgley
authors.forename: Takashi
authors.initials: T
authors.lastname: Sonobe
authors.forename: Keiji
authors.initials: K
authors.lastname: Umetani
authors.forename: Daryl O
authors.initials: DO
authors.lastname: Schwenke
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Fujii
authors.forename: Russell D
authors.initials: RD
authors.lastname: Brown
authors.forename: Darren J
authors.initials: DJ
authors.lastname: Kelly
authors.forename: Mikiyasu
authors.initials: M
authors.lastname: Shirai
authors.forename: James T
authors.initials: JT
authors.lastname: Pearson
mesh_terms: D000818:Animals; D017023:Coronary Angiography / Q000379:methods*; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000209:etiology / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications / Q000473:pathology*; D004195:Disease Models, Animal; D011464:Epoprostenol / Q000378:metabolism; D008297:Male; D008833:Microcirculation; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin / Q000009:adverse effects; D017356:Synchrotrons; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D009569:Nitric Oxide; D013311:Streptozocin; D011464:Epoprostenol