title: Flow-induced changes in pial artery compliance registered with a non-invasive method in rabbits.
abstract: OBJECTIVE
  This study was performed: 1) to assess the relationship between blood flow velocity in the internal carotid artery (CBF(ICA)) and pial artery pulsation (cc-TQ) and 2) to evaluate flow-induced changes in pial artery compliance.
  
  
  METHODS
  Experiments were performed on 10 crossbred male rabbits. Heart rate (HR), blood pressure (BP), left ventricle ejection fraction (LVEF), CBF(ICA), the systolic-diastolic blood volume fraction in the brain circulation (CBF(SDF)) and cc-TQ were recorded after glucagon and acetazolamide administration. cc-TQ was measured with near-infrared transillumination back scattering sounding (NIR-T/BSS), LVEF and CBF(SDF) with gated scintigraphy and BP and CBF(ICA) with electromagnetic pressure and flow transducers, respectively. Doses of drugs were chosen to exert a haemodynamic effect but not change BP or intracranial pressure.
  
  
  RESULTS
  Acetazolamide and glucagon evoked significant increases in cc-TQ, CBF(SDF), CBF(ICA), LVEF and HR. The following interdependencies were found: 1) changes after acetazolamide administration compared to baseline: CBF(SDF) vs. LVEF (r=0.73, p<0.05), cc-TQ vs. CBF(SDF) (r=-0.67, p<0.05), cc-TQ vs. LVEF (r=-0.76, p<0.05), 2) changes after glucagon administration compared to baseline: CBF(ICA) vs. BP (r=0.73, p<0.05), CBF(SDF) vs. LVEF (r=0.87, p<0.05), cc-TQ vs. HR (r=0.85, p<0.05), cc-TQ vs. CBF(ICA) (r=-0.74, p<0.05).
  
  
  CONCLUSIONS
  In the absence of systemic BP changes, pial arteries are significantly affected by changes in CBF(ICA). Pial arteries counteract changes in CBF(ICA) and CBF(SDF). The ability of pial arteries to stabilise CBF(ICA) is impaired after acetazolamide administration. Changes in cardiac output directly affect the brain's microcirculation. NIR-T/BSS recordings allow for non-invasive assessment of changes in pial artery compliance.
authors.affiliation: Institute of Human Physiology, Faculty of Health Sciences, Medical University of Gdansk, Tuwima Str. 15, 80-210 Gdansk, Poland.
authors.forename: Andrzej F
authors.initials: AF
authors.lastname: Frydrychowski
authors.forename: Magdalena
authors.initials: M
authors.lastname: Wszedybyl-Winklewska
authors.forename: Tomasz
authors.initials: T
authors.lastname: Bandurski
authors.forename: Pawel J
authors.initials: PJ
authors.lastname: Winklewski
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D001158:Arteries / Q000473:pathology*; D001783:Blood Flow Velocity / Q000502:physiology*; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply; D002560:Cerebrovascular Circulation; D005934:Glucagon / Q000378:metabolism / Q000494:pharmacology; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D008833:Microcirculation; D011817:Rabbits; D014159:Transducers
chemical_list: D000927:Anticonvulsants; D005934:Glucagon; D000086:Acetazolamide