title: Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats.
abstract: BACKGROUND
  The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage.
  
  
  METHODS
  A controlled graded bleeding (6 - 36% loss of estimated total blood volume: ETBV) was performed in streptozotocin-induced diabetic rats (STZ rats) under a conscious state. Hemodynamic and autonomic responses to acute hemorrhage were examined using analysis of BP-HR variability. The effects of dextran treatment after hemorrhage were also examined.
  
  
  RESULTS
  A significant reduction in mean arterial pressure began at 12% ETBV loss in STZ rats and 18% in the control rats, respectively. When blood loss reached 18% of TEBV, the decrease in HR was prominent in STD rats due to the activation of a parasympathetic drive, as indicated by the increase in high frequency (HF; 0.75~3.0 Hz) power in HR variability, while in the control rats this response was not observed. The administration of dextran prevented the activation of the parasympathetic drive in STZ rats during hemorrhaging. In the control rats, the dextran treatment sustained the initial increase in HR with reduced HF power in HR variability.
  
  
  CONCLUSIONS
  STZ rats showed different hemodynamic and autonomic responses to acute hemorrhage from the control rats. STZ rats were prone to develop bradycardiac hypotension characterized by marked parasympathetic activation during hemorrhaging. This finding suggests enhancement of the Bezold-Jarisch reflex in STZ rats. Dextran treatment to maintain a normovolemic hemorrhage state inhibits this reflex.
authors.affiliation: Department of Dental Anesthesiology Osaka University Graduate School of Dentistry, Suita, Japan. bokuaiji@dent.osaka-u.ac.jp
authors.forename: Aiji
authors.initials: A
authors.lastname: Boku
authors.forename: Mitsutaka
authors.initials: M
authors.lastname: Sugimura
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Morimoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hanamoto
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Niwa
mesh_terms: D000208:Acute Disease; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D001794:Blood Pressure; D001919:Bradycardia / Q000209:etiology / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D002319:Cardiovascular System / Q000294:innervation*; D003911:Dextrans / Q000008:administration & dosage; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects; D006454:Hemoglobins / Q000378:metabolism; D006470:Hemorrhage / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology; D008297:Male; D010952:Plasma Substitutes / Q000008:administration & dosage; D051381:Rats; D017208:Rats, Wistar; D012018:Reflex; D015656:Respiratory Mechanics; D013997:Time Factors
chemical_list: D003911:Dextrans; D006454:Hemoglobins; D010952:Plasma Substitutes; D002245:Carbon Dioxide