title: Changes in cardiovascular function on treatment of inhibitors of apoptotic signal transduction pathways in left ventricular remodeling after myocardial infarction.
abstract: BACKGROUND
  It has been suggested that apoptosis in cardiac remodeling after myocardial infarction (MI) occurs in cardiomyocytes and is critically involved in the process of postinfarct cardiac remodeling. We investigated the pathophysiological link between myocardial apoptosis and cardiovascular function by modulating apoptotic signal transduction pathways.
  
  
  METHODS
  Either a caspase-3 inhibitor (CasI) or a calpain inhibitor (CalI) was administered immediately after MI in a rat model of MI. Blood pressure (BP), heart rate (HR), and blood flow velocity (BFV) were measured, and pressure-rate product (PRP) was calculated to estimate the changes in cardiovascular function (n=6 for each group).
  
  
  RESULTS
  BFV showed no remarkable changes in any of the groups. Both systolic blood pressure (SBP) and HR changed significantly (P<.01) in the MI+CasI and MI+CalI groups at 1 day after MI and returned to control levels thereafter. In contrast, SBP and HR remained significantly (P<.01) altered in the MI group. PRP in the MI groups was significantly decreased (P<.05 in the MI and MI+CasI groups; P<.01 in the MI+CalI group) at 1 day after MI and returned to control levels at 4 days.
  
  
  CONCLUSIONS
  This study suggests that inhibition of apoptosis during left ventricular remodeling ameliorates cardiovascular function in remodeled hearts.
authors.affiliation: Graduate School of Information Science and Technology, Hokkaido University, Sapporo 060-0814, Japan.
authors.forename: Tadashi
authors.initials: T
authors.lastname: Saitoh
authors.forename: Takayuki
authors.initials: T
authors.lastname: Nakajima
authors.forename: Tatsuhisa
authors.initials: T
authors.lastname: Takahashi
authors.forename: Koichi
authors.initials: K
authors.lastname: Kawahara
mesh_terms: D000818:Animals; D017209:Apoptosis; D001783:Blood Flow Velocity; D002154:Calpain / Q000037:antagonists & inhibitors / Q000378:metabolism; D053148:Caspase 3; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism; D003331:Coronary Vessels / Q000601:surgery; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000201:enzymology / Q000473:pathology; D008026:Ligation; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D020257:Ventricular Remodeling
chemical_list: D061945:Caspase Inhibitors; D004791:Enzyme Inhibitors; D002154:Calpain; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases