title: Effects of angiotensin-I and ischemia on functional recovery in isolated hearts.
abstract: BACKGROUND
  Cardiac arrest resuscitation can present myocardial dysfunction determined by ischemic time, and inhibition of the angiotensin-converting enzyme (ACE) can reduce cardiac dysfunction during reperfusion.
  
  
  OBJECTIVE
  To investigate the effects of angiotensin-I and different periods of ischemia on functional recovery in isolated rat hearts.
  
  
  METHODS
  Isolated hearts from Wistar rats (n=45; 250-300 g) were submitted to different periods of global ischemia (20, 25 or 30 min) and reperfused (30 min) with Krebs-Henseleit buffer alone or with the addition of 400 nmol/L angiotensin-I, or 400 nmol/L angiotensin-I + 100 μmol/L captopril along the reperfusion period.
  
  
  RESULTS
  The maximal positive derivative of pressure (+dP/dt(max)) and rate-pressure product were reduced in hearts exposed to 25 min ischemia (~73%) and 30 min ischemia (~80%) vs. 20 min ischemia. Left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP) were increased in hearts exposed to 25 min ischemia (5.5 and 1.08 fold, respectively) and 30 min ischemia (6 and 1.10 fold, respectively) vs. 20 min ischemia. Angiotensin-I caused a decrease in +dP/dt(max) and rate-pressure product (~85-94%) in all ischemic periods and an increase in LVEDP and PP (6.9 and 1.25 fold, respectively) only at 20 min ischemia. Captopril was able to partially or completely reverse the effects of angiotensin-I on functional recovery in 20 min and 25 min ischemia.
  
  
  CONCLUSIONS
  These data suggest that angiotensin-II directly or indirectly participates in the post-ischemic damage, and the ability of an ACE inhibitor to attenuate this damage depends on ischemic time.
authors.affiliation: Universidade Federal o Rio Grande do Sul, Porto Alegre, RS, Brazil. biraoliveira@yahoo.com
authors.forename: Ubirajara Oliveira de
authors.initials: UO
authors.lastname: Oliveira
authors.forename: Alvaro Reischak de
authors.initials: AR
authors.lastname: Oliveira
authors.forename: Luiz Carlos
authors.initials: LC
authors.lastname: Kucharski
authors.forename: Ubiratan Fabres
authors.initials: UF
authors.lastname: Machado
authors.forename: Maria Claudia
authors.initials: MC
authors.lastname: Irigoyen
authors.forename: Beatriz D'Agord
authors.initials: BD
authors.lastname: Schaan
mesh_terms: D000704:Analysis of Variance; D000803:Angiotensin I / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D008297:Male; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000187:drug effects*; D013997:Time Factors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000803:Angiotensin I; D002216:Captopril