title: Sympathetic nervous activity and myocardial damage immediately after subarachnoid hemorrhage in a unique animal model.
abstract: OBJECTIVE
  Obvious cardiac dysfunction, including ECG abnormalities and left ventricular asynergy, is known to develop after subarachnoid hemorrhage (SAH). To clarify the close relationship between myocardial damage and sympathetic nervous activity immediately after SAH, a novel experimental animal model was used.
  
  
  METHODS
  SAH was provoked by perforation of the basilar artery with the use of a microcatheter inserted through the femoral artery in 18 beagle dogs. Hemodynamic changes were recorded, and plasma concentrations of noradrenaline, adrenaline, and 3-methoxy-4-hydroxy-phenylethylene glycol (MHPG) and serum levels of creatine kinase-MB (CK-MB) and troponin T were measured at 0, 5, 15, 30, 60, 120, and 180 minutes after SAH.
  
  
  RESULTS
  Noradrenaline (pg/mL), adrenaline (pg/mL), and MHPG (ng/mL) increased abruptly from 120+/-70, 130+/-70, and 1.3+/-0.5 before SAH to 1700+/-1200, 5600+/-3500, and 3.2+/-1.2 at 5 minutes after SAH, respectively. Aortic pressure, left ventricular wall motion, and cardiac output increased by 60%, 40%, and 30%, respectively (P<0.001) at 5 minutes and then decreased by 50%, 55%, and 40%, respectively (P<0.001) >60 minutes after SAH compared with baseline values. The peak value of CK-MB correlated positively with the peak values of noradrenaline and adrenaline (r=0.730 and r=0.611, respectively). The peak value of troponin T also correlated positively with the peak values of noradrenaline and adrenaline (r=0.828 and r=0.792, respectively).
  
  
  CONCLUSIONS
  These results suggest that the elevated activity of the sympathetic nervous system observed in the acute phase of SAH induced myocardial damage and contributed to the development of cardiac dysfunction.
authors.affiliation: Department of Rehabilitation, School of Medicine, Kitasato University, Sagamihara, Japan. tak9999@med.kitasato-u.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Masuda
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Sato
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Narihisa
authors.initials: N
authors.lastname: Matsuyama
authors.forename: Takao
authors.initials: T
authors.lastname: Shimohama
authors.forename: Atsuhiko
authors.initials: A
authors.lastname: Matsunaga
authors.forename: Shuichi
authors.initials: S
authors.lastname: Obuchi
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Shiba
authors.forename: Shinobu
authors.initials: S
authors.lastname: Shimizu
authors.forename: Tohru
authors.initials: T
authors.lastname: Izumi
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001921:Brain / Q000473:pathology; D002533:Cerebral Angiography; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004195:Disease Models, Animal; D018450:Disease Progression; D004285:Dogs; D004562:Electrocardiography; D004837:Epinephrine / Q000097:blood; D006331:Heart Diseases / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics; D007527:Isoenzymes / Q000097:blood; D008734:Methoxyhydroxyphenylglycol / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D020107:Troponin T / Q000097:blood; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D020107:Troponin T; D008734:Methoxyhydroxyphenylglycol; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D009638:Norepinephrine; D004837:Epinephrine